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Cell Bio Final > Nucleus/Cell Division > Flashcards

Nucleus/Cell Division Flashcards

(46 cards)

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1
Q

anucleate cells

A
  • not all cells have nucleus(mammalian RBCs and anucleate; avian/amphibian are not)
  • skin epidermis
  • lens of the eye (lens epithelial cells-> differentiate-> lens fibers)
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2
Q

nuclear envelope

A
  • 2 membranes
  • connected to the ER
  • nuclear pores
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3
Q

nuclear pores

A
  1. pass proteins via diffusions (>62,500 Daltons; ex: histones)
  2. Non-histones= much larger than 62,500 Daltons
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4
Q

nucleoplasmin

A
  • X. laevis(African Clawed Toad)– 10% of nuclear protein
  • first chaperone protein ever discovered
  • functions:
    1) gene stability
    2) transcriptional regulation
  • pentamer” 5x33,000=165,000 Daltons
  • receptor+ATP
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5
Q

Lamins

A
  • intermediate filaments= critical in supporting cellular membranes
  • lamins A, B, C ~60-70 kDa
  • karyoskeleton
  • lamins connect the chromosomes
  • nucleus in mitosis (nuclear envelope dissolution(disappears), inc MPF–> phosphorylation of lamins–> nuclear dissolutions)
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6
Q

MPF

A
  • maturation-promoting factor
  • promotes spindle assembly, chromatin condensation, and the breakdown of nuclear envelope
  • inc MPF= phosphorylates lamins= nuclear dissolution
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7
Q

cell fusion

A

causes chromosome condensation of the G1 cell

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8
Q

defects in Lamin A assembly

A
  • associated with Progeria (Hutchinson-Gilford Progeria Syndrome)
  • a precocious aging disease children age prematurely
  • mutation in LMNA gene which codes lamin A–> faresyl cannot be cut off lamin A and the protein piles up at the nucelar envelope= waek nuclear stiffness/fragility= inc cell death
  • drugs to combat progeria work by blocking the addition of famesyl
  • normal cells: farnesyl is added to lamin A which helps it to reach the nuclear lamina, once it gets there, it is cut off and lamin A can be incorporated into the lamina
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9
Q

Lonafarnib

A
  • farnesyltransferase inhibitor
  • used to treat Progeria
  • prevents proteins from building up and damaging cells
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10
Q

the cell cycle

A
  • following mitosis, daughter cells have 2n chromosomes in diploid organisms and 1n in haploid organisms
  • G1= period between “birth” of cell and following mitosis and initiation of DNA synthesis(beginning of S phase)
  • late G1 when cells become committed to enter the S phase= START/restriction point
  • end of S phase= cells enter G2 containing twice the number of chromosomes they had in G1 (4n or 2n)
  • end of G2= onset of mitosis
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11
Q

cell cycle facts

A
  • 1953= Howard and Pelc-Broadbean
  • defines cancer
  • embryogenesis
  • no mistakes allowed
  • you= 100 trillion cells= all come from one cell
  • cell division– cell death (ex= RBCs: half life is 120 days, new RBCs= 2.5x10^5/second
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12
Q

3T3 cells

A
  • commonly used for cell cycle and oncogene studies because they are easy to convert from normal to cancer cells
  • isolated from mouse embryo tissue
  • made famous by Arthur Pardee
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13
Q

G0

A

= “quiescent period”
- differentiated cell
- cell without intention of dividing

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14
Q

G1

A
  • 9 +/- hours out of 24 hour cycle period
  • requires growth period (PDGF, EGF, insulin)
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15
Q

restriction point

A
  • G1/S border
  • “go-no go” point
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16
Q

cell synchrony

A
  • typically: cells are going through different cell cycle phases at the same time
  • to understamd the bases of each individual cell cycle phase, need to have all cells go through select cell phases at the same time
  • cells only stay in synchrony for a few cycles given the extreme transit variability of the G1 cell cycle phase; then fall out of synchrony after the 4th/5th cell cycle
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17
Q

amino acid deprivation

A

all cells stall in G1

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18
Q

serum deprivation

A

all cells stall in G1

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19
Q

protein synthesis inhibitors

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A
  • all cells stall in G1
20
Q

Microtubule inhibitors

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A
  • all cells stall in M
21
Q

DNA synthesis inhibitors

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A

all cells stall in S

22
Q

cyclins

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A
  • control the cell cycle
23
Q

Ruderman and Hunt

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A
  • sea urchin egg experiment
  • discovered cyclins= master regulators of cell cycle
  • found that cyclins rose and fell in cyclical pattern during early cell divisions in fertilized sea urchin eggs
  • found that cyclins participated in synchronous cell divisions and degraded with each division–> peaked just before mitosis, destroyed after cell division, reappeared right before next round of division
  • cyclins activate cyclin-dependent kinases which control the progression of cells through different phases of the cell cycle
24
Q

