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Cell Bio > Cell Division > Flashcards

Cell Division Flashcards

0
Q

S and G2 cyclin

A

Cyclin A, inhibited by DNA damage

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1
Q

G1 Start

A

Cyclin E, inhibited by DNA damage

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2
Q

M phase cyclin

A

Up to meta/anaphase, cyclinB, inhibited by DNA damage and unreplicated DNA

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3
Q

M phase after anaphase to cytokinesis regulator

A

APC (anaphase promoting complex); inhibited by chromosome not being attached to the spindle

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4
Q

How do CDK and cyclin bind?

A

CDK binds ATP and binds cyclin in somewhat relaxed loop; CDK cyclin loop phosphorylated by CAK (cdk activating kinase) which causes loop to open more and bind cyclin; Wee1 phosphorylates again and deactivates the complex, cdc25 dephosphorylates and activates

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5
Q

What is the positive feedback mechanism that makes initiation into the cell cycle irreversible?

A

the cyclin CDK complex triggers a lot of cdc25 production and turns off Wee1; makes the start of cell division instantaneous and irreversible

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6
Q

How do we stop the cdk-cyclin ?

A

ubiquitylation and protesosome digestion of the cyclin

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7
Q

Ubiquitin

A

small polypeptide (70aa) also involved in regulating histones and acts as a marker for endocytosis receptors

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8
Q

How do proteins get ubiquitulated?

A

E1,E2, E3 complex
E1 bind to ubiquitin using ATP; E1 attracts E2 and E3 and transfers ub. to the E2 (E2 and E3 complexed); E2/E3 have a protein specific binding site (could be hydrophobic, etc). and transfer to ub to the protein; the ub protein is recognized by the proteosome cap and bound in an energy dependant step and then the ub/protein is degraded

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9
Q

What are microtubules?

A

polymers of a heterodimer of alpha and beta tubullin; polymerize into linear profilaments that are stacked (13) to create a cylinder with a hollow core; have a minus end and a plus end; polymerize from the plus end (grow); minus ends are stabilized by the microtuble organizing center MTOC

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10
Q

Astral microtubule

A

contact with cell membrane, position centrosomes

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11
Q

Kinetochore microtubules

A

bind to chromosomes and seperate them during anaphase; need to be bound to tubules from both centrosome to initiate anaphase

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12
Q

Interpolar microtubules

A

bind to eachother in center of the cell

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13
Q

How do the centrosomes maintain their positions in the cell?

A

Kinesin 5 (tetramer ) and dynein move the centrosomes towards the cell membrane and Kinesin 14 counteracts this movement to keep centrosomes from going all the way to the cell membrane

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14
Q

Chromokinesins

A

Walk to kinesin to the center of the cell so that kinetochore microtubules can bind and initiate anaphase; kinesins are highly specific to cell division so are a good target for cancer therapy (taxol)

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15
Q

How does APC work?

A

Anaphase promoting complex is an E3 ubiquitin ligase that ub. cyclin in the mitosis phase of cell division; it also triggers the degradation of cohesins (allowing the chromosomes to seperate)

Seperase (that degrades cohesin) is usually bound to securin in the cells; APC ubs securin

APC is active when bound to cdc20; unattached kinetochores inhibit cdc20 so cells can’t seperate chromosomes and arrests cell cycle

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16
Q

How to chromosomes move to opposite sides of the cell?

A

microtubules depolymerize

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17
Q

Which filaments and motor proteins drive cytokinesis?

A

actin filaments and myosin proteins for a ring at the center of the cell that constricts and causes cytokinesis

18
Q

Early prophase

A

centrioles divide and move apart, the nuclear membrane starts to disintegrate

19
Q

Late prophase

A

centrioles/centromeres are at opposite poles in the cell, the nuclear membrane and nucleous have almost disapeared

20
Q

Metaphase

A

Chromosomes line up at center of the cell

21
Q

Anaphase

A

centromeres (dots at hte middle of the chromosomes) split and half of the chromosomes move to one side of the cell and half to the oher; in late anaphase the chromosoems have almost reached the poles and the membrane starts to pinch

22
Q

Telophase

A

cell membrane completes constriction, nuclear membranes form around the separated chromosomes

23
Q

What is the series of protein/complexes that control DNA rep in the cell?

