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Lecture 17

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Department
Biology
Course
Biology 1002B
Professor
Tom Haffie
Semester
Winter

Description
Lecture 17: Development  Volvocine algae provide a productive model system o From last class… find time to look at lecture 16  Division of mortality… o Some cells need to die, some cell’s DNA will not make it to the next generation  Cause of (Cell) Death… o Maybe lysosomes, eat self o Starve to death, not enough nutrients o Viruses o Commit suicide at a specific time o Environmental factors, temperature too hot or cold, pH, chemicals that can denature the proteins o Toxin, like anti-biotic o Someone else eats you, got eaten o More beneficial to organism when some cells are dead  mutations o Suicide  Maybe its damaged, or got infected by virus, dying on purpose  Programmed Cell Death Mechanism o “executioner” caspases are proteases that cleave essential proteins, leading to a controlled, but irreversible, biochemical cascade causing cell shrinkage, chromatin fragmentation and cell death o Most cells use this o No signal  Signal from outside, (death signal receptor)  Active CED-9 protein inhibits activity of CED-4 protein  CED-4 inactive CED-3  CED-3 protein  Post translational control  Repressors, proteins can bind on to other proteins to shut them down  Can be degraded by adding ubiquitin  Competitive inhibition  Chaperons, how they fold  Get them away from others  Maybe regulate the availability to cofactors  Maybe you can cut them o Death signal  Inactivated CED-9 protein  Active CED-4  Active CED-3 (active by CED-4)  Activation cascade and active nucleases  Active proteases o It can also start from the inside, doesn’t have to be signal from outside o In silico methods have identified caspase orthologous in bacteria...  Study on the computer  How to inactivate proteins: (post translational to regulate protein) o Methylate them o Change shape, (environment) o Cofactor o Binding on to another protein  Bacterial plasmids can code for their own transfer o Parasites o Bacteria can code for itself and get into host’s DNA o By chance, one daughter cell might not get the plasmid and that daughter cell have an advantage, selected for, host want to get rid of the plasmid o Plasmid coded toxin (red) – antitoxin (blue)  Get rid of me you die  Bacteria produce both toxin and anti-toxin  Anti-toxin is degraded more quickly by protease (green) but is replenished  Protease degrades toxin and anti-toxin, but anti-toxin degrades way faster  Cells that lose the plasmid are killed by toxin  When cells born without plasmid, will not have enough anti-toxin to survive because anti-toxin degrades too fast and cannot produce anti-toxin  Sometimes, the anti-toxin gene gets imbedded onto the host DNA  Plasmid hates it, so it produce another toxin (anti-anti-toxin)  ARMS RACE o Cells may develop program cell death from getting infected by bacteria or viruses  Ancient mechanism o The toxin produced by bacteria might not work outside of the cytoplasm o Cascades, one cuts another, and cuts another… o Cells grab the toxin and anti-toxin gene and put it under control  So it can act as programmed cell death o When we took in the mitochondria, we took in programmed cell death o Apoptosis is associated with mitochondria, might be where we got it from  Drosophila are the basic studies of genetics o Fertilized egg (zygote) o The nucleus divides multiple times, multi-nuclear cell, but
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