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GMC > Block 4 - development > Flashcards

Block 4 - development Flashcards

1
Q

define growth

A

increase in size that doesn’t imply development

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2
Q

what is development

A

change with time involving:
morphogenesis - development of shape or form
differentiation - specialisation of function
both are independent of growth

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3
Q

what is embryogenesis

A

it occurs in animals and plants and is where the zygote starts to undergo differentiation and morphogenesis to produce rudimentary structures of the adult

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4
Q

describe the embryonic development of the zebra fish

A

it takes ~40hrs. ordered cell divisions produce various structures of the zebra fish. single cell zygote –> zygote change –> acquired polarity –> first cell division is uneven. this is followed by further divisions and morphogenesis

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5
Q

what is cell polarity

A

acquisition of asymmetry which determines subsequent cell division and fate

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6
Q

why is there a clear difference between the animal and vegetal pole of amphibians

A

because there is a difference in pigment

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7
Q

what happens to the algal zygote upon polarity change

A

it goes from spherical to pear

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8
Q

describe the development of multicellularity in the starfish

A

unfertilized egg –> 2 cell stage –> 4 cell stage –> 16 cell stage –> 32 cell stage

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9
Q

what does organogenesis ensure

A

that all the correct structures are produced in the right place at the right time

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10
Q

differentiation works in parallel with ……….

A

morphogenesis

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11
Q

cell ………… and …………….. are important in morphogenesis

A

movement

adhesion

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12
Q

differentiation is usually due to switching on sets of ….. when a particular cell type becomes established

A

genes

gene expression is a key control in development

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13
Q

what method allows visualisation of protein complexes inside of cells

A

EM methods

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14
Q

what is the forward genetics approach

A

create mutants and isolate, identify the gene that has become mutated, draw conclusion on gene function based on mutant function

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15
Q

what is a homeotic mutation

A

affects specification of organ type

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16
Q

what are 6 advantages of model organisms for genetics

A
  1. small and easy to grow
  2. rapid generation time
  3. lots of progeny
  4. preferably self fertile and able to be crossed
  5. easy to produce mutants
  6. multiple people working on it
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17
Q

what 3 advantages of model organisms for molecular biology

A
  1. small genome - enables full sequencing and gene isolation
  2. easy to genetically transform
  3. methods for isolating genes corresponding to mutants
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18
Q

what is the genome

A

the amount of DNA in the haploid form of the organism

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19
Q

describe c. elegans

A 
small bacterivorous nematode 
simple development 
usually self fertilising hermaphrodites 
3 day life cycle 
easy to manipulate 
short generation time 
lots of progeny 
each gender has exactly the same number of cells 
genome fully sequenced
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20
Q

describe drosophila

A 
male and female flies 
2 week life cycle 
easy to mutate 
learned a lot about pattern formation and morphogenesis from them 
genome fully sequenced
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21
Q

describe Arabidopsis

A 
small flowering plant 
self and cross fertile 
6 weeks life cycle 
genome fully sequenced 
easy to produce mutants 
small genome 
short generation time for a plant
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22
Q

what is fucus

A

brown algae

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23
Q

describe the early development of the fucus zygote

A
  • after fertilisation of the males and female gametes the zygote is immediately apolar
  • after 12hrs asymmetry develops
  • 15hrs - germinating rhizoid
  • 24hrs - first asymmetric division (right angles to the axis of symmetry). the lower cell produces the rhizoid which anchors the plant to the rocks. the upper cell divides further and develops into the thallus
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24
Q

on which side of the fucus plant does the rhizoid develop

A

the shaded side

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25
Q

the rhizoid appears at 12 hrs in the fucus. how and up to what point can the axis of polarity be changed

A

we can change the axis of polarity up to 10hrs

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26
Q

what determines polarity of the fucus - what factors affect it

A

fertilization (rhizoid at entry point)
heat (rhizoid develops at warm side)
pH and salt (rhizoid to alkaline pH and salt)
electrical gradient (rhizoid at -ve pole)

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27
Q

development of polarity is accompanied by production of ..………….. ………….. which generate an electrical potential

A

ionic gradients

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28
Q

how is calcium involved in fucus development

A
  • disruption of Ca gradients prevents polarity development
  • localisation of Ca channels is observed after 5-6hrs illumination
  • there is a Ca influx at the rhizoid end and efflux at the other end. initially Ca channels are evenly distributed but they become localised at the rhizoid end when polarity develops
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29
Q

why are some zygotes already polar upon fertilization

A

it is often due to egg cell gamete

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30
Q

what are localised cytoplasmic determinants

A

they are components in the cytoplasm that affect cell fate

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31
Q

how can we show that a component has an effect on development

A

we need to demonstrate its action e.g. removal or translocation

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32
Q

describe the ascidian regions of coloured cytoplasm

A

ascidian egg has regions of cytoplasm with different coloured inclusions that are linked to cell fate. pigmentation doesn’t control development but is localised in regions that have components that do control development. the cytoplasm contains localised cytoplasmic determinants

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33
Q

what is a downfall of fucus and ascidians as model organisms

A

neither of them allow easy mutant formation

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34
Q

in drosophila how is anterior-posterior polarity established

A

it is established in the eggs

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35
Q

why are body segments important in drosophila

A

they are important for producing organs

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36
Q

what is the egg precursor

A

oocyte

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37
Q

what is the roles of nurse cells

A

they synthesise macromolecules in the ovary that are transported to the oocyte as it develops via cytoplasmic bridges. some macromolecules become asymmetrically distributed

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38
Q

describe the drosophila bicoid mutant

A

the embryo lacks the head and thorax at the anterior end and instead has a second set of posterior structures. it is a single gene mutation. the phenotype can be rescued by injecting WT bicoid mRNA in the anterior end

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39
Q

what is the WT bicoid gene product required for

A

normal anterior development of the embryo. the bicoid mRNA/protein are localised at the anterior. mRNA is asymmetrically distributed so the protein accumulates the same

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40
Q

bicoid mRNA/protein is synthesised in the nurse cells and transferred to the oocyte

A

mRNA

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41
Q

bicoid localisation is established during oocyte development in the …………. …………….

A

maternal ovary

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42
Q

what is a maternal effect gene

A

when the female is responsible for expression of the phenotype of the developing embryo

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43
Q

what are other maternal effect genes involved in determining anterior-posterior polarity in drosophila

A

bicoid and hunchback regulate production of anterior structures
nanos and caudal regulate production of posterior structures

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44
Q

bicoid, hunchback and caudal are …. that regulate other genes controlling later steps in development

A

TFs

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45
Q

polar distribution of bicoid and nanos mRNA is established in the …………

A

ovary

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46
Q

describe the role of bicoid and nanos in drosophila development

A

bicoid and nanos are localised and translationally regulate hunchback and caudal bicoid inhibits translation of caudal mRNA at the anterior pole, resulting in accumulation of caudal towards the posterior. nanos inhibits translation of hunchback mRNA at the posterior so it accumulates at the anterior

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47
Q

describe the distribution of bicoid, nanos, caudal, and hunchback mRNA in drosophila and compare it to the protein distribution

A

mRNA - bicoid at the anterior and nanos at the posterior
hunchback and caudal throughout
protein - hunchback and bicoid at anterior and nanos and caudal at posterior

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48
Q

what is the cytoskeleton

A

an intracellular network of protein filaments of several types - microtubules, actin filaments and intermediate filaments

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49
Q

list some developmental aspects involving the cytoskeleton

A 
acquisition of polarity 
control of cell size and shape 
control of cell division 
intracellular movement of components 
cell movement and adhesion
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50
Q

describe microtubules structure

A
  • composed of alpha and beta tubulin dimers
  • both subunits bind GTP
  • only GTP bound to beta tubulin can be hydrolysed to GDP
  • they consist of 13 protofilaments each of which is a polymer of tubulin dimers
  • they are relatively big structures
  • they undergo continual disassembly and assembly regulated by GTP
  • tubulin dimers bound to GTP are added to the plus end of the microtubule. tubulin dimers are lost from the minus end
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51
Q

what is the microtubule GTP cap

A

it is at the plus end where both subunits of the dimer are bound to GTP

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52
Q

going down the microtubule, ……….. hydrolyses on …… subunits and dimers bound to GDP are lost at the ……. end

A

GTP
beta
minus

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53
Q

what happens to microtubules if [tubulin-GTP] is low

A

the rate of addition at the plus end is low and GTP hydrolysis will remove the GTP cap. Tubulin is rapidly lost from the plus end resulting in complete depolymerisation.

