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BIOL 2020 > 8: Cell Cycle > Flashcards

8: Cell Cycle Flashcards

1
Q

Why is cell cycle important

A
  • highly organized and regulated
  • cell cycle= repeated rounds of cell growth and division
  • primary goal= to divide the genetic materials and organelles accurately and equally
  • for reproduction in prokaryotes and eukaryotes
  • for replacing old cells with new cells
    • during would healing or cell damage
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2
Q

Why do we need to understand cell cycle/cell division

A
  • continuity and diversity

- mitosis ensures continuity

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3
Q

What is the basic role of the cell cycle

A
  • maintain chromosome number

- increase diversity among individuals and species

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4
Q

What is the overall theme of the cell cycle

A

-double, align, separate

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5
Q

M phase

A
  • mitosis (nuclear division)
  • cytokinesis (cytoplasmic division)
  • approx 30 mins
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6
Q

Interphase

A
  • growth phase
  • G1 (gap)
  • S (synthesis - DNA replicated)
  • G2 (gap)
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7
Q

S phase

A
  • DNA replication occurs
  • after replication, each chromosome consists of 2 sister chromatids, held together at the centromere
  • 2 sister chromatids will be separated during mitosis
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8
Q

Appearance of cell after S phase

A
  • cell material in synthesized
    • cell mass is higher
  • DNA has replicated
  • chromatin are diffuse and decondensed
    • DNA not organized
  • nuclear envelope intact
  • centrosomes have also duplicated
    • and double the organelles
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9
Q

Key experiment to deduce features of cell cycle

A
  • flow cytometry
  • add radioactive thymidine to an asynchronous cell culture (ie. cells at different stages of cycle)
  • lead 3Hthymidine in culture media for 30 mins
  • cells will incorporate it into DNA that is being replicated
  • refresh media and wait
  • use autoradiography to look for labeled DNA
  • similar to pulse-chase but with DNA
  • only cells that were going through DNA replication in that 30 min pulse will show up (only in S phase)
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10
Q

Observations of flow cytometry experiment

A
  • if cell was gong through mitosis, the DNA was not labeled
    • therefore, cells in mitosis are not replicating DNA
  • only a fraction of the cells were labeled
    • therefore, S is only a single, short phase of the cycle
  • there was a gap of at least 30 mind between the end of labelling and when the labelled DNA showed up in compact chromosomes
    • therefore there must be a G2 phase o at least 30 mind between S and M phase
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11
Q

Phases of mitosis

A
  1. Prophase
  2. Prometaphase
  3. Metaphase
  4. Anaphase
  5. Telophase
  • MPF = maturation promoting factor
    • initiates mitosis
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12
Q

Prophase

A
  • chromosomes start to condense
  • Centrosomes move to opposite poles
  • nuclear lamina breaks down (phosphorylation by kinases)
  • each chromosome consists of:
    1. 2 identical strands (chromatids)
    2. Joined at centromere
    3. Terminal regions (telomeres)
  • 2 proteins important in maintains compacted mitotic chromosomes
    • condensin: organizes DNA to maintain a condensed state. Activated by phosphorylation by MPF
    • cohesin: holds 2 sister chromatids together. Run entire length of chromosome but lost fro the arms in prophase (remains concentrated in the centromere)
    • condensin and cohesin work together during chromosome condensation and segregation
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13
Q

Centromeres

A
  • also called primary constriction
  • location of highly repeated DNA sequences
  • this DNA is not translated
  • repeated are an indication to cell that this is where kinetochore needs to be assembled
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14
Q

Kinetochores

A
  • structure on outer surface of centromere
  • more than 100 proteins
  • roles:
    1. Attachment site between chromosome and microtubules
    2. Location of some motor proteins involved in anaphase
    3. Involved in mitotic checkpoint

-MT plus end attaches to kinetochore

  • kinesin13 (depolymerase) found in kinetochore
    • plus a regular kinesin and cytoplasmic dynein
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15
Q

Centrosomes

A
  • composed of 2 perpendicular centrioles

- each centriole made of 9 triplet MTs + pericentriolar material (PCM)

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16
Q

S phase

A
  • DNA duplicates

- centrosome duplicates

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17
Q

Centrosome cycle

A
  • normally in G1 there is only 1 centrosome per cell

- during S phase new baby centrioles will emerge at right angles from each parent centriole

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18
Q

Prometaphase

A
  • chromosomes have finished condensing
  • nuclear envelope is gone
  • centrosomes at opposite poles
  • mitotic spindles start to form
  • attachment of MTs to chromosomes and the movement of chromosomes to equator
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19
Q

Mitotic spindle

A
  • composed of:
    1. Astral MT: radiate outward (shorter)
    2. Kinetochore MT: attach to sister chromatids
    3. Polar MTs: overlap and do not attach to sister chromatids

-plus end of MT associates with kinetochore

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20
Q

Movement of chromosomes to equator (congression)

