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Mitosis+Meiosis
Organisation of the Body
| Question | Answer |
|---|---|
| Human life cycle | There are around 10^14 cells in the human body with around 10^16 cell divisions needed to allow for replenishment of adult cells Haplophase - gametes formed by meiosis Diplophase - cells after fertilisation divide by mitosis |
| Cell Cycle events | Cells divide during mitosis/meiosis (chromosome segregation) DNA is replicated during Synthesis phase Growth and cell cycle progression, whilst often linked, are separatable processes E.g. early cleavage divisions show no growth |
| Visualising the cell cycle - Walther Flemming | Used stained and fixed salamander and plant cells Demonstrated arrangement of chromosomes and microtubules during the cell cycle |
| Visualising the cell cycle - Modern day | GFP- stains alpha tubulin allowing microtubules to be visualised mCherry - stains histone H2B, allowing chromatin to be seen Can be performed on living cells to see the cell cycle performed |
| Mitosis | Prophase - chromosomes condense and pair in sister chromatids Prometaphase - sister chromatids attach to spindle Metaphase - chromosome attached to each centromere by kinetochores Anaphase - chromatids separate Telophase - chromatids at each pole |
| What controls the cell cycle and how do we know | Identification of cell cycle genes - yeast Identification of cell cycle protein factors - frog eggs, marine invertebrates Fundamental cell cycle controls have been highly conserved during eukaryotic evolution |
| Fission yeast - Why use?? | Maintained as haploid or diploid - can have one copy of a gene so easy to identify mutations Straightforward genetics - can identify phenotypes then consider their genetics Small, simple genome - powerful molecular genetics e.g. gene isolation |
| Fission yeast cell cycle mutants | Random mutagenesis by chance generates temperature sensitive mutants that become arrested at distinctive cell cycle positions but continue to grow Occurs when shifted from 25-36 degrees They get longer but the nucleus cannot divide |
| cdc genes in mutant yeast | Conditional mutant strains identified following random mutagenesis were defined as cdc if they became reversibly arrested at a specific cell cycle stage when temperature shifted. cdc2 - required twice - if mutated cell will arrest at mitosis and G1 |
| Identifying cdc genes - functional complementation | Yeast genomic library in plasmid shuttle vector, one of these should complement the cdc gene and reverse its effect Genes transformed into cdc mutants at 25 degrees When temperature changed to 36 degrees, only the mutants with complementary gene survive |
| Identifying human cdc genes - functional complementation Lee and Nurse | Human cDNA library used to be transformed into cdc mutant yeast When temperature raised to 36 degrees only yeast with the complementary human gene will survive |
| The cdc gene - cyclin dependent protein kinase | First identified on basis of function in yeast Very highly conserved in function and amino acid sequence (63% between yeast and human) Activity depends on association with a cyclin partner protein and phosphorylated proteins to drive the cell cycle |
| Role of CDKs in yeast cell cycle | At mitosis - CDK1 associated with cyclin B At G1 - G1-CDK-cyclin At S - S-CDK-cyclin Yeast use a single CDK, sequentially partnered by different cyclins |
| The human CDK cycle | At mitosis - CDK1-cyclin B/A At G1 - CDK4/6-cyclin D At S - CDK2-cyclin E/A G1 is known as the restriction point Multiple CDKs and cyclins |
| S phase activation | Replication at replication origins is activated by S-CDK activation of helicase enzymes in the prereplicative complex DNA replication is semi conservative and semi discontinuous (only takes place in S phase) Mutations drive evolution and disease |
| Evidence for S-phase activation at replication origins | Incorporation of modified nucleotides at the replication fork allow the replication origin to be seen DNA synthesis detected by h3-thymine incorporation and autoradiography |
| Cell cycle check points | At S - detects DNA damage and prevents replication At S - detects if mitosis has not finished and prevents replication At Mitosis - detects if synthesis not finished and delays mitosis At Mitosis - detects if chromosomes not attached to the spindle |
| What happens when checkpoints are prevented | Cells are not able to identify if chromosomes are properly attached to the spindle If they are not attached properly the cell fails to recognise this so the chromosomes separate incorrectly in anaphase Leads to changes in chromosome number - aneuploidy |
| Dysregulation of the cell cycle in cancer | DNA replication and mitosis must be reasonably efficient but dysregulated cell cycle commitment is a key feature of most cancers Defects in cell cycle checkpoints contribute to genomic instability in cancer |
| Causes of genomic instability resulting from double strand breaks | Repair proteins cannot be assembled properly e.g. Rad51 in absence of BRCA2 One of the repair proteins is defective e.g. Nijmegen breakage syndrome (NDS1 mutation) No cell cycle response to the break signal e.g. Ataxia-Telangiectasia |
| Ataxia-Telangiectasia | Rare autosomal disorder Leads to cerebellar ataxia (poor movement control), dilation of blood vessels, T cell immunodeficiency and predisposition to leukaemia/lymphoma |
| What causes A-T | Chromosomal rearrangements Sensitivity to ionising radiation Causative mutations in the ataxia-telangiectasia mutated gene; encodes ATM protein kinase - acts in DNA damage checkpoint Cell cycle continues even when chromosomes are broken |
| Measuring checkpoint defects | Irradiate cells to induce DNA breaks With working checkpoints DNA synthesis should decrease as Radiation dose increases (reduced ratio of the dyes used) In mutated cells no response is seen |
| Meiosis | Homologues - one maternal and one paternal chromosome Sister chromatids - two identical chromatids after replication Homologous chromosomes pair, exchange DNA before segregating Sister/non-sister chromatids then pair up and divide Reduction division |
| Generation of oocytes | Arrest in meiotic 1 prophase until triggered to continue to mature by hormones Then arrest in mitotic 2 metaphase until fertilisation when meiosis is completed These arrest periods are associated with risk of chromosome disjunction |
| Meiotic segregation errors and maternal age | Failures of separation after meiosis 1 are more common in increased maternal age as the time spent in meiosis 1 depends on maternal age, whist time in meiosis 2 is not E.g. Down syndrome is more closely associated to maternal age than Edwards syndrome |
| Generation of variation | Crossing over during prophase 1 Independent assortment of paternal and maternal homologues Different male and female gametes fuse on fertilisation - each zygote carries a unique set of alleles due to the previous processes |
| Genetic linkage | Genes seperate independently if they are on separate chromosomes or far apart in a chromosome Genes close together on the same chromosome are less likely to be separated so are linked Allows linkage mapping - identifying genes based on proximity |
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