Brainscape's Knowledge GenomeTM

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


See full index

BIOC212 > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

3 parts of the cell cycle

A

Chromosome replication and cell growth

chromosome segregation

cell division

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

mitosis

A

nuclear division

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

cytokinesis

A

cell division

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

Longest phase of cell cycle

A

interphase

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

Short phase of the cell cycle

A

M phase

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

Three phases of interphase

A

G1, S, G2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What occurs in S phase

A

DNA replication

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

A comparison of the cell cycles of fission yeasts and budding yeasts

A

Fission vs budding

The fission yeast has a typical eucaryotic cell cycle with G1, S, G2, and M phases. In contrast with what happens in higher eucaryotic cells, however, the nuclear envelope of
the yeast cell does not break down during M phase. The microtubules of the mitotic spindle (light green) form inside the nucleus and are attached to spindle pole bodies
(dark green) at its periphery. The cell divides by forming a partition (known as the cell
plate) and splitting in two. The condensed mitotic chromosomes (red) are readily visible
in fission yeast, but are less easily seen in budding yeasts. (B) The budding yeast has
normal G1 and S phases but does not have a normal G2 phase. Instead, a microtubule based spindle begins to form inside the nucleus early in the cycle, during S phase. In contrast with a fission yeast cell, the cell divides by budding.

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

Cell cycle at permissive low temperature

A

normal

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

Cell cycle at permissive high temperature

A

restricted to G1 phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The morphology of budding

yeast cells arrested by a cdc mutation

A

In a normal population of proliferating
yeast cells, buds vary in size according to
the cell-cycle stage.

In a cdc15 mutant
grown at the restrictive temperature, cells
complete anaphase but cannot complete the exit from mitosis and cytokinesis. As a
result, they arrest uniformly with the large
buds, which are characteristic of late M
phase

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

Oocyte growth and egg cleavage in Xenopus

A

The oocyte grows without dividing for many months in the ovary of the mother
frog and finally matures into an egg

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

What happens after Xenopus fertilization

A

the egg cleaves very
rapidly—initially at a rate of one division cycle every 30 minutes—forming a
multicellular tadpole within a day or two. The cells get progressively smaller with
each division, and the embryo remains the same size.

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

Growth in Xenopus occurs when?

A

Growth starts only when
the tadpole begins feeding. The drawings in the top row are all on the same
scale (but the frog below is not)

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

the presence of an S-phase cell is evidence of

A

cell proliferation occurring

in response to damage

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

Analysis of DNA content with a
flow cytometer:

What are the key results?
Cells location and DNA content..

A

Most cells in G1 > G2 >S

DNA content G2 (2) > S > G1 (1)

The distribution of cells in
the case illustrated indicates that there are
greater numbers of cells in G1 phase than in G2
+ M phase, showing that G1 is longer than G2 +
M in this population.

those that
have an unreplicated complement of DNA and
are therefore in G1 phase, those that have a
fully replicated complement of DNA (twice the
G1 DNA content) and are in G2 or M phase, and
those that have an intermediate amount of DNA
and are in S phase

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

The control of the cell

cycle.

A

The essential processes of the cell cycle—such as DNA replication, mitosis,
and cytokinesis—are triggered by a cellc ycle control system.
By analogy with a
washing machine, the cell-cycle control
system is shown here as a central arm—
the controller—that rotates clockwise,
triggering essential processes when it
reaches specific points on the outer dial.

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

Three checkpoints in

the cell-cycle control system

A 
G1, G2, Metaphase
Information about the
completion of cell-cycle
events, as well as signals
from the environment, can
cause the control system to arrest the cycle at specific checkpoints.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

G1 checkpoint

when, question?

A

End of G1 to enter S

Is environment favourable

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

G2 checkpoint

when, question?

A

End of G2 to enter M

Is all DNA replicated?
Is environment favourable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

M checkpoint

when, question?

A

Middle of metaphase

Are all chromosomes attached to the spindle?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Two key components of the cell- cycle control system

A

A complex of cyclin with Cdk acts as a
protein kinase to trigger specific cell-cycle
events. Without cyclin, Cdk is inactive`

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

What interacts with a single Cdk in the cell cycle?

A

S-cyclin, M-cyclin

complex: s-cdk, m-cdk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

S-cdk triggers

A

DNA replication machinery

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

m-cdk triggers

A

mitosis machinery

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

Three D cyclins in mammals

A

cyclin D1, D2, and D3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q 
Match 
Cyclin-CDK- complex
- G1-Cdk
- G1/S-Cdk
- S-Cdk
- M-Cdk

Cyclin in vertebrates

  • E
  • B
  • A
  • D
A 
Match 
Cyclin-CDK- complex
D - G1-Cdk
E - G1/S-Cdk
A - S-Cdk
B - M-Cdk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 states of Cdk

A

inactive, partially inactive, fully active

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

inactive Cdk

A

without cyclin bound, the active

site is blocked by a region of the protein called the T-loop (red)