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54
Q

whether a microtubule grows or shrinks is dependent on what

A

[tubulin-GTP]
high –> microtubule growth
low –> microtubule depolymerisation

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55
Q

how can disassembly be seen in microtubules

A

frayed ends

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56
Q

what is the MTOC and how is it different in plants and animals

A

where microtubules assemble and radiate. in animal cells it is the centrosome which contains 2 centrioles. plants don’t have centrosome MTOC, instead they control polymerisation with local ion concentrations

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57
Q

what is microtubule stability affected by

A

low temperature causes depolymerisation

regulated by MAPs - proteins that interact with microtubules e.g. tam

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58
Q

mitosis spindle is made of ……………. - they move chromosomes. microtubules are also involved in movement of …………. and ………….

A

microtubules

vesicles and organelles

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59
Q

describe the process of movement along microtubules

A

it involved motor proteins kinesin and dynein which use ATP hydrolysis to move components to the plus or minus end of the microtubules
- kinesin moves cargo –> +end. it binds to the receptor protein on the vesicle and also to the microtubules. dynein works in the same way but instead moves cargo to the minus end

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60
Q

describe the structure of actin microfilaments

A
  • actin assembles as a filament but is not as large or as complex as microtubules
  • the globular actin monomer is called G-actin and it polymerises into F-actin filaments which can be dimers or trimers and are added to the growing filament
  • the filaments consist of tightly wound helix
  • actin binds ATP or ADP and hydrolysis of ATP follows polymerisation. monomers are added mainly at the + end. monomers bound to ADP are lost from the minus end
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61
Q

what is the effect of cytochalasin B on actin microfilaments

A

it binds at the + end preventing elongation

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62
Q

what proteins can bind to actin and regulate polymerisation and depolymerisation

A
  • cofilin promotes disassociation from the - end
  • profilin promotes ATP binding to actin and polymerisation
  • Arp2/3 proteins act as nucleation sites to stimulate assembly of new filaments
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63
Q

actin filaments can assemble as ………… or ……………… but what is the difference between these

A

bundles
networks
they have different types of cross-linking protein
the bundle is a string or parallel filaments of actin and is very strong
the network has looser cross-linking resembling chicken wire

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64
Q

describe the structure of intermediate filaments

A
  • they are strong but not dynamic
  • they associate with the PM and organelles
  • they are composed of various types of proteins
  • different filaments have the same basic structure N-head-rod-tail-C
  • there are no +/- ends, assembly involves multimerization
  • they are more stable than microtubules and microfilaments
  • they make dimer and tetrameric structures that are assembled into the protofilament –> filament
  • they associate with other cytoskeletal elements, the PM and organelles and help to increase mechanical strength and anchor components
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65
Q

what parts of the cytoskeleton are particularly important for controlling cell shape and explain their role

A

microtubules and actin filaments

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66
Q

explain the role of microfilaments in controlling cell shape

A

actin bundles/networks underlie and support the PM. the actin networks is connected to spectrin cross-linking protein and anchored to the PM by erythrocyte ankyrin (actin network makes shape and PM is spread over it)
actin bundles support microvilli of intestinal epithelial cells

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67
Q

actin microfilaments also have a role in ………… ………… in plants. several mutants in ………… …………. lack ……….. proteins required for normal actin filament production

A

trichome development
trichome development
Arp2/3

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68
Q

which components of the cytoskeleton are important in controlling intracellular movement

A

microtubules and microfilaments

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69
Q

using the bicoid examples explain why intracellular movement is critical in development and the role of the cytoskeleton

A

bicoid is synthesised in the nurse cells and transferred to the oocyte where it becomes localised at the anterior end. this movement is prevented by drugs that inhibit tubulin polymerisation. localisation requires mRNA binding to microtubules via linker proteins. mRNA protein complexes move along the microtubules bound to kinesin motor proteins

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70
Q

what is the cell cycle

A

the process that cells undergo to duplicate their contents to pass onto two identical daughter cells (mitotic). this involves both DNA replication and duplication of cellular constituents and their separation into 2 daughter cells (cell replication + cell division (cytokinesis))

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71
Q

in which is the cell cycle more complicated, eukaryotes or prokaryotes

A

eukaryotes

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72
Q

describe the prokaryotic cell cycle

A
  • takes 20-40 mins in e.coli
  • bacteria have circular DNA molecules
  • cellular growth and DNA replication are continuous throughout the cell cycle
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73
Q

describe prokaryotic DNA synthesis

A
  1. cleavage of DNA to produce 3’ end
  2. synthesis of RNA primer for DNA pol to allow DNA to be primed for creation of the complementary strand
    Other proteins are required e.g. type II
    as the cell gets bigger the DNA is replicated. when the cell reaches a certain size it divides into 2
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74
Q

cells with 2 copies or no copies of DNA …….

A

die

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75
Q

describe the eukaryotic cell cycle

A
  • takes longer - yeast 2hrs, humans 24 hrs - because the cellular constituents are much more complicated and the process is more complex to ensure production of 2 identical daughter cells
  • S phase - DNA replication occurs - NOT continuous
  • G phases - both contain crucial checkpoints
  • M phase - replicated chromosomes are separated into 2 daughter cells
  • cytokinesis - process by which the 2 cells separate
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76
Q

during mitosis chromosomes are condensed/decondensed

during interphase, chromosomes are condensed/decondensed

A

condensed

decondensed

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77
Q

how do we know the eukaryotic cell cycle is a well conserved process

A

proteins from yeast and humans are interchangeable

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78
Q

describe eukaryotic DNA synthesis

A
  • larger genome than prokaryotes s is more complicated
  • the ORC (origin or replication complex) is a complex of proteins which bind to DNA at specific sequences and have many roles in replicating DNA. they bind to DNA in the S phase and are stimulated to cause the replication of DNA. the cell coordinates this so that replication only occurs in the S phase
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79
Q

how is the ORC regulated

A

it is regulated by CDKs which bind to and activate the ORC which stimulates DNA replication in the S phase

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80
Q

what is mitosis and when does it occur

A

chromosome separation after the G2 phase

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81
Q

what are the 4 steps of mitosis

A

prophase, metaphase, anaphase and telophase

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82
Q

what is the product of mitosis

A

2 diploid cells

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83
Q

what happens in prophase

A

centrioles duplicate, centrioles move to poles, mitotic spindle forms

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84
Q

what happens in metaphase

A

chromosomes move to the equator of the cell forming the metaphase plate

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85
Q

what happens in anaphase

A

duplicated chromosomes split and move to opposite poles

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86
Q

what happens in telophase

A

nuclear membrane reforms around the chromosomes at each of the poles. nuclei reform and the cell divides

