lecture 10- post embryonic development Flashcards

(34 cards)

1
Q

describe the 3 processed of how growth occurs and give examples of each

A

1) proliferation, in most cells
2) cell enlargement in muscle fibres under exercise
3) accretion, the deposition of extracellular matrix in bones

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2
Q

which CDKs and cyclins are present in each stage of the cell cycle

A

G1-Cdk 4 and 6 and cyclin D
S- Cdk2 and cyclin E
G2- Cdk2 and cyclin A
M- Cdk1 and cyclin A/B

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3
Q

which stage of the cell cycle do fully differentiated cells sit it

A

G0

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4
Q

in drosophila, what controls Cdks and cyclins?

A

string, a phosphatase

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5
Q

describe drosophila cell division up to cycle 13

A

no G1 or G2 phases
syncytium produced
maternally supplied string activates Cdks

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6
Q

describe cell division in drosophila from cycle 13 onwards

A

G2 introduced
nuclei migrate to edge of syncytium and become surrounded by an involuting cell membrane
now, depending on precise location, each cell develops its own division rate
string is expressed under direct control of patterning genes

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7
Q

what is cellularisation

A

where a multinucleated cell (syncytium) is divided into individual cells, each containing one nucleus and surrounded by a plasma membrane.

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8
Q

what is a mitotic domain

A

where cells undergo mitosis in a coordinated manner, both in timing and often in orientation, due to having similar cell fates

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9
Q

why is mesoderm tissue an exception to the string involvement process

A

it has string present but doesnt divide for ages

due to it having tribble, a string inhibitor

tribble promotes mesoderm invagination by preventing cell division

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10
Q

what is the difference between extrinsic and intrinsic control of organ size and give examples of each

A

intrinsic = organ knows what size it should be, hippo pathway

extrinsic = cues tell organ what size it should be, IGF signalling

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11
Q

does the thymus use intrinsic or extrinsic control and how do we know this

A

intrinsic
when transplanted into body with thymus already, it grows normally to a normal size

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12
Q

does the spleen use intrinsic or extrinsic control and how do we know this

A

extrinsic
when transplanted, it only grows to half the size

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13
Q

which is more important for organ growth, dimensions or number of cells

how do we know this?

A

dimensions
organs are the same size whether the organism is haploid or triploid

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14
Q

what does the TOR pathway do

A

increases cell size

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15
Q

what is the inhibitor of the TOR pathway

A

Rapa

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16
Q

what does the Hippo pathway do

A

limits organ size

17
Q

describe the hippo pathway

A

pathway inactive= hippo or Mst1 inactive= YKi or Yap/TAZ in nucleus= growth and survival

pathway active = hippo or Mst1 active= YKi or Yap/Taz out of nucleus= no growth

18
Q

how is the overall size of an organism controlled

A

with the GH / IGF1 pathway

also due to maternal environment

19
Q

what is the proof that maternal environment has an impact on growth

A

women that have been malnourished during pregnancy have babies with increased diabetes

20
Q

how is molting/metamorphosis controlled

A

by short range signals
environment ->CNS -> hormones

21
Q

describe molting in arthopods

A

1)molting initiated by activation of stretch receptors in the cuticle

2)release of protothoracicotropic hormone from corpus alatum

3)release of ecdyson from protothoracic gland

4)cuticle seperates from epidermis

5)freed epithelial cells proliferate and secrete a fluid forming a barrier to make new cuticle

6) old cuticle sheds

22
Q

describe metamorphosis in frogs

A

corticotropin releasing hormone secreted
TSH secreted
T4T3 activated

23
Q

what causes metamorphosis to be irreversible

A

the processes positively feed back on eachother

24
Q

which tissues is cancer the most common in

A

tissues dividing through life as there is a higher level of division

25
what is a teratoma
a type of tumor that arises from pluripotent stem cells and contains a variety of different tissue types
26
what are the 3 ways loss of growth control can occur in cancer
1) proto oncogenes turn into oncogenes which forms cancer eg. Ras 2)tumour supressor genes become inactivated eg. retinoblastoma/ p53 3)loss of negative regulators of signal transduction so cant turn off signalling ->cancer
27
can cancer cells differentiate
no
28
which cancer develops from abnormal Wnt signalling
colon
29
which cancer develops from abnormal hedgehog signalling
basal cell carcinoma
30
which cancer develops from abnormal Nodal signalling
melanoma
31
which cancer develops from abnormal notch signalling
leukemia
32
which cancer develops from abnormal EGF signalling
lung breast
33
why dont mutations in BRCA1 and p53 directly cause cancer
they are tumour supressors so when they are mutated, they lead to odd development signals its these signals which cause cancer
34
describe the GH/IGF1 pathway
(GH) secreted by the anterior pituitary gland. GH binds to GH receptors, production of IGF-1 (Insulin-like Growth Factor 1). IGF-1 enters the bloodstream and acts on multiple tissues by binding to the IGF-1 receptor, a receptor tyrosine kinase. This activates intracellular pathways such as: PI3K/Akt pathway → promotes cell survival and growth MAPK pathway → promotes proliferation GH release is controlled by the hypothalamus via GHRH (stimulates) and somatostatin (inhibits). IGF-1 exerts negative feedback on both the pituitary and hypothalamus to regulate GH levels