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MCB - Cell Bio > cell cycle > Flashcards

cell cycle Flashcards

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Biology 101 flashcards
1
Q

animal cloning

A

iPSCs - induced pluripotent stem cells
extract nucleus (destroyed by UV), put other nucleus into empty egg, electricity induces cells to divide
only work 1/200 times

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2
Q

cancer

A

de-regulated cell cycle ignores stop signals

proliferate without control, no apoptosis, need blood supply so angiogenesis

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3
Q

benign tumour vs metastasis

A

stays in 1 place so can cut out

metastasis means invade other parts so colonies and spread

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4
Q

cancer and age

A

live longer more time for mutations and more exposure to carcinogens that damage DNA e.g. smoking

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5
Q

evolution of tumour

A

mutation causes mitogen (growth factor) independence so ignores signals
another mutation suppresses apoptosis so can’t stop proliferation
may cause unstable chromosomes and genetic instability

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6
Q

genetic instability

A

some chromosomes gone or fused with other

nuclei without correct number if chromosomes - if hit crucial genes then further degradation of genome

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7
Q

cell cycle stages

A 
Go
G1
S
G2
M
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8
Q

4 places where cell cycle can stop

and what are they controlled by?

A

between cycle phases

restriction point in G1
G1 to S (decides if replicate)
G2 to M (decide to divide)
M - metaphase to anaphase (decide if separate sister chromatids)

controlled by Cyclin-CDK activation/inactivation and have diff ones in diff transitions (on word)
activation triggers next one to activate and causes own destruction

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9
Q

how are Cyclin-CDK complexes activated?

A

need triggering event to put complex together

T-loop in CDK blocks active site (ATP binding site),

cyclin binding to CDK moves T-loop out of active site so CAK (CDK-activating kinase) can transfer phosphates to T-loop (CAK phosphorylates T-loop) and activates complex

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10
Q

CAK

A

CDK activating kinase

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11
Q

CDKI

A

CDK inhibitors bind CDK and keep inactive
target for degradation by ubiquitin

when enough phosphates, phosphate on CDKI recognised by F-box docking protein which brings SCF (E3 Ub ligase) so ubiquitylated and CDKI is sent for destruction so CDK/cyclin complex can be activated

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12
Q

restriction point (G1 checkpoint) + further checkpoints between phases

A

1) accumulation of cyclinD-CDK4/6 phosphorylates Rb tumour suppressor so removes it
2) so releases E2F (TF for replication) which causes expression of Cyclin E and A
3) CyclinE-CDK2 further phosphorylates Rb to activate E2F
4) p27 CDKI inhibits CyclinA-CDK2
5) Cyclin E-CDK2 gets rid of CDKI on CyclinA-CDK2
6) activation of E2F also causes transcription of genes for replication
7) CyclinE-CDK2 phosphorylates itself so destruction once activated because next cyclin activated

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13
Q

direct phosphorylation of cyclinB-CDK1

A

Wee1 kinase phosphorylates active site of CyclinB-CDK1 so blocks from using ATP (in G2)

Cdc25 inhibit Wee1 so removes phosphate to activate complex (G2/M)

feedback loop drives cell to next phase by activating pool of cyclin CDKs

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14
Q

how is Cyclin/CDK activated

A

transcription of cyclins
T-loop phosphorylation by CAK
proteolytic destruction of CDKI
dephosphorylation in active site by Cdc25
intracellular re-localisation of active cyclin/CDKs

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15
Q

how is Cyclin/CDK inactivated

A

CDKI blocks interaction of cyclin with CDK and blocks ATP binding and blocks substrate binding
phosphorylation of active site by Wee1 kinase
proteolytic destruction of cyclin

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16
Q

mitogens

A

a peptide or small protein that induces a cell to begin cell division

lack of mitogens means antiproliferation signals stop cell cycle and don’t go past restriction point

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17
Q

pseudotumour

A

pile of cells growing up from monolayer

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18
Q

protooncogenes vs oncogenes

A

Proto-oncogenes are normal genes that help cells grow which when mutated, becomes an oncogene. An oncogene is any gene that causes cancer