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87
Q

how can decondensed DNA in interphase be seen

A

if tagged with GFP

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88
Q

what is the first step in allowing mitosis to occur

A

condensation of chromosomes

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89
Q

describe the process of cytokinesis/abscission

A
  • constriction forms and separates the cells
  • contractile ring is made from actin microfilaments and it constricts the equator between the forming cells
  • abscission bridge forms and gets longer until we get a snap and a break which physically separates the cells
    actin ring –> constriction –> abscission bridge –> physical separation
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90
Q

why do we need redundancy in the cell cycle

A

if one mechanism goes wrong another one can compensate - belts and braces

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91
Q

what are the 3 levels of control in the cell cycle

A
  1. transcription - gene expression
  2. protein level and stability
  3. protein activity - post translational modifications e.g. phosphorylation
    they all work in parallel and allow for redundancy
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92
Q

give the sequence of a start codon

A

ATG

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93
Q

give the sequence of a stop codon

A

TAA

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94
Q

what are the 2 types of transcription

A
  • general gene expression - where the gene is transcribed constitutively e.g. housekeeping genes - expression not regulated at all. RNA pol binds to the TATA box in the promotor to produce mRNA. RNA pol is not regulated, it is just constitutively active-
  • specific gene expression - genes are only transcribed at a certain time/place. there is a more complicated promoter and extra TFs. RNA pol still binds to the TATA box. the enhancer is bound by a TF that stimulates RNA pol activity to create RNA but only at specific times (2 TFs control gene expression at particular times/places)
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95
Q

describe the fission yeast

A

unicellular eukaryote that is easy to grow in the lab and is used to study the cell cycle. good model organism. there is huge conservation of controls between yeast and humans.

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96
Q

are all the genes involved in the cell cycle expressed at the same time

A

no, different genes are expressed at different cell cycle times

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97
Q

what is the role of the MBF TF and MCB

A

they regulate gene expression at the end of G1/start of S phase

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98
Q

what is the outcome of MBF TF binding to MCB

A

the MBF complex binds to MCB enhancer DNNA sequence in the promotor and stimulates RNA pol to drive gene expression exclusively during the S phase. there are at least 20 yeast genes controlled like this. in each case there is an MCB with a simple motif: ACGCG. wherever an MCB is, that gene is expressed in the S phase because the sequence is bound by MBF

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99
Q

give 3 examples of S phase genes and their roles

A

cdc22+ - encodes ribonucleotide reductase, essential for making DNA
cdc18+ - encodes an important part of the ORC
cig2+ - G1 cyclin which has an important roles in regulating genes for the cell cycle and is important in controlling progression

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100
Q

mRNA is unstable and almost immediately …………., so we see fluctuation in the cell cycle of mRNA and protein

A

degraded

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101
Q

what is transcriptional control important for

A

cell cycle control

cell economy

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102
Q

describe the process of entering S phase from G1

A

cells don’t enter the S phase unless MBF is active. MBF = E2F in humans. E2F interacts with P53 and Rb and regulates gene expression at the start of S phase like MBF

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103
Q

how are ubiquination and the proteasome involved in regulating protein levels and stability

A

ubiquination causes specific degradation of protein through the proteasome.

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104
Q

why is it important that more stable proteins have a mechanism of being removed

A

because we would get a stepwise increase if they weren’t removed

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105
Q

what is the relationship between CDK1 and cyclin B

A

CDK1 (stable) is a master controller of the cell cycle and its activity is regulated by binding to the cyclin B molecule (unstable). CDK1 is inactive unless bound to cyclin B. binding to cyclin B is crucial for cell cycle progression from G2 –> M (allowed by active CDK1. to exit M CDK1 needs to be inactivated again by cyclin B being ubiquinated and targeted to the proteasome leaving inactivated CDK1

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106
Q

in order to activate CDK1 it needs to be bound by cyclin B but what else must also happen

A

it must be dephosphorylated - modifies protein activity

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107
Q

what are cell cycle checkpoints

A

surveillance mechanisms that ensure the cell cycle doesn’t progress until the previous stage has been completed. they can stop the cell cycle to allow repair mechanisms. checkpoint is only active when there is damage

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108
Q

what is the role of the G2 checkpoint

A

ensure M only occurs after S is complete. a defect in S results in the G2 checkpoint stopping the cell cycle

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109
Q

defective checkpoints are seen in many …………….

A

cancers

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110
Q

what happens when the checkpoint becomes activated

A

when the checkpoint is active due to damage, we see CDK1 inactivation by phosphorylation which leads to a delay in G2 to allow DNA repair then the cell cycle resumes when CDK1 is reactivated after the repair is complete

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111
Q

what is likely to result if damaged DNA enters the M phase

A

cancer

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112
Q

what is the epidermis

A

outer single cell layer covering the organs of the plant

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113
Q

what are the 3 cells types of the leaf epidermis and give a short description of each

A
  • pavement cells - undifferentiated/uncommitted epidermal cells
  • stomatal guard cells - can swell/shrink
  • trichomes - single branched cells projecting from the surface
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114
Q

are differentiated cells distributed evenly across the surface of the epidermis

A

reasonably evenly

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115
Q

describe root epidermal cells

A

there are hair cells and non-hair cells - root hairs are single cells that project from the root epidermis

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116
Q

describe seed epidermal cells

A

no differentiation of cell type

biosynthetic activity to make brown pigments that accumulate in the seed coat

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117
Q

how do we identify genes controlling epidermal cell fate

A

use forward genetic approach

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118
Q

what are common phenotypes of trichome mutants - how many genes have been identified to be involved in trichome development

A

altered in number, distribution or morphology of trichomes

25 genes can mutate and alter trichome development

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119
Q

describe the gl1 and ttg1 mutants and compare to WT

A

they have no trichomes. the WT genes are required for commitment of a leaf epidermal cell to differentiate into a trichome i.e. they are regulators of epidermal cell fate

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120
Q

what is the gl1 gene product

A

it is a TF that switches on genes to express trichomes

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121
Q

what is the ttg1 gene product

A

it is a protein that bind to GL1 and is required for GL1 action

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122
Q

describe gl3 mutants and the WT function

A

they have fewer trichomes than WT, so WT GL3 protein regulates trichome cell fate. GL3 is a TF that forms a protein complex with TTG1 and GL1.

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123
Q

describe the GL3, GL1 and TTG1 complex

A

the complex is a positive regulator that switches on genes in the trichome differential pathway. target genes include other TFs
complex –> target genes –> trichomes

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124
Q

why does the GL3 mutant still have some trichomes

A

there are other genes that have proteins similar to GL3. when GL3 is mutated, these proteins can take over the function - functional redundancy. the same function is carried out but not as well

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125
Q

what is the outcome when the GL3, GL1 and TTG1 complex is overexpressed

A

we see overproduction of trichomes

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126
Q

what happens if GL3 is overexpressed

A

there is more positive regulator and the transgenic plants are very hairy because there is more epidermal commitment to trichomes

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127
Q

what other signal do cells that commit to form trichomes produce

A

signals that repress trichome formation in adjacent cells i.e. negative regulators

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128
Q

describe triptychon and caprice mutants

A

they lack repressive signal that prevents trichome clustering

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129
Q

what are TRY and CPC

A

they are TFs that cause repression of trichomes

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130
Q

what is the number of trichomes on the surface of the leaf a compromise between

A

positive and negative signal

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131
Q

describe dis mutants

A

they have abnormal trichome morphology

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132
Q

the genes for morphogenesis function upstream/downstream of commitment genes

A

downstream

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133
Q

crossing mutants altered in commitment and morphogenesis results in …………..

