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Scientific Foundations > Lecture 23 > Flashcards

Lecture 23 Flashcards

Cell Cycle (Mitosis) and Regulation

1
Q

overview of cell cycle

A
  • each living cell undergoes growth and cell division resulting in the formation of two daughter cells, each of which contains the same genetic information as the parent
  • varies in length in different types of cells
  • repeated each time as cell divides
  • molecular events of the cell cycle are very strictly controlled/monitored to ensure that no errors are introduced and passed on to the progeny
  • homeostasis: balance between cell division and cell death
  • 4-stage process

pg 528

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2
Q

stages of the cell cycle

A

G1 phase, S phase, G2 phase, and M phase
* interphase: G1,S,G2 -> longest phase

pg 529

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3
Q

G1 phase (gap 1 phase)

A
  • lasts for hours to several days
  • cell grows and proteins are synthesized
  • restoring daughter cells to normal volume and size
  • cell preparing for S phase
  • restriction point: commits a cell to entering cell cycle or going to G0

pg 531

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4
Q

G0 phase (gap outside phase)

A
  • also known as quiescence
  • temporarily suspended in nondividing rest cells
  • cells are in a stable state
  • cellular processes in the cell are continuing as usual
  • cells may reenter the cycle to begin to divide again through growth factors or can be made to enter through other means
  • some cells like neurons, skeletal and cardiac muscles, RBCs do not need to undergo cell division any longer
  • liver cell damage and G0
  • bone marrow, gut epithelium, skin and hair follicles NEVER go to G0

pg 533

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5
Q

S Phase (synthetic phase)

A
  • 8-12 hours
  • DNA replication occurs
  • histone and non-histone protein synthesis occurs
  • duplication of chromosomes
  • at the end of S phase, chromosome consists of two double helix strands, i.e. sister chromatids held together at centromere -> G1 single stranded
  • cohesion applied to hold sister chromatids tightly together -> multi-protein complex comprised of four subunits, meiotic and mitotic complex differs by one subunit, also involved in other cellular processes

pg 535

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6
Q

cohesion complex and cohesionopathy

A

conserved protein complex known as cohesion

  • roles of cohesion: regulates sister chromatid cohesion during meiosis and mitosis, regulates DNA replication, DNA repair, and transcription
  • complex consists of 4 core proteins
  • several proteins regulate the cohesion complex’s interaction with chromatin

pg 536

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7
Q

function of cohesion complex

A

hold sister chromatids together as the chromosomes; if cohesion complex is not working, sister chromatids are already separating

pg 537

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8
Q

how premature sister chromatid separation affects meiosis and mitosis

A

chromatids are already separated so they can’t really separate during anaphase and the cell undergoes increased apoptosis

pg 538

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9
Q

cohesionopathies

A

abnormalities in these genes are associated with multisystem developmental disorders (cohesionopathies)
* SMC1A, SMC3, NIPBL, RAD21, HDAC8 -> Cornelia de Lange Syndrome (CdLS)
* STAG 1 -> intellectual developmental disorder, autosomal dominant 47
* STAG 2 -> Mullegama-Klein syndrome
* DDX11 -> Warsaw syndrome
* ESCO -> Roberts syndrome

not super worried about genes and syndromes -> just giving an idea

pg 539

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10
Q

G2 Phase (Gap 2 Phase)

A
  • 2-4 hours
  • extends to M phase
  • cells prepare for mitosis -> SECOND GROWTH PERIOD
  • high rate of cellular activity
  • energy required for the completion of mitosis is accumulated
  • RNA, proteins and tubulins for the spindle apparatus are synthesized

pg 542

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11
Q

M phase (mitosis)

A
  • occurs in somatic cells (meiosis occurs in germline cells)
  • no recombination -> daughter cells are identical
  • prophase -> prometaphase -> metaphase -> anaphase -> telophase and cytokinesis

pg 544-545

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12
Q

prophase & prometaphase

A
  • prophase: chromosomes begin to condense
  • centrosomes: made up of two centrioles at right angles, move to opposite poles of cell beginning formation of the spindle apparatus, nuclear membrane begins to break down
  • prometaphase: nuclear membrane completely broken down, chromosomes continue to condense, centromere attach to spindle fibers and chromosomes move toward midway point between spindle poles

pg 546

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13
Q

metaphase

A

M = middle

  • chromosomes become fully condensed by end of metaphase
  • chromosomes aligned on fibers of spindle apparatus at midway point
  • specialized proteins called kinetochores bind to centromeres and attach chromosome to spindle fibers

pg 547

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14
Q

anaphase

A

A = away
sister chromatids separate and move to opposite poles of spindle apparatus

pg 548

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15
Q

telophase & cytokinesis

A

telophase: chromosome begin to decondense, two nuclear membranes form
cytokinesis: formation of two new daughter cells by division of cytoplasmic contents

pg 549

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16
Q

mitotic mistakes contributing to human disease

A

non disjunction: both sister chromatids go to same pole in anaphase, produces both trisomic and monosomic cells - aneuploidy
anaphase lag: separated sister chromatid “lags” behind and not included within new nuclear membrane, micronucleus with lone chromosome forms in cytoplasm and is eventually lost, results in monosomic cell
mitotic recombination

pg 550

17
Q

restriction point (end of G1)