A

mitogens» cyclin D-CDK4» cylcin E-cdk2» cyclin A-cdk2» DNA rep

24
Q

What are the transcription factors that express cyclin E and how are they regulated?

A

E2F1-F4 activate cylcin E expression but cannot do so when they are bound to pRB (retinal blastoma protein= tumor suppresser) ; E2F4-5 inactivate cyclin E and are activated by binding of pRB

CyclinD-CDK4 phosphorylates pRB and allows cyclin E to be transcribed

Once cyclin E bind with CDK2, it phosphorylates pRB so once mitogens activate the cycle to produce cyclin E, they are no longer needed because of the positive feedback

25
Q

How do mitogens act?

A

Mitogens bind to a transmembrane protein receptor and activate Ras(GTP binding protein) that activates MAP KKK and transcribes MYC in the cell, MYC activates cyclin D and decreases activators of INK4

26
Q

How do antimitogens act?

A

Antimitogens bind to transmembrane receptors that activae SMads which express INK4 that binds competetively to CDK-4 instead of cyclin D

27
Q

What does p53 respond to?

A

hyperproliferative signals
DNA damage
telomere shortening
Hypoxia

28
Q

What does p53 cause?

A

cell cycle arrest
senescence
apoptosis

29
Q

What is the primary function of p53?

A

transcription factor that turns on p21 gene, p21 protein binds to CDK2-E and stops cell cycle

DNA damage activates ATM/ATR and CHK1/K2 kinases that phosphorylize mdm2 which changes shape to release p53, then p53 activates p21 which binds to CDK2-E

P53 also activates the box gene that makes a pore in the mitchondria membrane and allows cytochrome C to enter which triggers apoptosis by activating caspases via apotosomes (groups of apoptosis promoting proteins)

30
Q

What do ATM/ATR CHK1/2 kinases do besides activate p53?

A

phosphorylates cdc25 which ubs it and degrades it so the cell cycle can’t be turned on (remember that cdc25 dephosphorylates cdk-cyclin to activate it)

31
Q

How does the Ras cycle effect p53?

A

To much activation of Ras triggers p53 by transcribing PIQarf which causes Mdm2 to release p53 and activate, active p53 turns off the cell cycle

32
Q

What is the Haflick limit?

A

Number of times a cell can divide, determined by telomeres; shortened telomeres turn on p53 kinases

33
Q

What is the function of telomerase and how does it relate to cancer?

A

Telomerase can add telomere sequences to the end of DNA, normal cells express low amts, but it may be that cancer cells express more so they can over shoot the Haflick limit

34
Q

What are lamina and what is their role in the cell?

A

Lamina are intermediate filament type structures that lie under the inner membrane of the nucleus and 1) give structure/strength to the nucleus, 2) facilitate communication with the cytoskeleton/outside - mechanical information/stress on cytoskeleton- connected to cytoskeleton via KASH proteins 3) keep chromosomes in proper domaines (i.e. heterochromin on periphery and euchromin interior)

35
Q

Disease related to mutation in nuclear lamina

A

progeria

36
Q

How are mitchondria transported ?

A

bidirectionally, good ones from cell body out, and bad ones back for repair etc

37
Q

How does mitochondrial fission work?

A

DrP1 activates fission, polymerizes on the surface of the membrane and splits it in two

38
Q

How does mitochondrial fusion work?

A

mitofusions (like Snares) bring together outer membrane and Opa1 fuses inner membrane

39
Q

What diseases are related to mutations in microfusions?

A

neurodegenerative disorders, dead mitochondria in distal portions of axons can’t generate ATP and cannot be repaired

Charcot Marie Tooth type 2A sees neurdegeneration in skeletal muscles

40
Q

Why do mitchondrion fuse?

A

DNA in mitochondria has unique pieces and the enviro is not great for keeping it in tact (oxidative and not a good repair system) so mitchondria have more DNA than the nucleus (5-10 copies); when two mitochondria fuse, they exchange DNA so ones with bad DNA get wild type/non mutated DNA

Without fusion the mutation rate increases and there is a loss of mito DNA

41
Q

Why do mitchondria undergo fission?

A

Allow cells to get rid of damaged mitochondrial DNA, fiss off bad stuff and that is marked for destruction via mitophagy in autophagasomes

42
Q

How does mitochondrial fission occur?

A

PINK1 attracts Parkin (E3 ligase) that ubiquitylates bad vessels for destruction

Cell Bio (16 decks)

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