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Mol / Cel Biology > Lecture 8 > Flashcards

Lecture 8 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What is the cell cycle?

A

the life cycle of a cell, the period between

successive divisions of a cell.

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2
Q

What is binary fission? (prokaryotes)

A 
the normal life cycle of a bacterial cell
which involves:
Replication phase (R-phase = C-period);
Division phase (D-phase = D-period);
Interval phase (I-phase = B-period).
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3
Q

Which cells lack the ability to divide?

A

Highly specialized cells e.g. RBC, neurones.

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4
Q

What can liver cells, lymphocytes induce?

A

cell division by specific

stimulus.

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5
Q

Hemapoetic stem cells, epithelia cells e.g. have?

A

Relatively high

level of mitotic activity.

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6
Q

Interphase consists of (3)?

A

G1, S and G2 phases.

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7
Q

What is G1 phase?

A

The gap phase
after the cell division.

The first phase in the interphase.

Growth and biosynthesis
activity phase.

The duration
of the G1 phase is highly
variable, also among different
cells of the same species.

Check points before entering S phase.

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8
Q

What is S phase?

A

The DNA synthesis phase.
Starts with replication of DNA and finishes then the amount of DNA in the cell is doubled. Duplication of centrioles takes place.

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9
Q

What is G2 phase?

A

The gap phase after synthesis of DNA and before the cell division. The cell conducts a series of checks before entering the M phase.

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10
Q

What is M phase?

A

When cell actually divides.

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11
Q

What is G0 phase?

A

The «resting phase».
Some G0 cells can return to the cell cycle
and resume replicating.
Cells that can return are called quiescent (dormant).
Senescent (aging) cell cannot resume.

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12
Q

The key cell cycle regulation proteins?

A

Cyclin-dependent kinases (CDKs), which associate with one of different cyclins across the cell cycle to ensure accurate cell cycle progression.

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13
Q

Does cell-dependent kinases have kinase activity?

A

No, unless they are associated with a cyclin.

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14
Q

Concentration of cyclins in the cell fluctuates, Cyclin-dependent kinases concentration is?

A

Stable.

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15
Q

Which are the three main Cyclin-dependent kinases complexes?

A

G1 cyclin-CDK;
S-phase cyclin-CDK;
Mitotic cyclin-CDK (also known as maturation
promoting factor).

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16
Q

G1 cyclin-CDK includes CDK4 and CDK6 (Cyclin D’s). Which are their functions?

A

Reacts to exogenous signals like growth
factors and mitogen signals. Regulate the
phosphorylation state of the retinoblastoma
tumour suppressor (pRB) in G1, thereby
allowing the expression of genes required
for DNA synthesis.

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17
Q

G1 cyclin-CDK includes also CDK2 (Cyclin E). Function?

A

Important for transition from G1 to S-phase.

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18
Q

S-phase cyclin-CDK includes CDK2 and CDK1 (Cyclin A). Functions?

A

Promotes DNA synthesis. Targets are helicases and polymerases.

19
Q

Mitotic cyclin-CDK includes CDK1 (Cyclin B). Functions?

A

Important for transition from G2 to M-phase, activates APC/C complex. Regulate G2/M checkpoint.

20
Q

What are cell cycle checkpoints?

A

Surveillance mechanisms that monitor the order, integrity, and fidelity of the major events of the cell cycle.

21
Q

What are the major events of the cell cycle that has to be monitored?

A

growth to the appropriate cell size;
the replication;
integrity of the chromosomes;
accurate segregation at mitosis.

If the presence of a defect is detected, the arrest of cell
cycle progression takes place.

22
Q

G1/restriction checkpoint checks for?

A

Cell size, nutrients, growth factors, DNA

damage (environmental factors). Primary decision point.

23
Q

If damage is found in G1/restriction check?

A

G1 arrest and/or cell enters G0 phase

non-dividing state

24
Q

The S-phase checkpoint is?

A

A surveillance mechanism, that responds to DNA damage (spontaneous mutations).

The stabilization of DNA replication forks, which is critical for cell survival and genome stability.