A

epistasis

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134
Q

the genes altered in commitment ………… the effect of the genes in downstream morphogenesis

A

override

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135
Q

what is the phenotype of the gl1 and dis1 double mutant and provide an explanation

A

no trichomes - gl1 is epistatic to dis1. GL1 functions before DIS1 morphogenesis in the trichome differentiation pathway

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136
Q

of 2 genes the epistatic gene normally comes first/second in the pathway

A

first

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137
Q

are stomata evenly spaced over the leaf epidermis

A

yes

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138
Q

what are speechless, mute and fama

A

they are 3 TFs that control steps in stomatal formation - speechless initiates stomatal morphogenesis (commitment)
- mute and fama control later steps in stomatal development

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139
Q

describe the tmm mutant and the inferred WT function

A

it has clusters of stomata so WT controls spatial distribution of stomatal production

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140
Q

are mutants of stomatal development altered in trichome function

A

no, and trichome mutants are not altered in stomatal development. fates of leaf trichome and stomatal cells are controlled independently

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141
Q

in contrast to leaf hairs, root hairs arise in a ………… dependent manner

A

position

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142
Q

describe the commitment of a cells to become a root hair

A

we need positive regulators to commit epidermal cells to make root hairs. hair cells arise at junctions between adjacent cortical cells (under the epidermal cells). positional information is transmitted from the cortical cells to the epidermal cells. the positional and positive signals work together to produce hair

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143
Q

the root has files of ………… and …….-………. cells

A

hair

non-hair

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144
Q

where are cortical cells found

A

under the epidermal cells

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145
Q

describe the wer mutant and its inferred WT function

A

it shows ectopic root hair production - produces hair from non-hair cells. WT wer represses hair formation in non-hair cells i.e. it specifies non hair cell fate

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146
Q

what is the wer gene product

A

it encodes a TF and is expressed in non hair cells to switch on a gene that produces a repressor of hair production
WER –> repressor –I hair (non-hair cell)

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147
Q

other than the wer mutant, what other mutant has ectopic root hair production and what does this indicate about its function

A

ttg1 mutant - therefore ttg1 like wer specifies non-hair cell fate.

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148
Q

describe how wer/ttg1 are involved in root hair production

A

non hair cells produce a signal that represses the action of wer/ttg1 in adjacent cells. also a signal from cortical cells inhibits wer expression in hair cells - positional information.
non hair cell: wer/ttg1 –> repressor –I hair
hair cell: signal from non hair cell and cortical cells prevents production of the repressor so we get hair
in non hair cells, if either of wer/ttg1 is mutated we don’t get the repressor and we get hair production
(see diagram)

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149
Q

list the 3 types of epidermis that ttg1 works in

A

leaf, root and seed

150
Q

how is ttg1 involved in the seed epidermis

A

ttg1 associates with TFs to control synthesis of the brown pigments called condensed tannins. ttg1 mutant doesn’t make brown pigment so WT is required for the pigment biosynthesis. ttg1 facilitates the action of TFs, without this we don’t get brown pigment

151
Q

what are the 2 initial steps in morphogenesis and give a short explanation of both

A
  • acquisition of polarity - (sometimes already established in the female gamete) - involves spatial distribution of regulatory factors i.e. localised cytoplasmic determinants that control morphogenesis
  • pattern formation - development of structure, shape and form but in a predictable pattern manner
152
Q

in drosophila, pattern formation in the embryo results from sequential expression and action of sets of ………… Expression of …………. …………. ………… establishes gradients of TF distribution in the oocyte. Cascade of TF activities determines pattern formation

A

TFs

maternal effect genes

153
Q

explain how the initial distribution of TFs in the embryo determines subsequent events

A

the pattern of TF activity leads to production of body segments (14 body segments).expression of TFs in the segments determines segment specific patterns of organ formation, pigmentation etc
maternal affects genes –> segmentation genes –> 14 segments –> organs

154
Q

what are the precursors of body segments

A

14 parasegments

155
Q

what are the 3 types of segmentation gene and how do they interact with each other

A

gap genes regulate expression of pair-rule genes, which regulate segment polarity genes

156
Q

describe the distribution of gap gene, kruppel

A

expressed in broad transverse band covering a number off different parasegments as a result of the distribution of bicoid, hunchback, nanos and caudal TFs. distribution of maternal effect proteins that positively/negatively regulate kruppel transcription determine the pattern of expression

157
Q

how are other gap genes switched on

A

by other relative concentrations of TFs, so, in different positions along the developing embryo

158
Q

what is Kruppel and describe the mutant phenotype in drosophila

A

it is a TF that regulates pair rule genes. the mutant lacks series of segments as pair rule genes are not switched on which leads to abnormalities in the mature fly

159
Q

give 2 examples of pair rule genes and describe their expression distribution along with the mutant phenotype

A

even skipped (eve) (odd numbered parasegments)
fushi-tarazu (ftz) (even numbered parasegments)
they are both expressed in 7 stripes. the expression is dependent on gap genes TF giving positive/negative effects on transcription.
eve and ftz both regulate segment polarity genes.
the mutants lack parts of segments which alters pattern formation in the mature fly

160
Q

give an example of a segment polarity gene and describe the pattern of expression

A

engrailed gene - expressed in 14 stripes (in every parasegment). the pattern of expression is determined by the pair rule genes TFs

161
Q

describe the ftz mutant in terms of the segment polarity genes

A

the ftz mutant doesn’t express engrailed in even numbered parasegments.

162
Q

describe mutants of engrailed

A

they have duplications or defects in each segment which leads to abnormalities in the mature fly

163
Q

what do segment polarity genes ultimately regulate

A

morphogenesis of segments - organ formation - further TFs control the cascade

164
Q

describe the cells movement in the blastocoel

A

cell movement occurs in the blastocoel to rearrange the cells as we get gastrulation

165
Q

describe the developmental steps from zygote to gastrula

A

zygote (cleavage) –> 8 cell stage (cleavage) –> blastula (morphogenesis) –> gastrulation (invagination) –> gastrula

166
Q

what are the germ layers of the gastrula

A

endoderm
mesoderm
ectoderm
(the gastrula also contains the blastopore and the blastocoel)

167
Q

cells in the blastocoel rearrange by ……………. to form embryonic tissue layers during gastrulation

A

migration

168
Q

compare morphogenesis of plants and animals

A

both have commitment of cells and TF cascades in pattern formation
adjacent plant cells are fixed together via their walls. therefore,, cell movement and migration isn’t a feature of plant morphogenesis. instead plant morphogenesis involves:
- control of which cells undergo division
- control of orientation of plane of division
- control of direction and extent of cell expansion

169
Q

how is the cytoskeleton involved in plant cell division

A

the cytoskeleton regulates the plane of division through the pre-prophase band of microtubules. the ppb disappears and the microtubules reappear in the spindle. normal mitosis occurs and the chromosomes move to the poles of the cell and the microtubules reorganise into the phragmoplast. the phragmoplast microtubules then assemble the PM and cells wall (they recruit the cell plate - developing cell wall)

170
Q

what is the pre-prophase band of microtubules

A

a band of microtubules that marks the orientation of the plane of cell division

171
Q

why is the plane of division not always regulated

A

because it is not important in all cells

172
Q

what is the phragmoplast

A

an accumulation of microtubules which marks the original position of the ppb

173
Q

in plants the plane of division is pre-determined by ……

A

ppb

174
Q

why are ppb not found in animal cells

A

because animal cells can divide and move around so there is much less requirement to control the plane of division

175
Q

a committed leaf epidermal cell divides …………. (controlled by ………) to produce a small cell (…………..) that will divide further to produce the ………. ……. ……… and adjacent cells. the GMC divides longitudinally (………….) to form the ……. ……. The other cell divides and produces daughter cells that will be next to the ………. ……….. ………

