Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIOL 2030 > Ch. 18 Control of Cell #s and Size, M Phase, Mitosis, Cytokinesis > Flashcards

Ch. 18 Control of Cell #s and Size, M Phase, Mitosis, Cytokinesis Flashcards

1
Q

how can body and organ size be determined

A

cell growth, division, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the most common form of programmed cell death

A

apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why is apoptosis necessary

A

due to body/organ dynamism (constantly having to respond to environment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is dynamism controlled by

A

cell birth and death rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what process is apoptosis crucial to

A

sculpting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

compare apoptosis and necrosis

A
  • apoptosis: molecular pathways which complete internal degradation leading to engulfment by phagocytic cells (“clean”)
  • necrosis: spewing of cellular contents into environment (“messy”)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe necrosis and when it would occur

A

physical or chemical damage to cell (esp to plasma membrane) causes all cellular contents to release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what triggers apoptosis

A

caspase molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

draw out how apoptosis would would be triggered

A

main points: initiator procaspase dimerizes, activates, and cleaves into an active form (initiator caspase); this active form would activate executioner procaspases thru cleavage causing caspase cascade leading to apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe the initiator procaspase structure

A
  • adaptor binding region
  • protease domain which has protease properties
  • monomers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how can initiator procaspases be activated

A

when an apoptotic stimulus signals adaptor molecules to bind to them (dimerizes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do we mean by caspase cascade

A

positive(?) feedback loop of activated caspase molecules which cleave intracellular molecules leading to death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what type of a signal is apoptotic; how does this affect its control

A

all-or-nothing (i.e. irreversible); tightly controlled and regulated through Bcl2 proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe Bcl2 family of proteins

A

promoters or inhibitors of cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what Bcl2 proteins promote cell death; inhibit?

A

Bax and bak; Bcl2 protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

draw out the process of Bax or Bak molecules promoting cell death

A

main points: apoptotic stimulus on organelle (e.g. mitochondria), bax/bak will facilitate cytochrome c movement from organelle to cytosol, adaptor proteins bind to cytochrome c molecules, these units arrange into a wheel-like structure (apoptosome), procaspase molecules will attach to apoptosome and activate leading to caspase cascade and apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can Bcl2 affect bax/bak from promoting cell death

A

Bcl2 would inhibit Bax/bak from following through with their role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how does unicellular organism growth regulate

A

thru nutrient availability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how are multicellular organism cells regulated

A

by extracellular signal molecules for survival, growth, division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are some examples of extracellular signal molecules that regulate multicellular organism cells

A
  • soluble proteins secreted by neighboring cells
  • proteins bound to surface of neighboring cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the positive extracellular signal proteins

A
  • survival factors
  • mitogens
  • growth factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what do we mean by positive extracellular signal proteins

A

things that tell a cell to not go thru apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

define mitogens

A
  • proteins that induce cellular division or
  • enhance rate of division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

why do animal cells need survival factors

A

to prevent apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are target cells

A

cells that are beyond synapse of nerve cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how are survival factors used to avoid apoptosis (EX w nerve cells)

A

target cells release survival factors to nerve cells; cells that don’t receive survival factors will go thru apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the benefit of survival factors

A

target cells and survived cells match in number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are survival factors capable of suppressing and how

A

apoptosis by regulating Bcl2 family proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

draw out one way how survival factors can block apoptosis thru regulation of Bcl2 family proteins

A

main points: survival factor attaches to receptor and activates it; leads to signal transduction pathway that activates transcription factors, which begins transcription of Bcl2 gene; this makes the Bcl2 protein which blocks apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the two overall results that survival factor mechanisms can lead to

A
  • activation of proteins which inhibit apoptosis
  • inhibition of proteins that promote apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what do mitogen stimulate

A

cellular division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

draw out one pathway of how can mitogens work

A

main points: in a resting cell, mitogen receptor and transcription regulator are inactivated due to an active protein brake; the mitogen attaches to receptor leading to intracellular signaling pathway causing activated cdks; cdks will phosphorylate protein brake and inactivate it; transcription regulator activates and allows for transcription of genes for entry into s phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what was one of the first mitogens identified

A

platelet-derived growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the role of pdgf in the body, why?