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

Partially active Cdk

A

The binding of cyclin

causes the T-loop to move out of the active site, resulting in partial activation of the Cdk2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

active Cdk

A

Phosphorylation of Cdk2 (by CAK) at a threonine residue in the T-loop further
activates the enzyme by changing the shape of the T-loop, improving the ability of the
enzyme to bind its protein substrates

32
Q

inactive to partially active Cdk

A

binding of cyclin

33
Q

partially active to active Cdk

A

Phosphorylation of Cdk2 (by CAK)

34
Q

How is the cyclin–Cdk complex regulated by wee 1

A

turned off when the kinase Wee1

phosphorylates two closely spaced sites above the active site

35
Q

Wee1

A

inhibitory phosphorylation

Removal of
these phosphates by the phosphatase Cdc25 results in activation of the
cyclin–Cdk complex

36
Q

Regulation of cyclin–Cdk complex by a CKI

A

The inhibition of complex

The p27 binds to both the cyclin and Cdk in the complex, distorting the active
site of the Cdk. It also inserts into the ATP- binding site, further inhibiting the
enzyme activity

37
Q

The control of proteolysis (CKI) occurs by

A

SCF and APC during the cell

cycle

38
Q

The control of proteolysis by SCF

A

Degradation of CKI in proteosome

The phosphorylation of a target protein, such as the CKI shown, allows the protein
to be recognized by SCF, which is constitutively active. With the help of two additional
proteins called E1 and E2, SCF serves as a ubiquitin ligase that transfers multiple
ubiquitin molecules onto the CKI protein. The ubiquitylated CKI protein is then
immediately recognized and degraded in a proteasome.

39
Q

The control of proteolysis by APC

A

Degradation of M-Cyclin in proteasome

M- cyclin ubiquitylation is performed by APC, which is activated in late mitosis by the
addition of an activating subunit to the complex. Both SCF and APC contain binding sites
that recognize specific amino acid sequences of the target protein.

40
Q

S and G1 cell fusion

A

G1 phase nucleus immediately enters S phase

S phase nucleus continues DNA replication

41
Q

S and G2 cell fusion

A

G2 phase nucleus stays in G2

S phase nucleus continues DNA replication

42
Q

G1 and G2 cell fusion

A

G2 phase nucleus stays in G2

G1 phase nucleus enters S phase normally

43
Q

The initiation of DNA

replication in cell cycle

A

The ORC remains associated with a
replication origin throughout the cell cycle.
In early G1, Cdc6 associates with ORC.
Aided by Cdc6, Mcm ring complexes then
assemble on the adjacent DNA, resulting in
the formation of the pre-replicative
complex. The S-Cdk (with assistance from
another protein kinase, not shown) then
triggers origin firing, assembling DNA
polymerase and other replication proteins
and activating the Mcm protein rings to
migrate along DNA strands as DNA
helicases. The S-Cdk also blocks
rereplication by causing the dissociation of
Cdc6 from origins, its degradation, and the
export of all excess Mcm out of the
nucleus. Cdc6 and Mcm cannot return to
reset an ORC-containing origin for another
round of DNA replication until M-Cdk has
been inactivated at the end of mitosis

44
Q

The activation of M-Cdk

A

Cdk1 associates with M-cyclin as the levels of M-cyclin gradually rise. The resulting
M-Cdk complex is phosphorylated on an activating site by the Cdk-activating kinase
(CAK) and on a pair of inhibitory sites by the Wee1 kinase. The resulting inactive MCdk complex is then activated at the end of G2 by the phosphatase Cdc25.

45
Q

Active m-CDK feedback loops

A

Cdc25 is further
stimulated by active M-Cdk, resulting in positive feedback.
M-Cdk also inhibits Wee1.

46
Q

What is cdc25 stimulated by?

A

polo kinase

47
Q

Concentrations of Cdk during cell cycle

A

do not change and exceed cyclin amounts

48
Q

cyclin levels in G1

A

In late G1, rising G1/s-cyclin levels lead to formation of G1/S-cdk complexes that trigger proggestion through start transition

G1/S cyclin drops at start of S

49
Q

cyclin levels in G2

A

m-CDK complexes form during G2 but are held in an inactive state

they are activated at the end of G2 and tigger entry into mitosis at G2/M transition

50
Q

APC/C intiates

A

metaphase to anaphase transition

51
Q

The structure and function of cohesins and condensins.

A

Related

Both proteins have two identical DNA- and ATP-binding domains at one end
and a hinge region at the other, joined by two, long, coiled-coil regions. This flexible structure is well suited for their role as DNA cross-linkers.

Cohesins cross-link
two adjacent sister chromatids, gluing them together.

Condensins mediate
intramolecular cross-linking to coil DNA in the process of chromosome
condensation

52
Q

The triggering of sister-chromatid separation by the

A

APC

53
Q

The activation

of APC by … leads to …

A

The activation
of APC by Cdc20 leads to the ubiquitylation and destruction of securin, which normally
holds separase in an inactive state

54
Q

destruction of securin allows separase to

A

cleave a subunit of the cohesin complex holding the sister chromatids together

55
Q

In early embryonic cell cycles,

Cdc20–APC activity rises at the

A

end of metaphase, triggering Mcyclin destruction

56
Q

What keeps the Cdk activity supressed after mitosis which is required for a G1 phase?