A 
asymmetrically 
ppb
meristemoid 
guard mother cell 
symmetrically 
guard cells 
stomatal guard cell
176
Q

what is the function of speechless in stomatal development

A

TF required for initial commitment to produce meristemoid

177
Q

what is the function of mute in stomatal development

A

TF that controls generation of GMC from the meristemoid

178
Q

what is the function of fama in stomatal development

A

TF that regulates GMC cell division

179
Q

describe the process in developing a root hair

A

root hair committed cells show localised cell wall weakening followed by localised outgrowth of the PM, deposition of new cell wall material and nuclear migration into the hair. cell expansion is contributing to morphogenesis because root hairs alter morphogenesis

180
Q

control of which 2 processes in particular is important in root hair development

A

control of direction and extent of cell expansion

181
Q

what factors can affect root hair development

A
  • low pH stimulates cell wall loosening by activating expansins that break bonds between polysaccharides
  • auxin stimulates acidification and hence expansion (activates H+ pumps through gene expression
182
Q

describe the process of auxin and GA extension growth

A
  • unidirectional light causes phototropism (growth towards light). this involves auxin accumulating on the shaded side –> differential growth –> bend
  • photoreceptors suppress extension through the activity of growth regulators like auxin in response to light
  • auxin and GA promote extension. GA overcomes DELLA proteins that repress extension by inhibiting growth promoting TFs. light promotes an increase in DELLAs and GA destruction. Binding of GA to its receptor (G1D1) enables it to interact with DELLA proteins causing them to be targeted for proteolytic destruction. in the absence of light GA gets rid of DELLA to allow extension
183
Q

in drosophila, at the end of embryo development, we have all the components to make the adult fly. what is different compared to this in plants

A

in plants we end up with a very rudimentary structure. we see cotyledons, a stem and a rudimentary root and all the organs are produced subsequently

184
Q

what are meristems

A

small groups of dividing cells which produce most of the cells of the organism. they are found at the root/shoot apex as root/shoot apical meristems. meristems contain stem cells in a perpetuated undifferentiated state and have the capacity to produce new cells of the organism. they don’t differentiate but divide into cells that do.

185
Q

other than the root/shoot apical meristems what other type of meristems are there

A

lateral meristems which give rise to branches

186
Q

what are the 2 tissue types of the shoot meristem and give a short description of each

A

tunica - 2 layers of cells that cover the dome of the meristem (growing as the meristem and shoot grow
corpus - below the tunica and contains stem cells

187
Q

anticlinal divisions are found in the tunica layers of the shoot meristem. describe these divisions

A

the divisions are at right angles to the surface so we are gradually increasing the cell number that is covering the dome

188
Q

what kind of divisions are seen in the corpus of the shoot meristem

A

anticlinal and periclinal. anticlinal increases width and periclinal increase length of the meristematic region

189
Q

what happens spatially when cells divide in the meristem to allow the meristem to produce leaves

A

they are pushed laterally to produce a region of cell division which can give rise to leaf structures. we get production of leaf primordia

190
Q

describe the process of leaf formation from shoot meristems and how they form in the correct spatial orientation (organogenesis)

A
  • leaf primordia develop laterally from the shoot apical
  • leaf primordia divides and expands to produce the different tissues of the leaf
  • there is positional information in the meristem to ensure that leaf primordia are produced in the right positions (spiral arrangement of leaf primordia)
191
Q

what is phyllotaxy

A

it is the arrangement of leaves around the apex (genetically determined)

192
Q

define the L1, L1, CZ, PZ and RZ zones of the meristem

A

L! and L2 layers are the tunica which covers the shoot apical meristem
CZ is the central zone in the corpus where the SC are
PZ is the peripheral zone
RZ is the rib zone

193
Q

what happens in the meristem when SCs divide

A

when the CZ SCs divide they produce daughter cells both laterally and below. lateral cells go into the PZ and the cells below go into the rib zone. the cells start to differentiate in the PZ and RZ.

194
Q

how are SCs defined and how is the SC population in the meristem maintained

A

stem cells are defined by their position in the meristem (any cell in the CZ will be a SC, if the CZ size changes so would the size of the SC population. the population is maintained by wus - it regulates genes that regulate SC

195
Q

what is the phenotype of wuschel gene mutants

A

they lack functional SCs. it has cotyledons and a rudimentary stem and root but fails to differentiate other organs

196
Q

what is the WT function of the wus gene

A

it encodes a TF expressed just below the CZ. it is essential to generate the SC population and maintain the SC. it regulates genes that regulate SC. wus induces expression of genes characteristic of SC (positive regulator of SCs)

197
Q

what is CLAVATA3

A

stem cell gene expressed in the CZ where the SC are located

198
Q

describe the phenotypes of CLAVATA 1,2,3 mutants and the inferred WT function of the CLV genes

A

they have enlarged meristems because they accumulate SC, so CLV genes control SC population size (negatively regulate size). wus expression is also expanded in mutants of CLV so CLV must suppress wus in the WT

199
Q

describe the relationship between SC and wus that controls SC population

A

SC negatively regulate wus and wus positively regulates SC. the size of the population is controlled by the balance of positive signals from the organizing centre to the SC and negative feedback from the SC to the organising centre

200
Q

how do we know that the organising centre specifies formation of the SCs

A

wus is expressed before CLV3 expression appears

201
Q

what maintains the SC population in the seedling

A

wus/CLV relationship

202
Q

describe the basic process of the reproductive transition at the shoot apex

A

vegetative meristem –> inflorescence meristem –> each produce a single flower
- vegetative shoot receives signals to convert to a reproductive meristem. it stops producing leaves and starts producing inflorescences. inflorescence meristem grows and laterally produces floral meristems, each of which produces a flower

203
Q

what are inflorescences

A

structures that bear flowers

204
Q

describe the phenotype of lfy mutants and the inferred WT function

A

they have partial conversion of floral meristems into vegetative meristems so the WT promotes floral meristem identity

205
Q

what is antirrhinum majus

A

it is a plant used to study floral development and mutations are generated by movement of transposable elements

206
Q

what is a transposable element

A

piece of DNA which copies itself and excises out of the genome and potentially re-excises elsewhere in the genome. they encode transposase (which cuts the TE borders). we can speed up the TE movement by moving plants to a lower temperature

207
Q

describe the phenotype of the antirrhinum majus flo mutant and the inferred function of the WT gene

A

flo mutant shows conversion of floral meristems to vegetative meristems, so WT flo is involved in promoting floral meristem identity, similar to lfy in Arabidopsis

208
Q

what are the 4 organs of the flower

A

each floral meristem produces the appropriate number/type of floral organs in the correct positions. organs:

  • sepal (form flower buds)
  • inside the sepals are the petals
  • inside the petals are the stamens (male organs)
  • in the centre is the carpel (female organ)
209
Q

how are the flower organs organised

A

in 4 whirls

210
Q

describe the Arabidopsis apetela 3 mutants

A

single gene mutant - no petals or stamens

lacks gene B

211
Q

describe the Arabidopsis agamous mutant

A

single gene mutation - no male or female organs but lots (more than WT) of petals and sepals
lacks gene C
the mutant terminates floral meristem activity by inhibiting wus. without wus there is no SC production and no organ formation

212
Q

what type of mutations are the apetela and agamous mutations classed as

A

homeotic mutations

213
Q

what are homeotic mutations

A

they result in the incorrect positioning and number of organs

214
Q

describe the ABC model for flower morphogenesis

A
  • it was created by studying mutants
  • 3 genes - A, B and C all encode TFs that regulate floral organ genes
  • outermost whirl - A - specifies sepals
  • second whirl - A and B - specifies petals
  • third whirl - B and C - specifies stamens
  • fourth whirl - C only - specifies carpels
215
Q

what happens when a plant lacks expression of gene C

A

expression of gene C inhibits gene A and vice versa. by lacking C, A can now be expressed in all whirls. we get more petals from whirl 3 because A is expressed instead of C and the same thing happens in the 4th whirl and we get extra sepals

