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Cell Biology & Physiology BIOL1024 > Cell Cycle > Flashcards

Cell Cycle Flashcards

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1
Q

Overview of cell cycle

A
  • growth and reproduction
  • chromosome number duplicates and gene expression occurs
  • sister chromatids are separated during mitosis - M phase
  • cell divides forming 2 genetically identical daughter cells
  • during interphase, cells grow and duplicate their genome
  • s phase = duplication
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2
Q

Chromatin organisation - during interphase

A
  • mix of DNA and associated proteins (histones)
  • allows for DNA compaction and involved in regulation of DNA activity
  • nucleosomes - basic structural units of chromatin
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3
Q

Histone organisation during interphase

A
  • 4 types, H2A, H2B, H3 and H4
  • each core histone possesses 2 domains, amino terminal tail and histone fold
  • form dimers with eachother
  • 8 histones comprise 1 nucleosome - octamer structure
  • have tails which allow other proteins to bind
  • H1 sits outside nucleosome, interacts with DNA and determines overall nucleosome structure
  • individual nucleosomes are connected by linker histones and linker DNA, can change the path that DNA exits the nucleosome
  • SMC - structural maintenance of chromosomes - 2 complexes:
  • cohesin - organise chromatin during interphase
  • condensin - important during mitosis
  • chromatin organised into loops during interphase
  • loop domains are organised by cohesin complexes and CTCF dimer complex (DNA binding protein- stops looping)
  • loops are important for regulation of gene expression and chromatin compaction
  • after mitosis, chromosomes decondense in specific regions of the nucleus - chromosomal territories
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4
Q

Genome organisation during mitosis

A
  • 2 chromatids
  • joined by centromere
  • Telomeres - each mitotic chromosome = 2 DNA molecules = sister chomatids
  • each DNA molecule in a mitotic chromosome is 10000 fold shorter than its extended length
  • in early mitosis, condensins replace cohesins
  • condensins are loaded onto chromatin and cohesins are removed
  • forms loops - randomly, no regulation - very different than during interphase
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5
Q

G1 checkpoint

A
  • is the environment favourable?
  • sufficient cell growth?
  • damaged DNA?
  • if all passed, move to S phase
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6
Q

G2 checkpoint

A
  • is all DNA replicated?
  • is there any damaged DNA?
  • if passed, enter mitosis
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7
Q

M checkpoint

A
  • are all chromosomes attached to spindle?
  • metaphase to anaphase transition
  • if incorrect, initiation of sister chromatid separation can be blocked
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8
Q

Cyclin dependent kinases (Cdks)

A
  • when active, trigger specific cell cycle events - Cdk + cyclin = active Cdk
  • cyclin levels change throughout the cell cycle
  • Cdk activity also fluctuates - concentrations remain stable throughout
  • phosphorylation of proteins drives transition through the cell cycle - each Cdk/cyclin complex phosphorylates a different set of substrate proteins
  • cyclins also direct the activated Cdk to its target protein
  • accessibility of substrates changes throughout the cycle
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9
Q

Role of G1 cyclins

A
  • G1 cyclins = bind + activate Cdks that stimulate entry into new cell at start, concentration depends on rate of cell growth/on promoting signals (not phase of cycle)
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10
Q

Role of G1/S cyclins

A
  • activate Cdks that stimulate progression through start, results in commitment to cell cycle entry, concentration depends peaks in late G1
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11
Q

Role of S cyclins

A
  • activate Cdks necessary for DNA synthesis, conc increases and remains high during S phase, G2 and early mitosis, contribut to some early mitotic events
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12
Q

Role of M cyclins

A
  • activate Cdks necessary for entry to mitosis, conc rises at approach to mitosis + peaks in metaphase
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13
Q

Cdk activating kinases - mechanism 1

A
  • before cyclin binds, active site in Cdk is blocked by t-loop
  • when cyclin binds, t-loop unfolds = partially activated Cdk
  • phosphorylation of Cdk by CAK further activates the Cdk by changing the shape of the t-loop
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14
Q

Cdk activating kinases - mechanism 2 (regulatory pathway)

A
  • active cyclin/Cdk complex can be inactivated by Wee1 or Myt 1
  • dephosphorylation by phosphatase Cdc25 leads to reactivation (reversible reaction)
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15
Q