A
  • cell division/proliferation
  • blood clotting at wound site triggers platelets to release pdgf, which binds to receptor tyrosine kinases on surviving cells around wound
  • if liver is damaged then liver makes hepatocyte growth factor also leading to cell division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how are cells able to grow to completely different sizes

A

thru growth factor extracellular signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

cell growth and cell cycle control are _______ to e/o

A

independent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

draw a generic pathway of growth factors stimulating cellular growth

A

main points: GF binds to receptor causing an intracellular pathway, either leading to increase in protein synthesis or decrease in protein degradation; results in cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is myostatin

A

a type of inhibitory extracellular signal protein that limits cell growth and proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

define myoblasts

A

skeletal muscle cells

40
Q

how does myostatin affect myoblast growth and proliferation

A

by acting as a brake on skeletal muscle formation

41
Q

what were to happen if the myostatin gene is deleted/mutated

A

large and bulky skeletal muscles; larger overall organism size

42
Q

compare mitosis and cytokinesis

A

separation of chromosomes vs cytosol

43
Q

how many chromosomes do humans have normally; temporarily during cell cycle

A

46; 92

44
Q

if precise separation of chromosomes does not occur then what will happen to the cell

A

lack of full-functions

45
Q

what are sister chromatids

A

duplicated/identical chromosomes during M phase of mitosis

46
Q

how are sister chromatids held together

A

cohesin ring protein complexes

47
Q

if there are defective cohesin rings then, what will happen

A

major errors in chromosome segregations leading to fatal mutations

48
Q

all events in M phase are started by

A

m-cdk

49
Q

aside from —- what is m-cdk able to trigger ** check what last deck mentioned

A

chromosome condensation, mitotic spindle assembly

50
Q

draw out the positive feedback loop of m-cdk accumulation leading to metaphase

A

main points: inactive m-cdk is dephosphorylated by active phosphatase enzyme which causes m-cdk to become activated. this leads to a positive feedback loop where inactive phosphatase becomes active and helps inactive m-cdk to become active

51
Q

why is chromosome condensation required

A

allows for chromosomes to be more easily segregated into dividing cells

52
Q

what helps DNA to compact in chromosome condensation

A

protein complexes called condensins (similar structure to cohesin ring)

53
Q

what mediates mitosis and cytokinesis

A

cytoskeletal structures (actin, myosin, microtubules)

54
Q

what aids in physical separation of the chromosomes at the mitotic spindle

A

microtubules

55
Q

what aids in the physical separation of the two cells at the contractile ring (cytoplasm)

A

actin and myosin

56
Q

draw out how mitotic spindles form over the cell cycle (i.e. draw the centrosome cycle)

A

main points: initial centrosome (G1) replicates (S/G2); formation of aster and their migration to opposite pole ends (M); mitotic spindles form with replicated chromosomes (M); division of cells with eventual degradation of asters

57
Q

define an aster

A

divided chromosomes with microtubules sprouting out

58
Q

define mitotic spindle

A

two asters on opposing pole ends of cell with microtubules sprouting out

59
Q

what are the stages of nuclear (N) and cytoplasmic (C) division (M phase)

A
  • prophase (N)
  • prometaphase (N)
  • metaphase (N)
  • anaphase (N)
  • telophase (N)
  • cytokinesis (C)
60
Q

what occurs in prophase

A
  • chromosome condensation
  • mitotic spindle assembly (thru addition and removal of tubulin subunits by centrosomes/asters)
61
Q

what occurs in prometaphase

A

nuclear envelope breaks and this allows for spindle microtubules to bind chromosomes

62
Q

what occurs in metaphase

A
  • mitotic spindle gathers and aligns the chromosomes at the spindle centre (cell equator)
  • microtubules shrink
63
Q

what occurs in anaphase

A

sister chromatids separate from one another and move to opposite poles of cell

64
Q

what occurs in telophase

A
  • mitotic spindle disassembles
  • reassembly of two new nuclear envelopes
  • chromosomes decondense to normal interphase size
65
Q

what occurs in cytokinesis

A

cell separation by pinching of the cytoplasm

66
Q

describe interpolar microtubules; in what stage of M phase can we find these in

A
  • the microtubules from opposite polar centrosomes touching one another;
  • prophase
67
Q

microtubules are referred to as dynamically instable; however, there is a point during prophase where they gain stability. what instance is this referring to

A

interaction (physical touching) of microtubules from one centrosome to another (collective aster), which helps them to align at the cell equator

68
Q

what is a centromere

A

specialized DNA region needed for chromosome separation, generally more towards the centre of the cell but can be between the two telomeres of the chromosome

