Mitosis

Question 0

Cell phases

Answer 0

G1 - growth, longest phase by far
S - synthesis, replication of chromosomes and centrioles
G2 - growth, duplication of organelles, proteins for mitosis
M - mitosis, very short

Question 1

Functions of mitosis

Answer 1

Replicate DNA accurately, segregate chromosomes, replicate cell structures, divide cells

Question 2

Karyokinesis

Answer 2

Division of nucleus

Question 3

Cytokinesis

Answer 3

Division of cytoplasm and cell contents

Question 4

Interphase

Answer 4

Includes G1, S, G2

G0 if cell has left cycle

Question 5

Duplication of centrioles

Answer 5

Pair splits, each becomes nidus for new centriole
Reform gamma tubulin and capping proteins
MTs nucleate through gamma tubulin rings

Question 6

Deviations from cell cycle

Answer 6

G0 - quiescent phase (not good environment)

Gtd - terminal differentiation (muscles, nerves)

Question 7

Prophase

Answer 7

Chromatin condenses to chromosomes, nucleolus breaks down
Centrioles migrate, MTs develop

Late prophase - nuclear envelope breaks down

Question 8

Chromosome condensation

Answer 8

Condensin increases coiling

Cohesin binds sister chromosomes

Question 9

Dissolution of nuclear envelope

Answer 9

Occurs during “prometaphase”
M-CDK phosphorylates lamin
Breaks into small vesicles of lamin + membrane
Allows fast reassembly after mitosis complete

Question 10

Microtubules during mitosis

Answer 10

Astral
Polar (connect MT to MT in spindle, push against each other to separate centrosomes)
Kinetochore (pull chromosomes towards centrosome)

Question 11

Metaphase

Answer 11

Chromosomes migrate and align at equator of spindle via MT “tug of war”
MT’s attach to kinetochores

Question 12

Centromere

Answer 12

Region where sister chromosomes attach (DNA)

Kinetochore is complex of 30+ proteins that attach centromere to microtubules (plate structure)

Question 13

Separation of chromatids

Answer 13

Anaphase promoting complex (APC) is phosphorylated when aligned
Ubiquitinates securin which is inhibitor of a cohesin protease
Securin destroyed ->protease active -> cleaves cohesin

Question 14

Anaphase

Answer 14

A - chromosomes to centrosome via depolymerization of kinetochore MTs and dyneins on astral
B - poles apart via kinesins on polar MTs

Question 15

Telophase

Answer 15

MT’s depolymerize
Lamin, pore complexes dephosphorylated - nuclear membrane reforms
Chromosomes decondense
Actin contractile ring -> cytokinesis

Question 16

Time of mitosis

Answer 16

Very short! 2-3 hours total

G1 determines whether rate of cell division
Cells that get to G2 will go through mitosis

Question 17

Telomeres

Answer 17

Repeating sequences
Not always transcribed -> aging
Telomerase rebuilds and can extend lifespan

Question 18

Regulation of cell cycle

Answer 18

Cyclins only present for short time, activate CDKs
CDKs always present, but must bind to cyclin to be active
Also regulated by phosphorylation (checkpoints)
Many targets (transcription factors, kinases, activate other cyclins)

Conserved across species
Can cause cancer…

Question 19

S cyclin

Answer 19

Initiates DNA replication (S phase)

Joins with s-CDK
Phosphorylates pre-replicative complex which normally inhibits
Allows origin of replication complex (ORC) to begin fx

Question 20

Cyclins

Answer 20

Only present for short period - translated, then ubiquitinated
Carry out function via CDK

Question 21

Checkpoints

Answer 21

Regulate cyclins and CDKs based on "quality control"
G1 - env't favorable?
S - DNA damage?
G2 - DNA replicated?
M - sister chromosomes at equator?

Question 22

Retinoblastoma

Answer 22

Inhibits transcription of proliferative proteins (via inhibition of transcription regulators) based on env’t
G1/S cdk inactivates by phosphorylation, allowing replication to begin

Defects cause proliferation despite env’t (cancer)

Question 23

p53 mechanism

Answer 23

Always translated and broken down in cell

p53 is phosphorylated and stabilized if cell stress or DNA damage
Transcription upregulator of p21, which binds and inhibits G1/S-cdk
Also can initiate apoptosis

Most common cancer mutation (most cells)

Question 24

Apoptosis

Answer 24

Programmed cell death, not inflammatory
Normal part of development, degraded or damaged cells
Triggered by p53, TNF, cytochrome c in cytoplasm (vs mitochondria), lack of growth factors, bad env’t
Mediated by caspases
Nucleus and cell contents into vesicles -> phagocytosed

Question 25

BCL2

Answer 25

“B cell lymphoma” 2 gene
Blocks apoptosis
Upregulated in melanoma, breast, prostate, lung, etc