216
Q

C provides a stop signal for floral organ production, what does this mean for C mutants

A

in a C mutant there is no stop signal in the 4th whirl and the floral meristem keeps producing floral organs and the only ones it can produce are sepals and petals which are produced indefinitely

217
Q

what is the phenotype of plant mutants lacking A

A

they only have carpels and stamens

218
Q

describe the pattern of expression of A, B and C flower genes

A

they are expressed in the expected pattern of localisation from the ABC model

219
Q

morphogenesis in plants works through ………….

meristems determine the pattern of expression of genes which determines ……………. formation

A

meristems

organ

220
Q

what is the difference between morphogenesis in plants and animals

A

animals - TF cascade –> segments

plants - involves meristems and TF cascade

221
Q

give an examples of a protein hormone

A

insulin

222
Q

give an example of a peptide hormone

A

ADH

223
Q

give 2 examples of steroid hormones

A

estradiol and testosterone

224
Q

what is adhesion

A

when we combine sticking with signalling - selective

225
Q

what is juxtacrine signalling

A

when the receptor and ligand are brought together by contact

226
Q

what is the cause of Alzheimer’s and how does it come about

A

gamma secretase is involved in proteolytic cleavage of the amyloid beta precursor protein, creating the AB peptide, believed to be the causative agent of Alzheimer’s

227
Q

what kind of body plan does c.elegans have

A

tripoblastic

228
Q

where are the c.elegans gonads

A

between the body wall muscle layer and the intestine

229
Q

why is it useful that c.elegans are transparent

A

we can see all cell divisions and kill individual cells with lasers

230
Q

what is the cell lineage

A

the pattern of cell divisions

231
Q

how many somatic cells does the adult hermaphrodite and adult males c.elegans have

A

hermaphrodite - 959
male - 1031
and the map of cell divisions is largely invariant

232
Q

in c.elegans, how many larval stages are involved in egg –> adult

A

4

233
Q

name the 4 gonad cells stating their function

A

Z2, 3 - germline stem cells - make gametes

Z1, 4 somatic tissue of the gonad

234
Q

describe the divisions that take place from the Z1 and Z4 cells

A

Z1 and Z4 divide to produce 12 somatic cells by L2. Z1ppp and Z4aaa are great granddaughters of Z1 and Z4 respectively. they form an anchor cell (AC) and a uterine cell (VU). only one of each is always formed

235
Q

what happens at a cellular level in c.elegans upon L1 –> L2

A

germline cells are the same, Z1 and Z4 have undergone 3 divisions each to produce 12 cells. Z1ppp - 3 posterior divisions from Z1. Z4aaa - 3 anterior divisions from Z4. Z1ppp and Z4aaa will always sit adjacent to each other

236
Q

what experiments were done to investigate the control in production off the AC and VU cells

A

Z1ppp and Z4aaa differentiation - all killing by laser ablation

  1. leave all cells –> AC and VU always - never both
  2. kill all but Z1pp or Z4aaa –> always gives AC
  3. kill either Z1ppp or Z4aaa –> always get AC
  4. kill everything but Z1ppp and Z4aa –> always AC and VU
237
Q

what do the experiments on Z1ppp and Z4aaa differentiation tell us

A

Z1ppp and Z4aaa talk to each other

Ac is default state

238
Q

why is it likely something in the gonad that affects the differentiation of Z1ppp and Z4aaa cells

A

because it is surrounded by a thick basement membrane and it is unlikely a small molecule would get through

239
Q

in a screen for mutants with defect in AC/VU cell fate what 2 genes were identified. describe the phenotype

A

lin12
lag2
they both have the same phenotype. LOF mutations of either cause 2xAC cells and no VU cells. since the mutants fail to make a VU cell, their normal function is to make a VU cell

240
Q

what is the product of the lin12 gene

A

lin12 - the LIN12 protein is a TM receptor

241
Q

what is the product of the lag2 gene

A

lag2 - the LAG2 protein is a TM ligand that binds to the lin12 receptor

242
Q

describe the juxtacrine signalling of Z1pppa and Z4aaa in terms of lag2 and lin12 activation and differentiation

A
  • initially lin12 and lag2 are induced and go through the secretory pathway to end up on the cell surface
  • low levels of both lag2 and lin12 to start with
  • randomly, more lin12 is activated sooner in one cell than the other. activated lin12 turns on more lin12 and turns off lag2 (amplification and feedback).
  • the random unstable difference becomes stable and irreversible
  • one cell completely activates lin12, lacking lag2, and the other cell does the opposite. active lin12 is needed to keep making lin12 (unstable). lag2 is made when lin12 is off. lin12 cannot be activated without lag2on the other cell. either cell can make either type but we are guaranteed to make both
  • lin12 on –> AC
  • lag2 on –> VU
243
Q

what is the drosophila name for lin12

A

notch

244
Q

what is the lin12 pest sequence

A

it is a single protein sequence at the carboxy terminal end that targets a protein for degradation - allows for rapid turnover

245
Q

what is the lag2 drosophila name

A

DELTA

246
Q

how is notch activated

A

by binding to delta through repeats (juxtacrine signalling)

247
Q

what happens when notch is activated by binding to delta

A

we get ligand induced proteolytic cleavage just outside the membrane and presenilin (protease that is a component in the gamma secretase complex) mediated cleavage inside the membrane. the notch fragment interacts with protein CSL and activates target genes. Notch receptors are also TFs

248
Q

what is presenilin needed for in the notch signalling pathway

A

it is needed to release the intracellular domain so it can carry out its signal transduction

249
Q

what parts of mammalian development is notch important in

A

development of heart, angiogenesis, neurogenesis, intestinal cell differentiation (regulates proliferation/differentiation of intestinal SC) etc

250
Q

mutant versions of the notch receptor can be …………. Activating mutations are found in many human ….. …….…………….. …………/…………..

A

oncogenic

T acute lymphoblastic leukaemia/lymphoma

251
Q

…… signalling can repair myocardial injury

A

notch

252
Q

what is the problem with blocking the gamma secretase as an Alzheimer’s treatment

A

it reduces AB peptide but also blocks notch signalling which leads to the intestines falling apart

253
Q

what is meant by cell adhesion being xenophobic

A

differentiated cells only stick to the same cell type

254
Q

what structures are involved in cell-cell adhesion

A

desmosomes and adherens junctions - specific areas where sticky molecules relate to

255
Q

what structures are involved in cell-ECM adhesion

A

hemidesmosomes - exist at basement of cells where they contact the ECM

256
Q

describe adherens junctions

A

cadherins adhesive component

connect to actin

257
Q

describe desmosomes

A

cadherins adhesive component

connect to intermediate filaments

258
Q

describe hemidesmosomes

A

integrins adhesive component

connect to EM collagens, lamin, fibronectin etc

259
Q

different cells types have the same/different adhesion molecules

A

different - cell have signature mixes of adhesion molecules. this permits identification of and adherence to similar cells

260
Q

what does beta catenin do

A

it regulates the interplay between adhesion and cell behaviour

261
Q

what are homophilic interactions in terms of adhesion

A

the same cadherins stick together

262
Q

what are the ligands for integrins of hemidesmosomes

A

ECM proteins

263
Q

what are the 2 types of integrins

A

alpha and beta - different pairings of the 2 types provides specificity

264
Q

the beta subunit of integrins can form cytoskeleton attachment to …………

A

actin

265
Q

how many alpha and beta type of integrins are there

A

7 alpha and 5 beta

266
Q

what happens when integrins bind to the ECM

A

signalling molecules are recruited - different integrins cause different outcomes

