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Cellbiologi - cell division
Fichas del conjunto (40)
- 1Phases of the cell cycleInterphase: G1, S, G2
M-phase (mitosis and cytokinesis) - 23 main checkpointsBefore entering S-phase
Before entering mitosis
Before pulling duplicated chromosomes apart - 3How are the checkpoints contorlled?- intracellular signals
- extracellular signals - 4What are the effectors?Regulatory proteins ???
- 5Cdk-cyclin complex• triggers passage through different steps of the cell
cycle
• molecular switches to control the cell-cycle
machinery
• Cyclin = regulatory protein, as such no enzymatic
activity – binding to Cdk needed to become active =
Cdk-cyclin complex
• regulated by phosphorylation (kinases) and
dephosphorylation (phosphatases) - 6Concentrations of cyclins vary in a ...cyclic way
• Gradual increase of cyclin concentration by increasing transcription of cyclin genes
• Abrupt decrease of cyclin concentration by destruction of the protein:
- Degradation of cyclin depends on anaphase-promoting complex (APC) which works via ubiquitylination - 7G1 phase• Inactivation of S-Cdk and M-Cdk-activities from previous step
→ reset the cell cycle
• Cell growth (increasing cell volume)
• Synthesis of cell organelles
• Synthesis of proteins, lipids
• Prepare to replicate DNA
• Mitogens switching on cell-signalling pathways (MAPK) and
promote production of cyclins that triggers cell division
=> preparing for S-phase - 8What may arrest the cell cycle in G1 phaseDNA damage
• Phosphorylation of p53
• increased p53 protein concentration
and activity
• p53 = transcription regulator that
activates p21 gene
• p21 gene = encoding a Cdk-inhibitor
protein
• inactivation of G1/S-Cdk and S-Cdk = cell arrest
=> prevents replication of damaged DNA
• cell gets time to repair DNA or if too
severe DNA damage cell death
• loss of p53 function (mutations) is
associated with many forms of cancer - 9CdkCyclin dependend kinases
- 10S-phaseS-Cdk initiates DNA replication
- 11G2 phaseCell growth, protein synthesis, prepare for M
Cell-cycle control system:
prevents cell from dividing when incorrectly or incompletely replicated DNA
→ M-Cdk remains inactive (inhibited by phosphorylation)
- M-Cdk active by removal of Pi by phosphatase called Cdc25 - 12MitosisNuclear division
1) prophase
2) prometaphase
3) metaphase
4) anaphase
5) telophase - 13CYTOKINESEScytoplasmic division
- 14INITIATION OF M-PHASEM-Cdk:
• Accumulates in G2 phase
• Helps to prepare DNA for segregation
and assembly of the mitotic spindle
• Rearrangements of the cell content
• Cdc25 will activate M-Cdk complex
• Activated M-Cdk complex indirectly
activates more M-Cdk = positive
feedback loop - 15Mitotic spindlearray of microtubuli formed at the opposite poles of a
cell during mitosis and pulls duplicated chromosome sets apart
Duplication of the centrosome at the start of Sphase = microtubule organizing centre
Aster = star shaped array of microtubuli coming
from the centrosome - 16PROPHASECondensation of chromosomes
Assembly of the dynamic mitotic spindle
that starts to move apart - 17PROMETAPHASE- Breakdown of nuclear envelope
- Kinetochore microtubuli attach to
kinetochores
- Interpolar microtubuli move the
centrosome to opposite directions
Chromosomes attach to the mitotic spindle via kinetochores
+ active movement (chromosome) - 18Kinetochoreprotein complex that assembles on the centromere of a condensed
chromosome - 19Interpolar microtubuli:“interacting microtubuli”, motor
protein help to cross-link the 2
sets of microtubule - 20METAPHASEChromosomes line up to the centre of the cell
(equator) and form the metaphase plate
The kinetochore microtubules pull the sister chromatids back
and forth until they align along the centre of the cell - 21ANAPHASESister chromatids split synchronously and are pulled to the opposite ends of the cell =
chromosome segregation
Cohesin rings around the chromatids destroyed by separase - 22cohesin rings,Two copies of DNA remain tightly bound together
by cohesin rings, which is crucial for proper
chromosome segregation - 23anaphase-promoting complex (APC)activates separase by
degradation of securin and
triggers indirectly the
cleavage of cohesin - 24TELOPHASE• Disassembly of mitotic spindle
• Re-assembly of a new nuclear envelope around each set of chromosomes →
2 daughter nuclei
• decondensation of chromosomes → gene transcription possible
• Mitosis is complete at the end of the telophase - 25How does the nuclear envelope break down and reform during mitosis?The nuclear envelope breaks down by phosphorylation and reforms by dephosphorylation during mitosis
- 26Cytokineses• Overlapping interpolar microtubuli of the
mitotic spindle recruit proteins to start
creating a contractile ring
Dimension of the ring becomes smaller as cytokinesis progresses: equal size of
daughter cells - 27Contractile ringcomposed of actin and
myosin filaments - 28CONTROLL OF CELL NUMBER AND SIZENumber of cells in multicellular organism is in balance:
regulated by control of cell division rate and by control of cell death rate - 29Apoptosis(programmed cell
death)
The cell breaks apart into
apoptotic bodies by caspase
pathway – phagocytosis - 30NecrosisPlasma membrane rupture,
nuclear and cellular lysis causes
inflammation - 31Extracellular signal molecules are needed for cell survival, growth and divisionSurvival factors – cell survival
Mitogens – cell division (cell number )
Growth factors – cell growth (cell size ) - 32HYPERPLASIAan increase in the number of cells in
an organ or tissue. Normal appearance. They are
not cancer, but may become cancer - 33DYSPLASIAAbnormal appearance of cell (shape,
size, pigmentation…) - 34IN SITU CARCINOMA/NEOPLASMa group a
abnormal cells that remain in the place where they
were formed – cancer - 35INVASIVE CANCERa cancer which has invaded
beyond the membrane and has potential to spread
to other parts of the body → metastases - 36Some characteristics of cancer cells• Mutations in components of cell-signalling pathway (own
extracellular survival signals, Ras)
• Mutations in genes responsible for cell death (p53→
G1/S-Cdk and S-Cdk)
• Uncontrolled cell proliferation
• Overactive cell metabolism
• Invasive due to lack of adhesion molecules
• Survival and proliferation in abnormal locations - 37ONCOGENESGain of function
Normal gene induce normal cell proliferation
Mutation in pro-oncogene creates oncogene which
accelerates cell growth and division
Act in dominant manner - 38TUMOR SUPPRESSOR GENELoss of function
Normal gene prevent cancer
Normally inhibit cell division or induce apoptosis
Mutation creates cancer (= loss of function)
Act in recessive manner - 395 standard treatments fr cancersurgery, radiotherapy, chemotherapy, hormone therapy, tergeted therapy (a new generation of cancer treatments)
- 40Targeted therapy• signal transduction inhibitors (tyrosine kinase inhibitors)
• gene expression modulators
• apoptosis inducers
• immunotherapies (monoclonal antibodies, cancer vaccines)
• toxin delivery molecules
• angiogenesis inhibitors (block the growth of new blood
vessels to tumors)
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- Creado por Tova A · 14 feb 2021
- Copiado por Tova A · 19 feb 2021
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