Cdk inhibitor proteins - mechanism 3

A
  • p27 protein
  • binds to whole complex, causing structural changes, inhibits complex
  • usually in G1 or in response to inhibitory signals from environment or damaged DNA
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16
Q

Transition through G1 in favourable conditions

A
  • E2F - transcription factor
  • inhibited by protein Rb
  • Cdk/cyclin complex phosphorylates Rb and releases it from E2F
  • E2F can then transcribe genes important for S phase
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17
Q

Transition through G1 if DNA is damaged (start checkpoint/G1 arrest

A
  • ATM/ATR + Chk1/Chk2 pathways signal that DNA is damaged
  • triggers Mdm2 to release from P53
  • P53 is phosphorylated - active (acts as a transcription factor)
  • P53 binds to regulatory region of P21
  • P21 transcribed and translated
  • P21 is a Cdk inhibitor protein
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18
Q

Regulated proteolysis

A
  • ubiquitin pathway used to degrade proteins - controlled manner
  • 3 ubiquitin ligases are required: E1, E2 and E3
  • ubiquitin covalently attached to lysine, targeted for degradation
  • polyubiquitin chain produced
  • ubiquitinated protein broken down by proteasomes
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19
Q

What are Proteasomes

A
  • large protein complexes
  • proteolytic activity
  • responsible for degrading proteins marked by polyubiquitin modification
20
Q

Prophase

A
  • chromosomes condense
  • mitotic spindle assembles (produced by centrosomes)
21
Q

Prometaphase

A
  • nuclear envelope breaks down (only in some organisms) = open mitosis
  • chromosomes attach to spindle microtubules via kinetochores and undergo active movement
22
Q

Metaphase

A
  • chromosomes aligned at equator of spindle (metaphase plate)
  • kinetochore microtubules attach sister chromatids to opposite poles of the spindle
23
Q

Features of kinethochores

A
  • multiprotein complexes responsible for attachment of chromosomes to microtubules of mitotic spindle, assembled on centromeric chromatin
  • assemble during early mitosis
  • microtubules attach to outer kinetochore
  • each chromatid of a chromosome has its own kinetochore
  • 20-30 microtubules per kinetochore
  • correct attachment of all kinetochores is required for anaphase to begin
24
Q

Cohesion of sister chromatids

A
  • cohesins bind to sister chromatids, keeping them together
  • some of the cohesin is removed before anaphase
  • remaining cohesin is localised at the centromeric region
25
Q

How is cohesin removed? APC/C INACTIVE

A
  • APC/C remains inactive until all kinetochores are properly attached to microtubules
  • inhibited APC/C stops progression of cells in metaphase, allowing more time for correct kinetochore attachment
26
Q

How is cohesin removed? APC/C ACTIVE

A

1)
- cyclin B + Cdk bound
- APC/C ubiquitilates cyclin B
- degrading it
- leaves Cdk inactive
- allows mitotic exit

2) metaphase to anaphase transition
- enzyme separase, inhibited by securin
- APC/C ubiquitilates securin, degrading it
- separase now active
- separase cleaves cohesin ring
- triggering anaphase

27
Q

Anaphase

A
  • kinetochore microtubules shorten
  • pulling apart sister chromatids to form 2 daughter chromosomes
28
Q

Telophase

A
  • 2 sets of daughter chromosomes assemble at opposite poles + decondense
  • nuclear envelope reassembles around each set forming 2 nuclei
  • central spindle is formed
29
Q

Cytokinesis

A
  • contractile ring ( actin and myosin filaments) forms cleavage furrow
  • forms 2 genetically identical daughter cells each with 1 nucleus
30
Q

Centrosomes (Microtubule organising centres MTOCs)

A
  • contains centrioles - short cylindrical arrays of microtubules and pericentriole material
  • gamma tubulin - nucleates microtubules at centrosomes (polymerisation role)
  • centrosomes duplication mirrors DNA replication - during S phase
  • more than 2 centrosomes in a cell causes genomic instability - usually found in cancer cells
31
Q

Mitotic spindle assembly - animal cells

A
  • migrate around nuclear envelope to opposite poles of the cell - start to produce microtubules
  • microtubules attach to sister chromatids during prometaphase - not fully correct attachment
  • metaphase - spindle assembly checkpoint - all joined together
  • microtubules have inherent polarity, slowly depolymerise at (-) ends and rapidly polymerise or depolymerise at (+) ends
32
Q