A checkpoint is a cascade of signalling events that puts replication on hold until a problem is resolved.

25
Q

G2-phase checkpoint?

A

DNA damage checkpoint serves to prevent the cell from entering cell division (M-phase) with genomic DNA damage.

In response to extensive DNA damage, p53 activates gene expression for specific proteins to induce apoptosis.

26
Q

M-phase checkpoint?

A

Check for the mitotic spindle assembly.
Prevents separation of the duplicated chromosomes until each chromosome is properly attached to the spindle apparatus.
Arrest anaphase in the case of mistake.

27
Q

What is P53 protein?

A

Nuclear DNA-binding phosphoprotein, transcription factor.

28
Q

What is P53 protein able to do and when it is activated?

A

Is able to bind specific DNA sequences.

Is activated by increasing the protein’s half-life and the rate of translational initiation of its mRNA.

29
Q

Cell aging: cellular senescence is?

A

Irreversible arrest of cell proliferation.
The senescence arrest is considered irreversible.
Two main pathways are involved - p53/p21 and p16/pRB.

30
Q

What is apoptosis?

A

Form of cell death, also known as programmed cell death is a normal phenomenon, occurring frequently in a multicellular organism.

31
Q

Apoptosis takes place in?

A

Embryonic development,

Adult human body – cells with genomic damage,
senescent cells, cells which are not required anymore.

Human diseases – overactive initiation of apoptosis
(type 1 diabetes).

32
Q

What are caspases?

A

A family of proteases which are responsible for triggering apoptotic changes in the cell.

The protease cascade is irreversible - once a cell reaches a critical point along the path to destruction, it cannot turn back

33
Q

Apoptosis can be initiated by two different pathways:

A

Extrinsic pathway – extracellular messenger protein
called tumor necrosis factor (TNF).

Intrinsic pathway – activation is regulated by Bcl-2
proteins.

34
Q

After the cell death pathway is activated what happens to the cell?

A 
The cell shrinks and condenses.
The cytoskeleton collapses.
The nuclear envelope disassembles.
The nuclear DNA breaks up into fragments.
The cell surface is altered.
35
Q

DNA repair process exists in?

A

Both in prokaryotes and eukaryotes

36
Q

Control of DNA repair is closely tied to?

A

regulation of the cell cycle.

37
Q

What is mismatch repair (MMR)?

A

Repair DNA REPLICATION ERRORS – remove base mismatches and small insertion/deletion loops.

The mismatch repair mechanism is
strand-specific.

38
Q

What is Nucleotide excision repair (NER)?

A

Repairs DNA damages inducted by ENVIRONMENTAL FACTORS – radiation, mutagens (including chemical).

Important mechanism in excision of UV light inducted DNA damage.

39
Q

What is Base excision repair (BER)?

A

Removes damaged BASES in DNA sequence. Responsible for removing small, non-helix-distorting errors.

40
Q

BER (base excision repair) is initiated by?

A

DNA glycosylase that recognizes and removes the damaged base.

Two pathways exists:
short (removes one base lesions)
long (removes 2-10 base lesions)

41
Q

Homologous recombination repair (HR)

and Non-homologous end joining (NHEJ) can repair?

A

Both can repair DOUBLE-STRAND BREAKS
(DSB).

Homologous recombination repair (HR) uses a homologous DNA TEMPLATE and is highly accurate.

Non-homologous end joining (NHEJ) fixes the broken ends without using a template and is often accompanied by loss of some nucleotides.

NHEJ being more active in G1 and HR
dominating during S and G2 phases.

42
Q

Which two repair pathways exists for NER (nucleotide excision repair)?

A

Two repair sub-pathways exists - one for transcriptional active DNA (TC-NER) and one for global genomic (GG-NER).

43
Q

How does the progression of the cell cycle prior restriction checkpoint differ from cell cycle progression after the restriction checkpoint?

A

After the restriction checkpoint the progression of the cell cycle is no longer depending on growth factors!

44
Q

The binary fission begins after initiation of?

A

Mass is reached and DNA replication is initiated.

Mol / Cel Biology (17 decks)

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