Mitosis Flashcards

1
Q

What occurs during G1?

A

growth prior to DNA replication. It is the longest stage of the lifecycle

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2
Q

What is G0 and what are the two different types?

A

G0- cell temporarily leaves the cell cycle because conditions are unfit for replication

GTD- terminal differentiation, the cell will not re-enter the cell cycle.

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3
Q

What occurs during the S phase?

A

DNA duplicates, centrioles and centrosomes duplicate

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4
Q

What occurs during prophase?

A

chromatin condenses- mediated by cohesins and condensins
centrosomes migrate
MTs form
nucleolus disappears

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5
Q

What occurs during pro-metaphase?

A

nuclear envelop disappears

MTs attach to the kinetochores

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6
Q

How does the nuclear envelope degrade?

A

The process is caused by the phosphorylation of lamin, which causes the IFs to disassociate. Dephosphorylation post division will reassemble the membrane.

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7
Q

What happens during metaphase?

A

Chromosomes align- driven by tug of war between MTs

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8
Q

What are the 3 types of MTs present in mitosis and what do the do?

A

Kinetochore MTs- bind to kinetochore and pull on the chromatin (disassemble)
Polar MTs- attach to other pole’s MTs and push using kinesins
Astrial MTs- attach to periphery of cell membrane and pull centrosomes towards membrane via dyneins.

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9
Q

Differentiate- centrosome, centromere, kinetochore

A

centrosome- MTOC containing centrioles
centromere- region on chromosome containing kinetochore and heterochromatin
kinetochore- proteins within the centromere that bind the kinetochore MTs

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10
Q

What happens in anaphase?

A

Sister chromatids break apart and move towards poles
anaphase a- kinetochore MTs shorten to pull chromosomes to pulls, astrial pull towards membrane
anaphase b- polar mts push against each other

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11
Q

Differentiate between anaphase A and B

A

A is about “pulling”- astrial MTs use dynein and kinetochore MTs disassemble.

B is about pushing- kinetochore MTs use kinesin to push each other

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12
Q

How does sister chromatid dissociation occur?

A

anaphase promoting complex- enzyme that ubiquitinizes securin, which activates a proteolytic enzyme to destroy cohesin, which is the protein holding the chromatids together

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13
Q

What does cohesin do?

A

It is the protein that holds the sister chromatids together

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14
Q

What does securin do?

A

It is ubiquitinzed by the anaphase promoting complex. It inhibits a proteolytic enzyme from destroying cohesin. When it gets destroyed, it results in cohesin being destroyed and the sister chromatids come apart.

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15
Q

What happens in telophase?

A

Chromatids reach their poles and start to unbundle
lamina is dephosphorylated and reforms nuclear membrane
mts depolymerize
actin forms contractile ring

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16
Q

What are telomeres and why are they important

A

non-coding bases found at the end of chromosomes. Replication is inefficient and bases are lost off the end during every division. Because telomeres are non-coding, loss of telomere basis is not a loss of genetic information. the loss of telomeres can be a signal to stop dividing.

17
Q

What is the difference between kinases and phosphatases

A

kinases phosphorylate. phosphatases dephosphorylate

18
Q

What are the two types of proteins key in regulating the cell cycle?

A

cyclins- only present during certain parts of the cell cycle and form complex with CDK to move the cell forward

cyclin dependent kinases- always present, activated by binding with cyclin, allowing them to activate proteins that will progress the cell cycle

19
Q

What is a well known cyclin/CDK complex?

A

S-cyclin- promotes the advancement into the S phase. The origin of replication is where replication begins, and is activated by the origin recognition complex (ORC). The ORC is bound and inhibited by a pre-replicative complex. S-cycling phosphorylates the inhibitor and frees the ORC to being replication and thus the S phase

20
Q

How are cyclin/CDK complexes disposed of?

A

Cyclin is ubiquitinized and destroyed, freeing the CDK.

21
Q

What are some examples of checkpoints during the cell cycle?

A

g1- appropriate resources and growth factors
s- is their damaged dna?
g2- is their sufficient protein to move into M, any dna damage?

22
Q

What is retinoblastoma?

A

Rb inhibits transcription factors in healthy cells. Rb is deactivated by a cyclin/CDK phosphorylation, allowing transcription factors to initiate replication. mutations to Rb allow for unregulated growth- cancer

23
Q

What is p53?

A

A protein that when activated, prevents the cell from moving forward. It is constantly being produced and broken down. When phosphorylated, it is stabilized and does not break down, preventing the cell from moving forward. it prevents this by upregulating inhibitors of the cyclin/CDK complex. Enzymes that phosphorylate it are signaled by damaged DNA or cellular stress. It is also possible for p53 to induce apoptosis.

24
Q

What are the various mechanisms for apoptosis?

A

apoptosis is programmed cell death via fragmentation of the nucleus and budding of the cell into vesicles. This is usually mediated by caspase, but many different pathways can activate caspase. These include p53, Bcl2, cytochrome c, or TNF

25
Q

Why is caspase important?

A

It is the common pathway for apoptosis.

26
Q

What is BcL-2?

A

An anti-apoptotic enzyme that, when unregulated, can result in cellular dysfunction.

27
Q

What are the 4 functions of the cell cycle?

A
  1. copy/pass on genetic info
  2. segregate organelles and macromolecules appropriately
  3. create 2 identical daughter cells
  4. segregate genetic material accurately