A
  • chromosomes usually originally attach to the MT along its side
  • but then a kinesin will move it to the plus end
  • of that kinesin is missing, the chromosome will not get to the end of MT (ie. wont get to equator)
  • once both kinetochores are attached to MT from opposite poles, the chromosomes will be moved to the centre of the cell (congression)
  • MTs will either grow or shrink
    • whichever is required to get the chromosome to the middle
    • depolymerize on one side, while adding subunits on the other side
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21
Q

Metaphase

A
  • chromosomes are aligned at the metaphase plate
  • longest part of mitosis
  • once at equator, cell confirms that each chromosome is under tension, and bi-oriented (spindle assembly checkpoint)
22
Q

Anaphase

A
  • cohesin is cleaved by separase
  • sister chromatids pulled to opposite poles of the cell
  • normally separase (protease) is inhibited by securin (until needed)
    • mechanism to control when cohesin gets cleaved
    • MAD and BUB must confirm that every chromosome is bi-oriented and under tension
  • once all chromosomes are attached, mad and bub activate anaphase promoting complex (APC)
  • APC degrades securin once the chromosomes are attached
  • separase now active, and cuts cohesin
23
Q

Anaphase A

A
  • movement of chromosomes to poles
  • kinetochore MTs get shorter
  • depends on motor proteins
    • kinesin13 (depolymerase) to disassemble MT
    • cytoplasmic dynein just ahead of where MT is falling apart to walk to minus end
24
Q

Anaphase B

A
  • spindle poles move further apart
  • polar MTs get longer
  • depends on motor proteins:
    • 2 kinesin5 attached to each other (one on back of the other)
    • they bind between antiparallel polar MTs and slide apart to elongate the spindle
25
Q

Telophase

A
  • chromosomes decondense
  • nuclear envelope reforms (dephosphorylation by phosphatases)
  • spindle disassembles
26
Q

Cytokinesis

A
  • splitting of cytoplasm
  • contractile ring theory:
    • myosin II moves along a ring of actin in the cortex (just below cell membrane)
    • actin concentrated in a cleavage furrow
    • midbody: transient dense structure connecting 2 daughter cells at end of cytokinesis
    • abscission: final step of cytokinesis - splitting into 2
    • midbody is the last to be cut
27
Q

Cancer

A

-happens when the cell cycle becomes unregulated

28
Q

Growing cancerous cells in culture

A
  • dont require growth factors
  • will divide indefinitely
  • will pile all over eachother
29
Q

HeLa cells

A
  • first cancer cells to be grown in culture

- from Henrietta Lacks

30
Q

Cell cycle length

A
  • varies in different cells
  • usually depends on G1
  • constantly replicating cells have short G1
  • mature nerve cells almost always in G1
    • hard to repair
  • liver cells live in G0 but then divide if activated by trauma
31
Q

Cell cycle check points

A
  • metaphase-anaphase transition
  • restriction point
  • G2-M transition
32
Q

Cell fusion experiment

A
  • helped us to figure out how the cycle was controlled

- heterokaryon=a single cell with 2 genetically different nuclei

33
Q

Fusion experiment 1

A
  • fuse G1-phase cells and S-phase cells
  • DNA in G1 nucleus immediately started to replicate
  • ie. there is a molecule in the S phase that triggers replication
34
Q

Fusion experiment 2

A
  • fuse G1 cells and M phase cells
  • DNA in G1 nucleus immediately started to compact and nuclear envelope started to disintegrate
  • ie. there must be a molecule in M phase cells that triggers prophase
35
Q

Progression through cell cycle

A
  • relies on cdks and cyclins
  • CDk is a kinases and phosphorylates other proteins to trigger different phases of the cell cycle to start
    • only when activated by a cyclin
    • CDK= cyclin dependent kinase
  • concentration of cyclin varies throughout the cell cycle
  • CDk usually always same concentration
36
Q

Work on control of cell cycle

A
  • Hartwell
  • Nurse
  • Hunt
  • Nobel prize 2001
37
Q

G2-M transition

A
  • G2 checkpoint
  • mitotic cyclin + mitotic CDK = MPF (maturation promoting factor)
  • once activated, CDK will phosphorylate other proteins to cause cell to progress into mitosis
  • M phase cyclin peaks just before M phase

-MPF complex must be phosphorylated before it is active

  • ATR recognizes and binds to broken DNA
    • ATR phosphorylates Chk1
    • Chk1 phosphorylates cdc25
    • a phosphorylated cdc25 is retained in the nucleus
    • therefore cdc25 cannot removed the inhibitory phosphate
      • mitosis will not start, cell must repair DNA
38
Q

Fission yeast experiment

A
  • fission yeast reproduce by growing and then splitting into 2 equal sized cells
  • we can predict exactly when they should divide (we know their normal length)
  • yeast cdks and cyclins and human cdks and cyclins are almost identical
  • yeast have cdk called cdc2 (cell division cycle)
    • CAK = kinase
    • Wee1 = kinase
    • cdc25 = phosphatase
39
Q