Microtubules of mitotic spindle

A
  • (+) ends of the microtubules project away from the spindle pole
  • (-) ends are anchored at the spindle pole
  • kinetochore microtubules connect the spindle poles with the kinetic horse of sister chromatids
  • interpolar microtubules from the 2 poles interlock at the spindle equator
  • astral microtubules radiate out from the 2 poles into the cytoplasm and contact the cell cortex
  • plant cells do not contain centrosomes but they have fully functional mitotic spindles
33
Q

Inhibitors of microtubule dynamicity

A
  • e.g. colchicine - binds at beta tubulin interface and blocks polymerisation of microtubules, leading to cell shortening
  • unattached kinetochores trigger spindle assembly response
34
Q

How are cancer cells made?

A
  • colonal evolution = division in an uncontrolled, autonomous way
  • tumour develops through repeated rounds of mutation + proliferation - gives clone of fully malignant cancer cells
  • normal cell division + apoptosis = homeostasis (normal)
  • increased cell division + normal apoptosis = tumour
  • normal cell division + decreased apoptosis = tumour
35
Q

External factors regulating cell division

A
  • mitogens - stimulate cell division (trigger G1/S - Cdk activity)
  • growth factors - stimulate cell growth (synthesis of proteins)
  • survival factors - promote cell survival (suppress apoptosis)
  • all, via receptors, induce signalling pathways/cascades affecting cell cycle progression (induce G1/S gene regulators, prevent passing start checkpoint = Ras pathway)
36
Q

Mutations leading to cancer development

A

E.g. mutant receptor (protein kinases) could be constantly active - doesn’t require signals
E.g. amplified receptor - excessive receptor activity

  • mutation of ANY component of a signalling pathway may lead to cancer development
37
Q

Feature of cancer cells

A
  • bypass normal proliferation controls
  • altered control of growth
  • can colonise other tissues
  • derive from a single abnormal cell
  • contain + accumulate somatic mutations
  • require multiple mutations to form
  • ability to survive stress and DNA damage
  • genetically unstable
38
Q

Oncogenes

A
  • a gene whose protein product promotes cancer, generally because of mutations in a normal gene (proteo-oncogene) have resulted in a protein that is overactive/overproduced
  • dominant, require 1 mutation to have an effect
  • proteo-oncogenes regulate cell growth and division
39
Q

Tumour suppressor genes

A
  • encodes a protein that restrains cell proliferation
  • if mutated, can cause tumours
  • recessive, requires mutation in 2 alleles of a gene to eliminate the tumour suppressor gene - promotes cell transformation
40
Q

Meiosis

A
  • nuclear division leading to haploid cells
  • produces 2 gametes
  • similar control systems to mitosis
41
Q

Meiosis 1 - Prophase 1

A
  • long process during meiosis
  • 2 closely aligned duplicated homologs called a bivalent
  • homologs joined by a protein complex called a synaptonemal complex (SC)
42
Q

Synaptonemal complex

A
  • each homologs organised around a protein axial core
  • the synaptonemal complex forms when these homolog axes are linked by rod shaped transverse filaments
  • the axial core of each homolog interacts with cohesin complexes that hold sister chromatids together
43
Q

Homolog synapsis and desynapsis during prophase 1

A
  • in a single bivalent: at leptotene, the 2 sister chromatids coalesce and their chromatid loops extend out from a common axial core
  • assembly of the synaptonemal complex begins in early zygotene and is complete in pachytene
  • the complex disassembles during diplotene
  • followed by diakinesis
44
Q

Crossing over

A
  • thin connection between homologs called a chiasmata
45
Q

Products of meiosis 1 & 2

A

Meiosis 1: haploid cells with chromosomes containing 2 chromatids
Meiosis 2: haploid cells with chromosomes containing 1 chromatid

46
Q

Meiosis vs mitosis

A
  • homologs separate rather than sister chromatids
  • sister kinetochores in a homolog must be stably attached to the same spindle pole
  • chiasmata hold homologs together allowing their bi-orientation at the equator
  • centromeric cohesin stays on during anaphase 1, this allows sister chromatid pairs to correctly bi-orient during meiosis 2

Cell Biology & Physiology BIOL1024 (3 decks)

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