Stages of Cell cycle Flashcards

1
Q

Name the 6 stages of the cell cycle?

A
Prophase
Prometaphase
Metaphase
Anaphase
Telophase
Cytokinesis
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2
Q

What happens to the chromosomes and mitotic spindle in prophase?

A

Replicated Chromosomes, consisting of 2 sister chromatids condense and move appart
Outside the nucleus the mitotic spindle assembles between the 2 chromosomes which have replicated

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3
Q

What happens in prometaphase?

A

Nuclear envelope breakdown

Chromosomes attach to spindle microtubules via their kinetochores and undergos active movement

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4
Q

When does open and close mitosis occur?

A
Open= when nuclei dissolves before cell division
Close= nuclei remains intact
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5
Q

What happens in metaphase?

A

Chromosomes align at the equator of spindle. midway between spindle poles
Kinetochore microtubules attach sister chromatids to opposite poles of the spindle

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6
Q

What happens in anaphase?

A

Sister chromatids synchronously seperate to form 2 daughter chromosomes and each s pulled towards a spindle pole.
Kinetochore microtubules get shorter and spindle poles move appart

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7
Q

What happens in telophase?

A

2 sets of daughter chromosomes arrive at the poles of the spindle and decondense
A new nuclear envelope forms
Central spindle is formed
Division of cytoplasm begins with contraction of contractile ring

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8
Q

What happens during cytokinesis?

A

Cytoplasm is divided into two by a contractile ring of actin and myosin filaments

This pinches the cell in 2 to create 2 daughter cells

Mitotic cyclins are destroyed and proteins are dephosphorylated

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9
Q

What are kinetochores?

A

multiprotein complexes that are responsible for the attachment of chromosomes to the microtubules of the mitotic spindle, are assembled on the centromeric chromatin

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10
Q

When are kinetochores assembled?

A

assembled early during mitosis on centromeres (centromeric chromatin)

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11
Q

Define centromere

A

part of the chromosome where the primary constriction is; a fragment of DNA, which allows for chromatid segregation during mitosis; a region on the chromosome where kinetochore is assembled

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12
Q

How are chromosomes attached to the mitotic spindle?

A

Attached via kinetochores

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13
Q

How does plant cell cell cycle differ?

A

Plant cells do NOT contain centrosomes but they have fully functional mitotic spindle

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14
Q

In which phase is the DNA and centrosome replicated?

What is established immediately after this and what is responsible for this?

A

S phase

Sister chromatid cohesion is established by cohesin (mostly) and DNA catenation

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15
Q

Give 3 reasons why spindle checkpoints are useful

A

1) detects incorrect attachment at kinetochores
2) Arrests cells in metaphase
3) provides more time to correct improper attachments When SAC is satisfied (meaning: all kinetochores are properly attached to the microtubules of the mitotic spindle), APC/C becomes activated.

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16
Q

What keeps APC/C inactive and when does it become active?

A

APC/C remains inactive, until all kinetochores are attached properly to microtubules. Spindle Assembly Checkpoint (SAC) keeps APC/C inactive

17
Q

What are the two major functions of APC/C

A

❶ Ubiquitinates Securin, which – after Securin destruction – releases (activates) Separase. Separase removes cohesin from centromeres, which triggers anaphase.
❷ Ubiquitinates Cyclin B, what – after Cyclin B destruction – inactivates Cdk1, which in turn leads to the mitotic exit

18
Q

What has inherent polarity?

A

Mitotic spindle assembly Microtubules have an inherent polarity.

Dynamic nature of microtubules: slowly depolymerising at (-) ends, rapidly polymerising or depolymerising at (+) ends.

Metaphase .The plus ends of the microtubules project away from the spindle pole, while minus ends anchored at spindle poles,

19
Q

Explain how colchicine blocks microtubule dynamicity

A

Colchicine binds at the alpha/beta tublin interface and blocks polymerisation of microtubules.
Leds to shortening and depolymerisation of microtubules and unattached kinetochores and trigger SAC

20
Q

Define Cancer

A

A cancer is an abnormal type of tissue growth in which some cells divide and accumulate in an uncontrolled, relatively autonomous way.

21
Q

What are the 3 categories of external factors on extracellular signalling molecules?

A

Mitogens
Growth Factors
Survial Factors

22
Q

Describe Mitogens

A

stimulate cell division, primarily by triggering a wave of G1/S-Cdk activity that relieves intracellular negative controls that otherwise block progress through the cell cycle.

23
Q

Describe Growth factors

A

stimulate cell growth (an increase in cell mass) by promoting the synthesis of proteins and other macromolecules and by inhibiting their degradation

24
Q

Describe survival factors

A

promote cell survival by suppressing the form of programmed cell death known as apoptosis. All of them, via specific receptors, induce particular signaling pathways/cascades that affect the cell cycle progression

25
Q

What causes cell proliferation

A

G1 cyclin–Cdk complexes trigger the activation of gene regulatory proteins that stimulate the expression of numerous G1/S genes, including genes encoding G1/S cyclins, S cyclins and the proteins that carry out the events of the early cell cycle. The resulting waves of G1/S– and S–Cdk activities result in irreversible commitment to cell division.

26
Q

Describe the difference between Receptor Tyrosine Kinases in normal and cancer cells.

A

(a) Normal receptors exhibit tyrosine kinase activity only after a growth factor has bound to them, (b) Some oncogenes encode mutant receptors whose tyrosine kinase is permanently activated, (c) Other oncogenes produce normal receptors but in excessive quantities, which leads to excessive receptor activity.

27
Q

Define oncogene

A

: a gene whose protein product promotes cancer, generally because mutations or rearrangements in a normal gene (the proto-oncogene) have resulted in a protein that is overactive or overproduced.

28
Q

Define protoncogene

A

generally regulate cell growth, cell division, cell survival, or cell differentiation

29
Q

Define tumour suppressor gene

A

: a gene that encodes a protein that normally restrains cell proliferation or tumorigenesis, such that loss of the gene increases the likelihood of cancer formation

30
Q

What is the role of p53 protein?

A

a cellular stress sensor. In response to hyper-proliferative signals, DNA damage, hypoxia, telomere shortening, and various other stresses, the p53 levels in the cell rise

31
Q

Name 5 features of cancers

A

They can bypass normal proliferation controls, this includes independence of mitogens, suppression of apoptosis
They can colonise other tissues
Most cancers derive from a single abnormal cell
Cancer cells contain and accumulate somatic mutations
A single mutation is not enough to change a normal cell into a cancer cell
Cancers develop gradually from increasingly aberrant cells
Cancer cells display an altered control of growth (e.g. they are not contact inhibited) Cancer cells have an altered sugar metabolism
Cancer cells have an abnormal ability to survive stress and DNA damage They can escape a built-in limit to cell proliferation
Cancer cell are genetically unstable
Cancer cells create their own micro-environment (niche), where they evolve → Check MBOC pages 1091 through 1103 for detail

32
Q

Define genetic instability

A

an abnormal increase in the rate at which genes and chromosomes are mutated, rearranged or lost.

33
Q

Define chromosomal instability

A

Chromosomal instability (CIN) – an abnormally high incidence of defects in chromosome number or chromosome structure