Regulation of MPF activity by phosphorylation

A
  1. MPF is phosphorylated by CAK and Wee1
    • CAK (CDK activating kinase) puts 1 activating phosphate on cdc2
    • Wee1 puts 2 inhibitory phosphates on cdc2 (inactivates it)
  2. Cdc25 will remove the 2 inhibitory phosphates
  3. MPF now active
  4. Once cell has gone through mitosis the activating phosphate is removed and mitotic cyclin is degraded
40
Q

Mutating Wee1 and cdc25

A
  • if Wee1 mutated, there is no brake applied and mitosis begins prematurely
    • daughter cells smaller than normal
  • if cdc 25 mutated, the brake is not removed and mitosis is delayed
    • cells longer than normal
41
Q

Ras-MAP pathway and cdk/cyclins

A
  • Ras-MAP pathway results in transcription of cdks and cyclins
  • the G1 cdk-cyclin complex phosphorylates Rb so E2F is able to transcribe other genes required for S phase
42
Q

P53 and restriction point

A
  • ATM = protein that detects and binds to damaged DNA (similar to ATR)
  • this leads to phosphorylation of p53
  • if p53 phosphorylated it will:
    1. Activate transcription of p21 which will inactivate G1 cdk
    2. Trigger apoptosis if damage is irreparable
  • p53 gene mutated in 50% of all tumors
    • if p53 doesnt halt cell cycle or induce apoptosis the cell becomes permissive and allows sick cells to divide
43
Q

Apoptosis

A
  • Greek=falling off
  • programmed cell death
  • apoptosis clears out cells between mammalian digits, in plans
44
Q

C. Elegant

A
  • used to study apoptosis
  • transparent round worm about 1mm long
  • lifespan 3 days
  • only 1090 cells produced during development so each can be followed with precision
    • 131 cells programmed to die at specific time
  • key proteins in apoptotic pathway named ced (ie cell death)
    • homologous proteins found in mammals (caspases)
45
Q

Features of apoptosis

A
  • cytoplasm shrinks, cell shrivels and becomes lobed
  • loss of adhesion
  • nucleus and organelles fragment
  • DNA digested by a DNAse in regular intervals (laddering) 200bp
  • flippant inserts phosphotidylserine into the outer leaflet of PM
    • usually in cytoplasmic leaflet
    • signal for macrophage to cut it
  • blebbing
  • cell dismantled into small apoptotic bodied
  • phagocytic cells ingest the apoptotic bodies
  • neighbouring cells protected from damage by potentially harmful digestive enzymes
46
Q

Necrosis

A
  • cell swells
  • organelles swill
  • cell contents leak into surrounding environment
  • leads to inflammation
  • bad for tissues
47
Q

Caspases

A
  • cysteine proteases (cysteine in active site)
  • cleaves at an aspartic acid residue
  • produced as inactive PROcaspases
    • activated by cleavage
    • leads to proteolytic cascade
48
Q

Caspase targets

A
  • lamins
  • cytoskeletal proteins
  • endonucleases (cut DNA)
49
Q

Extrinsic pathways

A
  • direct, death signal
  • death signal (eg. TNF) binds to a dearth receptor in PM
  • 2 adaptor proteins (FADD and TRADD) are recruited
  • 2 procaspases-8 also recruited
  • procaspases-8 cleave eachother to make the mature enzyme (caspase-8)
  • caspase-8 is an initiator caspase
  • caspase-8 initiates apoptosis by cleaving and activating downstream executioner caspases like caspase-3
50
Q

Intrinsic pathway

A
  • indirect
  • mitochondria mediated
    1. survival factor (trophic factor) binds a RTK
    2. causes protein called BAD to be phosphorylated (keeps cell alive)
    3. Mitochondrial outer membrane contains channel proteins called BAX
    • normally anti-apoptotic Bcl protein will keep this channel closed
    • if BAD loses is phosphate it will inhibit Bcl proteins and BAX channel will open
      1. Cytochrome c will be released from mitochondria
    • triggers apoptosis
      1. In the cytosol, cytochrome c recruits an adaptor protein Apaf-1 and another initiator caspase (procaspase-9) to form an apoptosome
      2. The apoptosome will activate (cleave) caspase-3 (executioner caspase)
51
Q

P53 in apoptosis

A
  1. P53 will bind to puma
  2. puma will bind to Bcl-2
  3. This allows cytochrome c to be released into cytoplasm… forms apoptosome with Apaf-1 and procaspase-9
  4. Apoptosome will activate caspase-3
52
Q

Anastasis

A
  • “rising to life”
  • cells avoiding suicide may play role in spread of cancer
  • even while undergoing apoptosis, cell holds onto a life line that could bring it back if situation improves/cell becomes healthier

BIOL 2020 (8 decks)

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