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19
Q

proto-oncogenes

A

in signal transduction pathways
cause proliferation and survival, rare
genetically dominant or from overexpression
from point mutation or translocation

e.g. Ras, Myc, Fos, Jun, Raf, EGFR, PDGF

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20
Q

what does mitogen cause? (process)

A

mitogen recognised by receptor
activates Ras GTPase which activates Raf (kinase) which activates MAP kinase cascade, MAP kinase enters nucleus, activates dimeric Fos/Jun TF trigger immediate early gene expression,

Fos/Jun induce Myc TF (induce delayed response gene expression and activates Cyclin D in G1 so cell cycle continues and replication

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21
Q

tumour-suppressor genes

A

inhibit proliferation/survival, promote apoptosis, sense DNA damage, need to lose both copies on 2 chromosomes to cause cancer

e.g. Rb

22
Q

Rb

A

inhibit G1/S expression
mutation leads to retinoblastoma

hereditary retinoblastoma = inherit 1 faulty Rb and 2nd by somatic mutation, can surgically remove

sporadic retinoblastoma = both fine till 2 somatic mutations cause 2 faulty Rb, hard to treat

23
Q

mitotic recombination

A

1 mutated chromosome, bits of chromosome swap

so segregation cause 1 normal homozygous allele and 1 mutant homozygous

24
Q

mis-segregation

A

1 mutated heterozygous

checkpoint goes wrong so 3 chromosomes in 1 cell and other one dies so 1 hetero and 1 homo mutant

25
Q

mutated Rb

A

can’t sit on E2F repress so pass restriction point even without signal
or oncogene mimics signal so pass restriction point

26
Q

mutated p16INK4

A

normally keep CDK4/6 away from cyclin even with signal but now allow and cell passes restriction point

27
Q

other tumour suppressors

A

work on other mitogenic signalling pathways like neurofibromatosis when Ras not restrained so APC loss and proliferation

and forced proliferation without enough nucleotides so ssDNA breaks and rpelication stress

28
Q

DNA damage

A 
cellular metabolism (mitochondria create free radicals)
radiation
chemical exposure (smoking)
replication errors
virus

causes cell checkpoint activation, DNA repair, apoptosis

29
Q

caretaker genes

A

repair, prevent DNA damage, enzymes

30
Q

major DNA damage repair pathways

A

1) X-rays, alkylating agents, O2 radicals = single stranded breaks don’t affect structure but still replication problems, so use BER
2) UV radiation, chemical mutagens = bulky lesions, crosslinks, cause DNA kink, so use NER
3) replication error, wrong nucleotide paired, cause bulge in DNA, so use MMR

31
Q

BER

A

base excision repair
for damaged nucleotides

1) DNA glycosylases scan DNA
2) damaged bases removed, single stranded break (short/long patch)
3) polymerase corrects DNA with other strand then ligate

32
Q

NER

A

nucleotide excision repair
for when damage caused kink e.g. crosslinks or pyrimidine dimers

1) recognition and remove segment with lesion
2) undamaged strand used to polymerase complementary sequence
3) ligation with DNA ligase

loss of enzymes in NER causes XP (xeroderma pigmentosum, sensitive to UV so tumours on skin

33
Q

MMR

A

mismatch repair
for when wrong nucleotide causes bulge

1) recognition by MMR proteins, endonuclease cuts phosphodiester bonds of backbone
2) exonuclease removes base and repair polymerase adds correct one
3) ligation reattach backbone

mutations in this cause hereditary non-polyposis colorectal cancer (HNPCC)

34
Q

double strand break repair by non-homologous end joining (NHEJ)

A

both strands separated and ends of chromosomes can invade others and get fusion of chromosomes

ends are joined to fix break with ligase

35
Q

what happens in imprecise repair during NHEJ?