Sae urchins

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A
  • absence of cancer despite some species being long-lived
  • possess high regenerative capacity
  • lack adaptive immune system
  • cancer resistant animal model
25
cyclins and CDKs
- when cyclin binds to CDK, it activates it so that it can phosphorylate specific target proteins - they will phosphorylate specific proteins at different times, pushing the cell forward through growth, DNA replication, and division
26
Cyclin D
- required for G1 passage
27
G1 transit time
- how to determine is cell cycle transit time is the same in normal cells versus cancer cells - synchronize cells so all are in G0 then add 3H-thymidine--> look for appearance of radioactive cells
28
S transit time
- how to determine is cell cycle transit time is the same in normal cells versus cancer cells - use randomly cycling cells and add 3H-thymidine--> count percent in S and multiply by total cell cycle time
29
G2 transit time
- how to determine is cell cycle transit time is the same in normal cells versus cancer cells - use randomly cycling cells, add 3H-thymidine for 30 mins--> look for radioactive M cells
30
M transit time
- how to determine is cell cycle transit time is the same in normal cells versus cancer cells - use randomly cycling cells--> count percent in M and multiply by total cell cycle time
31
is there a difference in cell cycle transit times in normal vs cancer cells?
no difference between cancer vs normal cells
32
S phase
- entry into S phase is defined by the unwinding of origins of DNA replication - CDKs trigger initiation of DNA synthesis by phosphorylating and recruiting MCM helicase activators to DNA replication origins - eukaryotic chromosomes are replicated from multiple replication origins - S phase CDKs allow DNA replication to be initiated only at G1-S phase transition and prevent re-initiation from origins that have already been fired - when CDKs phosphorylate MCM, DNA begins to be unwound--> DNA Polymerases are recruited to origins--> initiation of DNA replication on both leading and lagging strands
33
replicons
- DNA that is copied from a single origin - process of creating and fusing the replicons ensures that each DNA strand is copied only once, maintaining the correct gene copy number each time a cell replicates - "replication bubbles"
34
What happens in G2
- cell verified that all of the DNA has been correctly duplicated and all DNA errors have been corrected - chromosome condensation is initiated - early organization of the cell cytoskeleton - mitotic cyclin dependent kinases initiate activity
35
36
mitosis
- m phase - Prophase: chromatin condenses into chromosomes, spindle fibers begin to form from centrosomes, nuclear envelope starts to break down - Metaphase: chromosomes line up in the middle, spindle fibers attach to centromeres - Anaphase: sister chromatids are pulled apart to opposite sides of the cell (each chromatid is a separate chromosome) - Telophase: chromosomes arise at pole and de-condense into chromatin, nuclear envelopes re-from around each set of chromosomes, spindle fibers disassemble
37
Lamin B phosphorylation
- lamin B phosphorylation by MPF - required for nuclear dissolution
38
reassembly of nuclear envelope
- extensions of the ER associate with each decondensing chromosome and then fuse with one another, forming a double membrane around the chromosome - De-phosphorylated nuclear pore subcomplexes reassemble into nuclear pores, forming individual mini-nuclei called karyomeres - enclosed chromosome further decondenses, and fusion of the nuclear envelopes of all karyomeres at each spindle pole forms a single nucleus containing a full set of chromosomes
39
MPF
1. Maturation Promoting factor 2. Mitosis Phase Factor
40
Maturation promoting factor
- egg arrested in G2--> meiosis I--> blastula - induces entry into meiosis and oocyte maturation when injected into G2 arrested oocytes
41
Mitosis Phase Factor
- induces mitosis in all eukaryotic cells
42
cyclin B
- mitotic cyclin - binds to CDK1---> activity rises through cell cycle until mitosis where is falls abruptly due to degradation
43
Ruth Sager
- discovered tumor suppressor genes - halt growth of cancer - identified genes that are not mutated but whose expressions are altered in cancers
44
p53
- "guardian of the genome" - tumor suppressor gene - normally unstable transcription factor - ATM/R can phosphorylate p53--> stable - p21 is triggered - G1 CDKs--> blocked
45
Budding Yeast and the Cell cycle
- start - G1: spindle pole body duplication, bud emergence - S: DNA replication - S/G2: Spindle formation; nuclear migration - M: Chromosome segregation; nuclear division, cytokinesis - Parent cell and daughter cell
46
Fission Yeast and the Cell Cycle
- Start - S: DNA replication - G2: cell growth, spindle pole body duplication - G2/M: chromosome condensation - M: spindle formation, chromosome segregation, nuclear division - 2 daughter cells

Cell Bio Final (5 decks)

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