A 
the
drop in M-Cdk activity in late
mitosis leads to the activation of
Hct1–APC (as well as to the
accumulation of CKI proteins, not
shown). This ensures a continued
suppression of Cdk activity after
mitosis, as required for a G1
phase.
57
Q

The control of G1 progression by Cdk activity in budding

yeast

A

As cells exit from mitosis and inactivate M-Cdk, the resulting increase in
Hct1 and Sic1 activities results in stable Cdk inactivation during G1. When
conditions are right for entering a new cell cycle, the increase in G1-Cdk
and G1/S-Cdk activities leads to the inhibition of Sic1 and Hct1 by
phosphorylation, allowing S-Cdk activity to increase

58
Q

What are the mehcnisms controlling S phase intiation in animal cells?

A

G1-Cdk activity initiates Rb phosphorylation –> inactivated Rb

Freeing E2F

E2F acts back to stimulate the transcription of its own gene, forming another
positive feedback loop

Aperance of G1/S-cdk and S-cdk is a positive feedback loop

59
Q

What happens to the mass of cell with/without nutritional cell cycle control

A 
If cell division
continued at an unchanged
rate when cells were starved
and stopped growing, the
daughter cells produced at
each division would become
progressively smaller respond to some
forms of nutritional deprivation
by slowing the rate of progress
through the cell cycle so that
the cells have more time to
grow. As a result, cell size
remains unchanged or is
reduced slightly
60
Q

How does yeast cells coordinate cell growth?

A

G1-cyclin bind to DNA bound proteins

once all are bound, the free G1-cyclin is able to bind to Cdk and proceed into S phase

61
Q

How DNA damage

arrests the cell cycle in G1

A

When DNA is damaged, protein
kinases that phosphorylate p53 are
activated

p53 usually bound to Mdm2 and causes destruction

phosphorylation blocks binding and causes high tranlation of gene that encodes CKI

CKI inactivated G1/S-Cdk and S-CDK, arresting the cell in G1

62
Q

CAK

A

phosphoylates an activiting site in Cdk

63
Q

Wee1

A

phosphorylated inhibitory sites in Cdks, involved in controlling entry to mitosis

64
Q

Cdc25 phosphatase

A

removes inhibitory phosphates from Cdks

  • cdc 25A, B, C
  • Cdc25C is the activator of cdk1 a the onset of mitosis
65
Q

Sic1

A

supresses cdk activity in G1, phosphorylation by cdk1 triggers it destruction

66
Q

p27

A

supresses G1/s-Cdk and S-cdk activities in G1

helps cells to withdraw from cell cycle

67
Q

p21

A

SUPRESSES G1.S-CDK, s-cdk activities following DNA damage in G1

68
Q

Why is the tail lost from the tadpole to frog

A

undergo apoptosis in tail due to stimulated by an increase in thyroid hormone in the blood

69
Q

The binding of mitogens to cell-surface

receptors leads to the activation of

A

Ras

and a MAP kinase cascade

70
Q

Ras

and a MAP kinase cascade activation results in

A

increased production of

the gene regulatory protein Myc

71
Q

what does Myc increase

A

transcription of several
genes, including the gene encoding cyclin
D and a gene encoding a subunit of the
SCF ubiquitin ligase. The resulting
increase in G1-Cdk and G1/S-Cdk
activities promotes Rb phosphorylation and
activation of the gene regulatory protein
E2F, resulting in S-phase entry

usually functions as a heterodimer

72
Q

MYC leads to increased ___ activity which leads to entry into _____

A

E2F

S phase

73
Q

Abnormally high levels of Myc cause the activation of

A

p19ARF, which binds and inhibits
Mdm2 and thereby causes increased p53 levels

Depending on the
cell type and extracellular conditions, p53 then causes either cell-cycle arrest or
apoptosis.

74
Q

activation of cell- surface
receptors leads to the
activation of … which promotes…

A 
activation of cell- surface
receptors leads to the
activation of PI 3-kinase,
which promotes protein
synthesis, at least partly
through the activation of
eIF4E and S6 kinase.
Growth factors also inhibit
protein breakdown (not
shown) by poorly understood
pathways.
75
Q

Why do some nerve cells apoptose

A

The number of nerve cells is much greater than target cells and thus some receive insufficient survival factors –> apoptosis

76
Q

Two ways
in which survival factors suppress
apoptosis

A

the binding
of some survival factors to cell surface receptors leads to the activation of various protein
kinases, including protein kinase B
(PKB), that phosphorylate and inactivate the Bcl-2 family member
Bad.

When not phosphorylated,
Bad promotes apoptosis by binding
and inhibiting Bcl-2. Once
phosphorylated, Bad dissociates,
freeing Bcl-2 to suppress
apoptosis. As indicated, PKB also
suppresses death by
phosphorylating and thereby
inhibiting gene regulatory proteins
of the Forkhead family that
stimulate the transcription of genes
that encode proteins that promote
apoptosis.
77
Q

What does ploidy affect

A

chromosomes
and size

as n increases, size increases too

BIOC212 (7 decks)

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