A

can lose nucleotides so frameshift and nonsense mutation so inappropriate NHEJ causing translocations and telomere fusion so cancer

36
Q

double strand break repair by homologous recombination (HR)

A

sister chromatid for template
proteins recognise break
single stranded break can invade strand on partner sister chromatid and create double holliday junction
unzip junction to form 2 wild type chromatids

37
Q

BRCA1 in double-strand break repair

A

mutation could lead to breast cancer/ovarian/testicular

38
Q

cell cycle checkpoint experiment on budding yeast

A

made rad mutants which is radiation sensitive
damaging cell causes no replication so no nucleus in new bud and delays cell cycle in G2

Rad9 mutants can’t stop cell cycle so divides and fragmented DNA so chromosome instability (because wild type rad9 usually senses DNA damage and checkpoint stops progression)

39
Q

p53 in humans (function in cell cycle, destroyed)

A

for genome stability
part of checkpoint between G1/S and G2/M
binds DNA promoters and acts like TF, only when DNA damage
absent in 100% proteins/low levels unless damage

produced but destroyed by Mdm2 E3 ligase

if low damage: bind promoters like p21 to stop cycle and allow repair
if high damage: apoptosis

40
Q

DNA common repair pathways (no matter what DNA damage - common activation of pathway but diff outcomes)

A

proteins recognise pathway and cause signalling cascade (ATM/ATR kinase activation and Chk1/Chk2 kinase activation) so phosphorylation of p53 so not recognised by Mdm2 (so not destroyed by Mdm2 E3 ligase) so act on regulatory genes like p21 CDK inhibitor (transcribed) so CDKI inactivates CDK/cyclin complex and can’t progress in cell cycle

p53 and p21 stay until damage repaired

diff pathway:
Chk1/2 (checkpoint 1 and 2) inhibit Cdc25 so can’t activate CyclinB-CDK1 complex and G2/M transition doesn’t happen till repaired

41
Q

mutated p53

A

cell cycle continues and can’t apoptosis so accumulates more mutations and cancerous

42
Q

fail safe pathway

A

replication stress by activation of oncogenes Ras and Myc
accumulation of INK4 (p16 ink4 is CDKI) inhibits CyclinD/CDK4 complex
ARF regulator of p53 stops replication and drives death

43
Q

why is the ability to segregate so important?

A

so cells have same number of chromosomes so no aneuploidy and have genome stability

44
Q

APC

A

anaphase-promoting complex

multisubunit protein complex with ubiquitin ligase activity that regulates chromosome segregation and anaphase progression by targeting key factors for degradation

E3 ligase polyubiquitinates 2 proteins

45
Q

mitosis phases

A 
prophase
prometaphase
metaphase
anaphase A
anaphase B
telophase

only separates when same no. chromosomes in each cell - can sense when complete

46
Q

cohesin complex

A

ring around DNA

2 coiled coils (Smc1, Smc3) and Kleisin subunit (Scc1) and other accessory proteins (Scc3)

47
Q

function of cohesin complex (when is it present and when do some go away?)

A

concentrate near centromere during G1 phase,

replication fork passes ring which leads to 2 chromatids being inside the ring,

most rings go away before metaphase leaving only a few near the centromere so 2 arms are free and seen as a )( shape

Smc side open to allow fork past and then close when 2 chromatids

48
Q

cohesin complex during mitosis (function)

A

concentrates around centromeric region and resists pulling by MTs attached to kinetochore so tesion for biorientation

49
Q

removing cohesin complex

A

when chromatids bi-oriented on mitotic spindle
E3 ligase APC/C activated by Cdc20 ubiquitinates Securin (inhibitor protein for Separase) which releases Separase which cleaves Kleisin subunit of cohesin so opens ring to allow chromatids to separate

APC also targets Cyclin B (between metaphase to anaphase transition) to destroy in proteasome which inactivates CDK1 kinase so chromosomes move to poles for anaphase A and stimulate motor protein activity so 2 poles separates in anaphase B

50
Q

bi-orientation

A

need to sense that pairs have MTs correctly attached before separation

incorrect would be if only 1 kinetochore attached to MT, wrong MT side to wrong chromatid, inappropriate number attached
if forces are not equal it prevents activation and separation

correct if same force on both sides

51
Q

Cdc20

A

if correct bi-orientation of chromosomes then Cdc20 binds to APC to cleave cohesin, destroy cyclin B and depolymerise MTs to pull chromatids apart

Cdc20 bound on 6 checkpoint proteins means APC is inactive

MCB - Cell Bio (3 decks)

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