267
Q

what are ras and src

A

oncogenes

268
Q

upon adhesion what does cell signalling do

A

it tells the cell that it has stuck to the right thing

269
Q

explain why cell adhesion is structural and regulatory

A

it involves gluing (structural) and juxtacrine signalling (regulatory)

270
Q

in what 2 ways can adhesion alter cell behaviour

A

via signalling pathways and cytoskeleton changes

271
Q

what is necrosis

A

accidental death of cells and living tissue. generally results in swelling and bursting of the cell, release of digestive enzymes from lysosomes, and local inflammatory response

272
Q

what is apoptosis

A

a regulated controlled cell death process. the cell becomes rounded, chromatin condenses and then fragments. phagocytes are attracted. membrane bound apoptotic bodies form. apoptotic bodies are phagocytosed. cellular contents are not released so no inflammation

273
Q

what are the cellular changes seen in apoptosis

A 
DNA fragmentation 
membrane blebbing (reducing size of cellular but they're still membrane bound)
274
Q

inter-nucleosomal DNA fragmentation is a classic sign of apoptosis/necrosis in mammals

A

apoptosis

275
Q

describe the process of DNA being fragmented in apoptosis

A

chromosomal DNA is cut up by a non-specific nuclease. we get a ladder of small fragments. the fragmentation is a result of the chromatin structure. the linker DNA is cut by the endonuclease. the smallest fragments are the distance between one nucleosome and the next. the cell can’t recover - irreversible

276
Q

what is tunnel staining

A

labels free ends of broken DNA strands. the more chopped up –> the more fluorescence

277
Q

what process removes the tissue between our fingers and toes, playing a critical role in limb morphogenesis

A

apoptosis - cell death in the mesenchyme of interdigital spaces accompanies the formation of free digits

278
Q

explain why apoptosis is essential for the immune system

A
  • negative and positive selection requires apoptosis (removal of unreactive and autoreactive lymphocytes)
  • removal of excess B lymphocytes requires apoptosis
  • removal of proliferated B lymphocytes after infection requires apoptosis
279
Q

what can enhanced lymphocyte apoptosis result in

A

it can cause immunodeficiency

280
Q

what can result from inhibition of apoptosis in the immune system

A

autoimmunity or lymphoma

281
Q

how is apoptosis involved in neurogenesis

A

half of the healthy neurons born in brain development undergo apoptosis
motor neuron survival depends on synapse with muscle. more powerful input destabilises less powerful input. there is selection for the strongest synapses and these survive

282
Q

how many cells in c.elegans are born only to undergo apoptosis

A

131

283
Q

describe the c.elegans ced-1 mutant

A

the 131 cells are not engulfed by phagocytosis. worms with the extra cells are viable in the lab with no other obvious phenotype

284
Q

what happens to c.elegans if we lose ced-3 or ced-4

A

there is no apoptosis and the 131 extra cells live

285
Q

what happens to c.elegans when we lose ced-9

A

all cells apoptose

286
Q

what is ced-4 equivalent to in mammals and what does it do

A

it is homologous to APAF-1 and activates downstream caspases

287
Q

what is a caspase

A

a class of protease

288
Q

what is ced-3 and what is it equivalent to in mammals

A

it is a caspase homologous to mammalian caspases

289
Q

what is the relationship between ced-3 and ced-4

A

ced-3 is present in all cells. it is regulated by the protein encoded by ced-4. ced-3 stays inactive without ced-4 activation.

290
Q

what is the relationship between ced-4, ced-3 and ced-9

A

ced-4 is negatively regulated by ced-9. if we remove ced-9 function, ced-4 activates which activates ced-3
- ced-9 –I ced-4 –> ced-3 –> apoptosis

291
Q

where id ced-9 found and what does it do to ced-4

A

it site on the surface of the mitochondria in c.elegans and sequesters ced-4 and prevents it interacting with ced-3

292
Q

what does ced-4 do to ced-3 when they interact

A

it physically changes ced-3s conformation. it undergoes an autoregulated internal proteolytic cleavage which activates the cysteine protease (caspase) of the protein

293
Q

proteases are made of …………… that are inactive. they are activated only when needed

A

pro-proteins

294
Q

what is the human equivalent of ced-9

A

bcl2

295
Q

what happens when bcl2 negative regulation is removed

A

if the negative regulation is removed by an upstream protein, part of the process results in cytochrome C being released from the mitochondria - part of the activation process of APAF1 –> caspase –> apoptosis

296
Q

ced-9/bcl2 are proapoptotic/antiapoptotic

A

antiapoptotic

297
Q

EGI-1 and other BH3 only members of the bcl2 family are pro-apoptotic/antiapoptotic

A

proapoptotic

the balance between proapoptotic and antiapoptotic makes the life/death decision

298
Q

where is oncogenic bcl2 often overexpressed and what does this cause

A

B cells - a translocation takes place adjacent to the immunoglobulin heavy chain enhancer. this causes follicular lymphoma (B cell lymphoma). B cells cannot apoptose

299
Q

list factors that can induce apoptosis

A

DNA damage, oncogene activation, unfolded proteins, loss of growth factor stimulation, gain of TGF beta signalling (predominantly anti-proliferative role)

300
Q

what is p53 and what does it do

A

tumour suppressor - it protects against cancer and can induce apoptosis. it integrates multiple stress/damage sensing systems in the cell and can activate the death pathway

301
Q

what is the p53 response to moderate damage

A

induce DNA repair and the cell returns to normal

302
Q

what is the p53 response to severe genome damage

A

senescence

303
Q

what is the p53 response to sever genome damage and hyperproliferation

A

apoptosis

304
Q

what are some functions of TGF beta signalling

A

it has tumour suppressor functions, is involved in cell division, dorsal ventral specification, growth control (inhibition of cell division), cellular homeostasis (promoting apoptosis in some breast cell tissues). how a cell responds to TGF beta signalling depends on its context

305
Q

how is TGF beta involved in cancer

A

many tumours have either inactivating mutations in TGF beta receptors or smad proteins. most pancreatic cancers have a deletion in the gene encoding smad 4. many cancers are unresponsive to TGF beat growth inhibition. mutations block TGF beta signalling, causing resistance to growth inhibition and failure to undergo TGF beta mediated apoptosis

306
Q

smad genes act up/down stream of TGF beta

A

downstream

307
Q

TGF beta is a critical extrinsic/intrinsic regulator of apoptosis in the developing limb

A

extrinsic

308
Q

what are the 3 hallmarks in apoptosis

A

decision to die –> dying process –> dead cell

309
Q

what are the 3 principle axes of the body

A

anterior/posterior - defines mouth and anus
dorsal/ventral - defines back and front
left/right - defined automatically once A/P and D/V are established

310
Q

what is gastrulation

A

a movement and reorganisation of cells from the blastula that is linked to creation of 3 layers of SC - ectoderm, mesoderm, endoderm

311
Q

all ..………. are tripoblastic

A

bilateria

312
Q

what is meant by tripoblastic

A

have a mouth, gut and anus (A/P), a back and front (D/V) and a left and right

313
Q

when are the 3 body axes in c.elegans established and what defines them

A

from the first 2 cell division we create 4 cells where the A/P and D/V and L/R axes are already established
D/V - vulva on ventral side
L/R - 20 epidermal cells at either side

314
Q

in c.elegans there is symmetry and ……….. symmetry

A

broken

315
Q

the hermaphrodite c.elegans has 2 arms to the gonad whereas the male only has one - what process allows for this