69
Q

what is a kinetochore

A

specialized protein complexes that attach to mitotic spindle

70
Q

what happens to kinetochores during prophase

A

proteins assemble into large complex on each centromere facing in opposite directions

71
Q

label a chromosome with the following terms: cohesins, kinetochore, centromere, sister chromatid, non-sister chromatid, telomere, mitotic spindle microtubules

A

…

72
Q

why are the chromosomes in the nucleus and why can’t the mitotic spindles access them in prophase

A

nuclear envelope is not broken down at this point

73
Q

define bi-orientation

A

chromosomal orientation to opposite poles of the bipolar spindle before cell division

74
Q

why do the spindle microtubules “bump into” chromosomes in prometaphase

A

the nuclear envelope has been disassembled

75
Q

what happens to kinetochore microtubules during prometaphase

A

since there are 2 kinetochores on the entire replicated chromosome (1 per sister chromatid), the microtubules for each kinetochore will link to one spindle pole (opposite) – biorientation

76
Q

why is tension required at the kinetochore

A

to act as a checkpoint for the cell cycle

77
Q

what are the classes of microtubules that make up the mitotic spindle

A
  • aster
  • kinetochore
  • interpolar
78
Q

describe aster microtubules

A

microtubules emanating from the aster but are not attached to the microtubules from the opposite aster or chromosomes

79
Q

describe kinetochore microtubules

A

microtubules (20-40) emanating from asters that bump into and attach to chromosomes

80
Q

describe interpolar microtubules

A

microtubules that link up two polar sides, forming a stable region in middle

81
Q

the sister chromatids constantly oscillated and adjusted during metaphase, so how do they align at the middle of the cell

A

microtubules that are attached to the chromosomes are still going thru constant growth and shrinkage and the net result is to lie in the middle

82
Q

how are kinetochores separated in anaphase

A

cohesin rings are broken by separase (cohesin proteolysis)

83
Q

what is separase

A
  • aka separin
  • cysteine protease enzyme that hydrolyses cohesin
84
Q

draw out the pathway of separase cleaving cohesins during anaphase

A

main points: inhibtory protein (securin) attached to inactive proteolytic enzyme (separase); active anaphase promoting complex ubiquitylates and degrades inhibitory protein making proteolytic enzyme active; proteolytic enzyme cleaves and dissociates cohesins present (in metaphase) during anaphase

85
Q

APC degrades the inhibitory protein limiting anaphase (ex securin) but can also degrade

A

M-cyclin

86
Q

describe the checkpoint for spindle assembly; what is its importance

A
  • chromosomes without microtubule attachment send out a stop signal
  • stop signal blocks APC activation
  • hence no chromosomal separation until all sister chromatids are attached with kinetochore microtubules under tension
  • even one unattached chromosome will result in mutant cells
87
Q

what are the processes of anaphase

A

anaphase a and anaphase b

88
Q

describe anaphase a

A
  • kinetochore microtubules shorten rapidly
  • physical poles are moving apart
  • both result in chromosomes pulled towards poles
89
Q

describe anaphase b

A
  • poles pushed toward centre via sliding fence mechanism generated b/w interpolar microtubules
  • poles pulled apart
  • microtubules growth at plus end of polar microtubules
90
Q

telophase is often described as the _____ period

A

restoration

91
Q

what happens in telophase that triggers cytokinesis(?)

A

nuclear proteins enter thru nuclear pores of envelope, causing swelling

92
Q

why can’t chromosomes complete gene transcription during mitosis

A

due to extreme condensity

93
Q

draw out nuclear envelope cycle

A

main points: interphase nuclear pore proteins and lamins phosphorylate; prometaphase nuclear pore proteins and lamins dephosphorylate; fusion of nuclear envelope vesicles

94
Q

what is the mechanism of nuclear envelope cycle control

A

(de)phosphorylation of nuclear pore proteins and lamins

95
Q

what is the first sign of cytokinesis 1 (during anaphase 1)

A

furrowing of plasma membrane (indentation along middle) due to contractile ring under plasma ring

96
Q

in reference to the mitotic spindles, cleavage furrow always orients in what direction; why?

A
  • perpendicular
  • to ensure one pole is in each daughter cell
97
Q

describe cytokinesis 2

A
  • actin and myosin filaments overlap
  • sliding filaments generate force (similar to skeletal muscle)
  • contractile ring disassembles after cell division

BIOL 2030 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions