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BIOL2200 > MODULE 1: cell cycle > Flashcards

MODULE 1: cell cycle Flashcards

1
Q

interphase

A
  • chromosome duplication
  • cohesion of chromosomes (cohesions = proteins that hold sister chromatids together)
  • centrosome duplication
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2
Q

prophase

A
  • breakdown of microtubule display
  • replacement by mitotic asters (centrosomes + microtubules)
  • chromosome condensation
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3
Q

prometaphase

A
  • nuclear envelope breaks down

- chromosomes captured, bi-orientated and bought to spindle equator

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4
Q

metaphase

A
  • chromosomes aligned at metaphase plate
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5
Q

anaphase

A
  • APC/C activated and cohesions degraded
  • chromosome movement to poles
  • spindle pole separation
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6
Q

telophase

A
  • nuclear envelope reassembly

- assembly of contractile ring

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7
Q

cytokinesis

A
  • reformation of interphase microtubule array
  • contractile ring forms cleavage furrow
  • cell separates in two
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8
Q

chromosome movement during mitosis

A

microtubules shrink (break down) on one side and grow on the other, allowing chromosome movement

kinesin-7 connects microtubules to kinetochore, pulling chromosomes along as microtubule grows and shrinks

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9
Q

meiosis 1

A

DNA replication

homologous chromosomes pair

recombination occurs between homologous chromosomes (alleles exchanged –> genetic diversity)

homologous chromosomes separate, sister chromatids in tact

cell division

daughter cells are 2n and contain different sets of chromosomes (parental or maternal)

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10
Q

meiosis 2

A

sister chromatids separate

cell division

four gametes (1n) formed

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11
Q

kinase

A

enzyme that adds phosphate to its target

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12
Q

phosphatase

A

enzyme that removes phosphate from its target

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13
Q

CDKs at different stages in cell cycle

A 
M phase - M CDK
G1 phase - G1 CDK + S CDK 
S phase - S CDK
G2 phase - G2 CDK + M CDK
G0 - inactive CDK

G1 CDK = CDK4 + cyclin D
G1/S CDK = CDK2 + cyclin E
S CDK = CDK2 + cyclin A

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14
Q

how to test for CDK activity

A

combine in a test tube:

  • cell lysate
  • control / cyclin / CDK antibodies

purify Ab protein complexes

add substrate and radioactive ATP

load reaction products on SDS page gel to see CDK activity

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15
Q

mechanics of regulation - ubiquitination

A

ubiquitination - protein ligases attach to Ub to target a protein

process repeats = polyubiquitination

proteasome recognises polyubiquitination and destroys the protein

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16
Q

anaohase promoting complex or cyclosome (APC/C)

A

involved in metaphase to anaphase + anaphase to telophase transitions

APC/C degrades securin, activating separase which splits chromosomes

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17
Q

phosphorylation vs ubiquitination

A

phosphorylation is temporary and reversible (molecular switch). phosphorylation is quick and easy

ubiquitination is permanent and irreversible (destruction)

18
Q

G1 to S phase transition

A

very abrupt transition

PATHWAY

  • CK1 bound to S cyclin/CDK
  • G1/S cyclin/CDK polyubiquinates CK1, allowing SCF to recognise it
  • SCF degrades CK1 and S cyclin/CDK activates
  • SCF binds to S cyclind/CDK until cell is ready for S phase
  • SCF is degraded by Ub-protein ligase when cell is ready
19
Q

cohesin

A

“rubber band” around centromere on sister chromatids

20
Q

temperature sensitive mutants in yeast cells

A

yeast cells used to examine cell cycle

foudn that cells elongate then divide

cell growth uncoupled from cell division i.e. keep growing independent of cell cycle stage

yeast cells grown cells at permissive temp then shifted to restrictive temp

cells that survived after shift contained ts mutations

mutated cells grown up an mutations characterised

  1. cdc2+ (wild type) = cdc is a CDK
  2. cdc2- (recessive) = long phenotype, no mitosis
  3. cdc2º (dominant) = wee phenotype, lost regulatory function, mitosis too often
  4. cd13 (mitotic cyclin) = mutants also give long phenotype
21
Q

regulation of mitosis (cdc25 + wee1)

A

cdc25 (phosphate) drives mitosis
wee1 (kinase) inhibits mitosis
wee1 phosphorylates tyrosine 15, cdc25 acts on same tyrosine

elongated cells = increased G2 = deficit of cdc25 OR excess of wee1

small cells = decreased G2 = deficit of wee1 OR excess of cdc25

cascade of kinase and phosphate activity controls entry into mitosis

  • mitotic cyclin forms complex with CDK
  • inactive because wee1 immediately phosphorylates Y15 and blocks substrate binding site
  • in G2, CAK phosphorylates T161 (near Y15) to begin activation
  • when checkpoints passed, cdc25 removes phosphate from Y15 and cell can undergo mitosis
22
Q

mitosis promoting factor (MPF)

i.e. mitotic cyclin/CDK

A

MPF drives mitosis

MPF produced in G2 phase

kept inhibited (phosphorylated) until cell is ready for mitosis

once active, MPFs phosphorylate:

  • chromatin associated proteins
  • nuclear envelope proteins
  • microtubule associated proteins
  • kinetochore proteins
  • many more
23
Q

mitotic checkpoint pathway

A

is DNA replication complete?

ATR1 (protein) detects single strands of DNA, usually associated w/ replication forks

active ATR1 activates CHK1 (kinase). CHK1 in turn inhibits cdc25 to prevent mitosis

24
Q

metaphase to anaphase transition

A

APC/C initiates transition by inducing cohesin removal at centrosome

when all kinetochores bind MTs, cdc20 binds to APC/C

APC/C polyubiquinates securin (bound to separase, inhibiting it)

securin uninhibits separase and it cleaves scc1,

cohesins composed of Smc proteins and Scc1, cohesin falls apart when scc1 degraded

chromatids free to separate = anaphase

25
Q

degredation of mitotic cyclins (APC/C)

A

APC/C specificity changes in late anaphase once chromatids have separated

Cdn1 becomes active and leads APC/C complex to mitotic cyclins for degredation

this is necessary for chromatin decondensation and depolymerisation of microtubules –> needed to get to telophase

26
Q

necrosis definition

A

unplanned cell death

27
Q

apoptosis

apoptosis signalling pathway

A

programmed cell death = common cell fate

cell chopped up and packaged for removal. DNA is fractioned, cell membranes pinch off into small structures

fragments are labelled for macrophages so that they will be cleaned up through phagocytosis

apoptosis adjusts number of nerve cells to a target. survival factor released by target cells

SIGNALLING PATHWAY

CED-9 (protein) sits on mitochondrion and binds to CED-4

EGL-1 induces release of CED-4 from CED-9, initiating cell death

CED-4 forms large octamer complex in cytoplasm

interacts with CED-3 to form capsule holoenzyme

capsule destroys vital proteins to cause cell death

once active, CED-3:

  • cleaves lamins –> nuclear envelope dissolves
  • activates endonucleases –> DNA digested
  • attacks cytoskeletal structure
  • attacks cell-cell adhesion proteins
  • cleaves itself
28
Q

selection of cancer cells

A

tumours developed through selection process

cancer cell has mutation with growth advantage

selection of cell with growth advantage= more mutations

29
Q

proto-oncogenes

A

normally promote cell growth

once mutated (typically gain of function) or amplified they become oncogenes (Ras, myc, src)

can duplicate DNA

30
Q

colon cancer

colon cancer pathways

A

early pollops can be identified and removed

stages I-III = benign

right before stage IV, p53 activated = cell death, cell cycle arrest, sensescence

common genes mutated along progression

APC (adenoma polyposis coli protein) ——| wnt signalling —–> myc proto-oncogene —–> proliferation advantage (benign)

Ras (growth factor) —–> MAPK (mitogen activated protein kinase) —–> proliferation

31
Q

metastasis

A

spread of cancer cells from their site of origin and establishment of secondary growth

most cancer deaths arise from metastasised tumours

as more cells become mutated, they can detect GFs and move towards source

  1. penetrate basement membrane by acquiring enzymes
  2. migrate on ECM fibre down to blood vessel
  3. travel to anywhere in body (1 in 1000 land somewhere to make tumour)
32
Q

retinoblastoma

diagrams of hereditary and sporadic mutations

A

rare childhood cancer

if caught early, 95-98% cure rate

caused by mutations in Rb gene

1) hereditary retinoblastoma
- RB+ and RB- (from parents)
- somatic mutation
- RB- and RB-
- homozygous cells give rise to tumours in retina

2) sporadic retinoblastoma
- RB+ and RB+
- two somatic mutations
- RB- and RB-
- homozygous cells give rise to tumours in retina

33
Q

restriction point in cell cycle

A

cell is committed to another round of cell division once it passes restriction point and is no longer mitogen-sensitive

8 hours between restriction point and S phase - cell can still exit cycle within this period

Rb is a transcriptional repressor of E2F (a TF of genes required for DNA replication). Rb is also a substrate for G1 cyclin/CDK. hyper-phosphorylation of RB = restriction point passed, cell mitogen-independent and committed to cell cycle

34
Q

APC/cdh1 activity in mitosis

A

APC/Cdh1 degrades mitotic cyclin so DNA can be decondensed = region of gene called destruction box

APC/Cdh1 can degrade many proteins required for S-phase (such as E2F) so it needs to be inactivated before cells enter S-phase