A

apoptosis kills off the other part of the gonad in males

316
Q

describe the c.elegans body muscle symmetry

A

4 segments each with 2 internal segments

317
Q

describe the broken symmetry in c.elegans

A

intestine displaced to one side and the gonads to the other

318
Q

in c.elegans the unfertilised egg has polarity/non polarity

A

no polarity

319
Q

what defines the posterior end of c.elegans

A

sperm entry

320
Q

describe the 2 cell stage of c.elegans

A

there is an AB cell at the anterior end and a P1 cell at the posterior end

321
Q

describe the 4 cell stage of c.elegans

A 
ABp cell at the dorsal side 
EMS cell at the ventral side 
ABa at the anterior side 
P2 at the posterior side 
P1 --> P2 + EMS 
AB --> ABa + ABp
322
Q

describe the 1st cell division in c.elegans

A

it is asymmetric

AB is larger and molecularly distinct from P1

323
Q

the point of sperm entry determines the posterior end OR the point of sperm entry is defined by the posterior end

A

the point of sperm entry determines the posterior end

324
Q

describe the PIE-1 mutant and its WT function

A

PIE-1 is a maternally supplied c.elegans protein present in the oocyte. in the mutant the P2 cell is transformed into a second EMS cell. the mutant has 2xEMS cells and no posterior end. EMS makes 20 epidermal cells but we get 40 in the mutant. PIE-1 WT role is to define the difference between a posterior cell (P2) and EMS (ventral cell)

325
Q

what happens when sperm enter the egg in c.elegans

A

pseudodivision - cleavage furrow makes it look like division is about to occur. the sperm and egg nuclei then fuse then the 1st cell division occurs. PIE-1 concentrates in the posterior end

326
Q

…… ……………… segregate to P1 then P2

A

P granules

327
Q

how do PIE-1 become distributed after fertilization

A

it is segregated to P1 then P2 and rapidly degraded in EMS

328
Q

what makes P2 different from EMS

A

in PIE-1 mutants blastomere P2 develops as EMS. therefore PIE-1 makes P2 different from EMS

329
Q

at the stage in development where P2 and EMS become different, are ABa and ABp different

A

no - they are still the same at this stage

330
Q

WT EMS has/doesn’t have PIE-1

A

doesn’t have

331
Q

describe par mutants and what is the WT function

A

they are defective in A/P polarity. PIE-1 is not differentially segregated. par proteins correctly localise PIE-1
par protein –> PIE-1 –> posterior determination

332
Q

what divides first AB or P1

A

AB

333
Q

describe what happens when AB divides

A

the bottom cell moves more anterior and ventral and the other cell moves more posterior and dorsal

334
Q

what happens when P1 divides

A

its more ventral cell moves under ABa and ABp (EMS) an the other cell (P2) sits at the back

335
Q

describe the poking a cell and moving it backwards experiment

A

P1 is forced to divide in a different direction
ABa is now more dorsal and ABp more anterior
ABa is in contact with P2, not ABp
the EMS position still determines the ventral side. EMS is displaced vertically by pushing ABa and ABp round
ABa and ABp positions have switched places

336
Q

how do we know that ABa and ABp have the same developmental potential

A

they can carry out the other cells role when their positions are switched. the difference must result from their spatial position

337
Q

ABa and ABp both make the …………. receptor

A

GLP-1

338
Q

P2 becomes different to EMS when ………. localises

A

PIE-1

339
Q

because of PIE-1, P2 turns on ………. and ……….

A

APX-1 and MOM-2

340
Q

what is MOM-2

A

a signal for the wnt pathway

341
Q

EMS makes the ………… receptor (wnt pathway receptor)

A

MOM-5

342
Q

wnt signalling regulates the behaviour of ……… in its subsequent divisions

A

EMS

343
Q

what is the ligand for GLP-1

A

APX-1 (notch pathway)

344
Q

what does APX-1 do

A

it tells the more posterior cell (ABp) to become ABp and not ABa

345
Q

P2 acts as a ………… ………….. ………….

A

posterior signalling centre

346
Q

what makes the EMS daughters (E ams MS) different

A

MOM-2

347
Q

what is induction

A

communication between cell that induces changes

348
Q

why are xenopus laevis good model organisms for studying development

A

they have big eggs which are easy to study

349
Q

the xenopus egg is polar/apolar

A

polar - cytoplasm is different colour at different ends due to protein localisation

350
Q

which body axis does the xenopus animal/vegetal axis correspond to

A

the anterior/posterior axis

351
Q

what is the role of the TF, VegT

A

it accumulates in and determines the vegetal (posterior) end

352
Q

how is sperm entry different in xenopus from c.elegans

A

sperm enter at the animal pole and the polarity is defined before sperm entry - the sperm will only enter at a certain place

353
Q

describe the xenopus 4 cell stage

A

it is divided into dorsal/ventral halves which are defined by sperm entry and the nieuwkoop centre

354
Q

the ventral half of the xenopus 4 cell stage lacks a …….…….… ……………. and develops into a ………… …………

A

nieuwkoop centre

ventralised embryo

355
Q

the dorsal half of the xenopus 4 cell stage develops into a …………. embryo

A

dorsalised

356
Q

sperm entry in the xenopus causes …………… of protein

A

relocalisation

357
Q

the NC is at the same/opposite side of sperm entry in xenopus

A

opposite

358
Q

describe the 1st cell cleavage in the xenopus

A

it usually bisects sperms entry and the NC to give the left/right axis

359
Q

describe the 2nd cleavage in xenopus

A

it cleaves the cells into dorsal/ventral halves

360
Q

how can we graft cells and give a transplant example

A

suck single cell with glass pipette. transplant cell
e.g. transplant NC to ventral –> twinned dorsals –> dorsalised embryo. graft cell instructs adjacent cells to become dorsal

361
Q

do graft cells contribute to mesoderm and ectoderm

A

no they remain endoderm

362
Q

does grafting ventral –> dorsal have an effect

A

no

363
Q

describe the NC

A

endoderm with dorsalising abilities

364
Q

what pathway allows communication between graft and host cells

A

an unusual form of the wnt pathway

365
Q

describe what happens upon fertilisation in the xenopus

A

there is complete movement of cytoplasm when sperm enters. vesicles are moved to an area opposite the point of sperm entry by the cytoskeleton. these define the NC.

366
Q

the wnt pathway:
microtubules that mediate ……………. ……….. also transport membrane vesicles from the vegetal pole. these vesicles transport dishevelled protein (part of the wnt pathway) injected into the cell. in the wnt pathway there is a receptor (………) normally on the outside of the cell that binds dishevelled (activated receptor activates pathway) and stabilises ……… …………… . elevated beta catenin plus vegetal side creates the NC

A

cortical rotation
frizzled
beta catenin

367
Q

in xenopus, how is the wnt pathway activated

A

from a source internal to the cell - from internal vesicles

368
Q

how do we know beta catenin is involved in dorsal axis specification

A

injection of beta catenin into vegetal cells induces a second dorsal side

369
Q

describe the 4 steps involved in the specification of axes

A
  1. vegT accumulates and defines vegetal (posterior) end
  2. beta catenin accumulates in and defines dorsal side (initiated by sperm entry which results in localisation of wnt signalling vesicles)
  3. concentration differences mark a molecular map of axis formation
  4. outcome - differential expression of nodal related proteins in endoderm
370
Q

what are nodal proteins

A

members of the TGF beta superfamily

371
Q

highlight the differences and similarities in development between c.elegans and xenopus

A
  1. in both, differential localisation of factors in the zygote help establish the A/P axis
  2. signalling establishes D/V axis. Notch and wnt in c.elegans and wnt then subsequently nodal in xenopus
    3 xenopus - wnt-dorsal, lack of wnt-ventral
    c.elegans - notch-dorsal, wnt-venral
372
Q

nodal related proteins are ……………..

A

organisers

GMC (4 decks)

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