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| Question | Answer |
| Phases of the cell cycle | Interphase: G1, S, G2 M-phase (mitosis and cytokinesis) |
| 3 main checkpoints | Before entering S-phase Before entering mitosis Before pulling duplicated chromosomes apart |
| How are the checkpoints contorlled? | - intracellular signals - extracellular signals |
| What are the effectors? | Regulatory proteins ??? |
| Cdk-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) |
| Concentrations 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 |
| G1 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 |
| What may arrest the cell cycle in G1 phase | DNA 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 |
| Cdk | Cyclin dependend kinases |
| S-phase | S-Cdk initiates DNA replication |
| G2 phase | Cell 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 |
| Mitosis | Nuclear division 1) prophase 2) prometaphase 3) metaphase 4) anaphase 5) telophase |
| CYTOKINESES | cytoplasmic division |
| INITIATION OF M-PHASE | M-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 |
| Mitotic spindle | array 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 |
| PROPHASE | Condensation of chromosomes Assembly of the dynamic mitotic spindle that starts to move apart |
| PROMETAPHASE | - 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) |
| Kinetochore | protein complex that assembles on the centromere of a condensed chromosome |
| Interpolar microtubuli: | “interacting microtubuli”, motor protein help to cross-link the 2 sets of microtubule |
| METAPHASE | Chromosomes 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 |
| ANAPHASE | Sister chromatids split synchronously and are pulled to the opposite ends of the cell = chromosome segregation Cohesin rings around the chromatids destroyed by separase |
| cohesin rings, | Two copies of DNA remain tightly bound together by cohesin rings, which is crucial for proper chromosome segregation |
| anaphase-promoting complex (APC) | activates separase by degradation of securin and triggers indirectly the cleavage of cohesin |
| TELOPHASE | • 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 |
| How does the nuclear envelope break down and reform during mitosis? | The nuclear envelope breaks down by phosphorylation and reforms by dephosphorylation during mitosis |
| Cytokineses | • 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 |
| Contractile ring | composed of actin and myosin filaments |
| CONTROLL OF CELL NUMBER AND SIZE | Number of cells in multicellular organism is in balance: regulated by control of cell division rate and by control of cell death rate |
| Apoptosis | (programmed cell death) The cell breaks apart into apoptotic bodies by caspase pathway – phagocytosis |
| Necrosis | Plasma membrane rupture, nuclear and cellular lysis causes inflammation |
| Extracellular signal molecules are needed for cell survival, growth and division | Survival factors – cell survival Mitogens – cell division (cell number ) Growth factors – cell growth (cell size ) |
| HYPERPLASIA | an increase in the number of cells in an organ or tissue. Normal appearance. They are not cancer, but may become cancer |
| DYSPLASIA | Abnormal appearance of cell (shape, size, pigmentation…) |
| IN SITU CARCINOMA/NEOPLASM | a group a abnormal cells that remain in the place where they were formed – cancer |
| INVASIVE CANCER | a cancer which has invaded beyond the membrane and has potential to spread to other parts of the body → metastases |
| Some 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 |
| ONCOGENES | Gain of function Normal gene induce normal cell proliferation Mutation in pro-oncogene creates oncogene which accelerates cell growth and division Act in dominant manner |
| TUMOR SUPPRESSOR GENE | Loss of function Normal gene prevent cancer Normally inhibit cell division or induce apoptosis Mutation creates cancer (= loss of function) Act in recessive manner |
| 5 standard treatments fr cancer | surgery, radiotherapy, chemotherapy, hormone therapy, tergeted therapy (a new generation of cancer treatments) |
| Targeted 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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