  • APC inactive at G1/S boundary
  • APC inactive in S phase
  • APC active in mitosis
  • region between inactive APC and start of DNA replication = cells cannot exit cell cycle = new committment point

G1/S CDK phosphorylates Cdh1

Emi1 leads another Ub ligase to destroy Cdh1

35
Q

Cell stress pathway

Mutations in cancer cells

A

cell stress —–> p16 —–| G1 cyclin/CDK (cyclin D + CDK4) —–> Rb —–| E2F —–> transcription of genes that control entry into S-phase

  • under stress, p16 sits atop G1 cyclin/CDK complex
  • this prevents CDK/cyclin complex from hyper-phosphorylating Rb
  • Rb sits atop E2F to prevent gene transcription
  • no hyperphosphorylation = no Rb release from E2F = no gene transcription

in presence of mitogens, p16 is inactive –> G1 cyclin/CDK active –> Rb phosphorylated and removed from E2F –> E2F transcribes genes for S-phase

cancer cells frequently:
- delete/inactivate p16
- over express/amplify G1 cyclin
- delete/inactivate Rb
tumours have only one of these mutations, indicating that regulation of this genetic pathway needs to be disabled for growth
36
Q

tumour suppressor pathway

A

p53 = tumour supressor
detects conflicts within cell (DNA damage, telomere shortening, etc) and can activate several different pathways to resolve conflicts (cell cycle arrest, apoptosis)

ATR —| MDM2 —| p53

  • p53 controls WAF1 gene - an inhibitor of CDKs
  • therefore, p53 activity inhibits cell cycle progression
  • MDM2 degrades p53

cancer cells have GOF mutation in MDM2 or LOF mutation in p53 = excessive proliferation
50% of tumours have mutations in p53 pathway/gene

37
Q

types of gene regulation

A

transcriptional regulation: distinct genes turned on/off controlled via various mechanisms

translational regulation: distinct mRNAs translated or repressed and localised to different regions of cell

epigenetic regulation: marks on DNA that regulate gene expression are inherited by daughter cells but independent of DNA sequence

38
Q

mechanisms of cell specification: asymmetric cell division

A

cells contain factors which provide unique info related to cell

factors localised to particular region of cell

cell divides to produce two identical cells in terms of DNA, but different regarding cytoplasmic contents

39
Q

mechanisms of cell specification: cell-cell interactions

A

cell fate determined bu interactions with neighbouring cells

  • back cells in blastula form back tissue
  • transplant these back cells into belly regions
  • these cells then go on to form belly tissue
40
Q

mechanisms of cell specification: morphogen gradients

bicoid and nanos

diagram of bicoid, nanos, hunchback and caudal

A

morphogen gradients are typically TF’s that are “master gene regulators” i.e. determine whether it is head or tail region of animal

example: drosophila embryos
- bicoid = head and nanos = tail
- mother deposits mRNA in unfertilised egg
- egg already polarised
- mRNA localised at poles of egg
- egg fertilised, DNA replicated with no cell membranes —> gradients of cell specificity factors
- exposure to amount of factors determines cell fate

bicoid and nanos are tranlational inhibitors and transcription factors

inhibity translation of two other mRNAs involved in early patterning of embryo, hunchback and caudal

hunchback and caudal not localised

bicoid binds to caudal and prevents it being made into protein (same re. nanos and hunchback)

41
Q

transcriptional regulation: molecular level

A

Dna contains elements that allow for cell specific gene regulation

TFs - proteins that promote or inhibit gene expression

enhancers - TF binding sites

histones - proteins that package DNA and can be modified to regulate gene expression. positively charged tails interact with negative phosphate backbone of DNA

epigenetic marks - histone acetylation and methylations as well as DNA methylation. modify histones to allow DNA translation

acetyl and methyltransferases - enzymes that add epigenetic marks to histones and DNA

in general, modifications that decrease histone tail interactions with DNA open up the chromatin

acetylated histones –> open chromatin, transcriptionally active
deacetylated histones –> close chromatin, transcriptionally silent

42
Q

terminal differentiation

terminal differentiation pathway

A

permanent cell cycle exit

differentiated cells become refractory to proliferative signals (respond in different way)

G1/S CDK inhibitor and Rb family members play major role in cell cycle exit

terminal differentiation distinct from senescence

cell fate determining TFs *

  • —-> G1/S CDK inhibitors
  • —-| substrates for cycling CDKs become dephosphorylated (less phosphorylated Rb)
  • —-> Rb recruits epigenetic modifying complexes that permanently repress E2F transcriptional activity
  • cell fate inhibits cdc25 and activates eigenetic regulators. Rb recruits epigenetic regulators to locus in genome and mark histones and DNA to permanently silence it

BIOL2200 (7 decks)

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