cell cycle Flashcards

1
Q

division in specific cells

A

cells divide at different rates eg embryonic vs adult cells depends for necessity for renewal eg intestinal cells

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2
Q

cell division in tumours

A

apart from mutations in TMS/aneuploidy, solid tumours are aneuploidy (abnormal chromosome number)- contact inhibition of growth (when cells know when to stop growing) not present, of protein levels of cell cycle regulators affected

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3
Q

stages of cell cycle

A

interphase (duplication)- not just DNA, but also organelles and protein synthesis M phase ie mitosis: nuclear and cytoplasmic (cytokinesis) division coordination

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4
Q

vulnerable period of cell cycle and why

A

M phase, as cells more easily killed, and DNA damage can’t be repaired

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5
Q

phases of interphase

A

G0- cell cycle machinery broken down, cell resting G1 (gap)- decision point S- DNA/protein synthesis+ replication of organelles G2 (gap)- is all DNA produced

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6
Q

centrosome

A

double barrel composed of 2 centrioles- forms microtubule organising centre and (polymerisation of them occurs from them) mitotic spindle

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7
Q

DIAGRAM what occurs in prophase

A

chromatin condense- forms two sister chromatids with a centromere in the middle, with kinetochores on each side centrosomes also go on opposite side

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8
Q

DIAGRAM spindle formation and interaction

A

radial microtube arrays (called asters) from AROUND each chromosome, and meet in the middle to form polar microtubles

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9
Q

early prometaphase

A

early- nuclear breaks down, which spindle formation having already occurred: chromosomes attach to spindle microtubules via KINETOCHORES

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10
Q

late prometaphase

A

chromosomes attached to each pole go to middle

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11
Q

DIAGRAM anaphase and subphases

A

sister chromatids separate (COHESIN hold chromatids together) anaphase A- cohesion broken down, microtubules contract and get shorter anaphase B- DAUGHTER CHROMOSOMES pulled to opposite poles AND spindle poles (centrosomes) move outwards

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12
Q

telophase

A

daughter chromosomes arrive at spindle, nuclear envelope forms again, and contractile ring forms (needed for cytokinesis)

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13
Q

spindle assembly checkpoint and proteins needed- also where occurs

A

make sure that chromosomes are aligned at equator, and that chromosomes are attached to microtubules- occurs between prometaphase and metaphase needs BUB kinases and CENP-E

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14
Q

DIAGRAM misattachment of microtubules to kinetochores- types and overall

A

monotelic attachment- only 1 sister chromatid attaches syntelic- both chromatids attach to same tubule= go to same daughter cells/pole merotelic- multiple microtubules attach to same sister chromatid= chr LOSS in cytokinesis leads to aneuploidy amphelic- normal

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15
Q

aberrant centrosome/DNA duplication

A

leads to more than 2 centrosomes= more than 2 daughter cells= aneuploidy

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16
Q

how anti-cancer therapy works and examples and their mechanisms

A

cause GROSS chromosome missegregation, meaning cells is unviable so dies chekpoint kinase (checkpoint in G2) inhibitors taxons and vinca alkaloids change microtubule mechanicsms, unattached kinetochores, and long term mitosis (ie more vulnerable)

17
Q

what happens in sth goes wrong during cell cycle

A

cell cycle arrest at checkpoints: often temporary OR apoptosis if DNA damage too great/chromosome abnormalities

18
Q

DIAGRAM how tumours affects checkpoint

A

growth factors affect G1 checkpoint, allowing S phase to occur- tumour affect this tumours also effect G2 checkpoint (for DNA damage) or metaphase checkpoint (for alignment)

19
Q

G0 and how tumours affect it

A

tumours also prevents exit of cell cycle at G0, so no resting state in this stage, cells are not dividing, but are NOT dormant the exit from G0 back into cell cycle needs growth factors, which activates a signalling cascade

20
Q

DIAGRAM how peptide growth factors work

A

dimeric ligand binds to a monomeric receptor, forming dimers, as the 2 kinase domains brought together and are phospohrylated receptor protein tyrosine kinase involved, activating the receptor

21
Q

how phosphorylation occurs

A

negative phosphate from ATP added to hydroxyl group of serine, threonine or tyrosine- causes change in shape- doesn’t just phosphorylate kinase domain, but also other sites too, causing a kinase cascade

22
Q

kinase cascade

A

kinases are regulated by other kinases- 1 kinase is phosphorylated, and it phosphorylates a second kinase this phosphorylation is reverse by PHOSPHATASES