A

influenced by: growth factors, nutrients, cell size, and DNA damage
prevents cell from going to S phase

pg 554

18
Q

G2-M transition

A

influenced by: cell size, DNA damage, DNA replication

pg 554

19
Q

anaphase-promoting complex (APC)

A
  • ubiquitin ligase that controls levels of M-phase cyclins
  • controls the initiation of sister chromatid separation which begins at the metaphase-anaphase transition

pg 554

19
Q

metaphase-anaphase transition

A

influenced by: chromosome attachments to spindle

20
Q

cyclins and cyclin dependent kinases (CDKs)

A

work together like a complex

  • initiate/induce cell progression through the cell cycle
  • progression can be STOPPED by various checkpoints -> accuracy of cellular events is monitored
  • cyclin-dependent kinase (CDK) key player for cell cycle regulation
  • CDKs require cyclins (activators) for their activity
  • different cyclins expressed at different stages of cell cycle; each cyclin has distinct expressive pattern; each pair targets a particular set of cellular processes involved in cell cycle

pg 555

21
Q

G1 Phase

A
  • Cyclin D: helps passage of cells through restriction point in late G1 phase
  • Cyclin E: helps cells at end of G1 phase to commit to DNA replication and enter S phase
  • enable cell to enter/advance to S phase

pg 557

22
Q

checkpoints at G1 phase and S phase

A
  • replication of DNA is monitored
  • if errors are detected, the cell cycle cannot continue until errors are corrected

pg 558

23
Q

S phase

A
  • Cyclin A: enables cell to leave S phase and enter G2 phase
  • necessary for the initiation of DNA synthesis
  • cyclin B manufactured

pg 559

24
Q

Checkpoints at G2 phase

A
  • unreplicated DNA checkpoint: DNA that hasn’t been replicated cannot pass, making sure S phase occurred
  • G2 DNA damage checkpoint: prevents the continuation of the G2 phase if errors are present in the replicated DNA

pg 560

25
Q

G2 phase

A

Cyclin B: induces the cell to leave the G2 phase and enter the M phase

pg 561

26
Q

Checkpoints at M phase

A
  • Spindle Assembly Checkpoint: beginning of M phase and monitors spindle apparatus; if spindle apparatus is faulty, cell cannot leave the M phase
  • Chromosome Segregation Checkpoint: end of M phase and monitors condition of chromosomes; if any of the chromosomes are sticking to each other, cell is not permitted to leave M phase

pg 562

27
Q

how are Cdk-Cyclin complexes regulated?

A
  • activation of mitotic Cdk-cyclin involves the addition of inhibiting and activating phosphate groups
  • followed by the removal of the inhibiting phosphate groups by a phosphatase
  • once removal has begun, a positive feedback loop is setup: the activated CDK-cyclin complex generated by this reaction stimulates the phosphatase thereby causing the activation process to proceed more rapidly
  • transcription factor E2F activates the expression of cyclin A, cyclin E, and CDK2

pg 563

28
Q

G1 checkpoint and retinoblastoma (RB) protein

A
  • tumor suppressor RB normally halts cells in the G1 phase of the cell cycle
  • in normal, resting cells, the RB protein is unphosphorylated -> RB prevents a cell’s entry into S phase by binding to E2F and its binding partner DP1/2 which are critical for the G1/S transition
  • RB normally prevents progression out of early G1 and into S phase in a resting cell

pg 564

29
Q

RB and retinoblastoma

A
  • RB protein is a tumor suppressor
  • plays an important role in regulating the progression of proliferating cells through the cell cycle and the exit of differentiating cells from the cell cycle
  • affects two functions by sequestration of other transcription factors and by promoting deacetylation of histones, a chromatin modification associated with gene silencing
  • pathogenic variants cause retinoblastoma

pg 565

30
Q

two DNA damage checkpoints

A
  • ATM and ATR produced in response to damaged DNA
  • leads to activation of p53 which in turn stimulates transcription of p21
  • p21 binds to CDKs in G1 and S preventing progression of cell cycle until DNA damage is repaired
  • if DNA too damaged to repair, p53 initiates apoptosis
  • checkpoint proteins also associated with cancer initiation and/or progression

pg 568

31
Q

TP53 and Li-Fraumeni

A
  • transcription factor p53 responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism
  • p53 appears to induce apoptosis through nontranscriptional cytoplasmic processes
  • pathogenic variants cause Li Fraumeni syndome -> multitude of cancers

pg 569

Scientific Foundations (46 decks)

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