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Lecture 17

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Biology 1002B
Denis Maxwell

Lecture 17: Development 1. Posttranslational regulation controls mRNA availability to ribosomes  Changes in pre-mRNA processing o Alternative splicing – remove diff combinations of exons and introns creating family of proteins  Masking proteins bind to mRNAs and make them unavailable for protein synthesis  Rate of mRNA breakdown o Steroid hormone slow or increase rate o If 5’UTR is transferred from one mRNA to another, the half-life is the same  Controlling sequences in 5’ UTR of mRNA recognized by proteins that regulate stability  Regulation of expression by small noncoding single stranded RNA interference (RNAi) bind to mRNA 2. Identify the various mechanisms for regulating the activity of proteins after they are translated.  Rate of translation = rate of protein synthesis  Adjusting length of poly A tail increases translation  Post translational regulation controls the availability of functional proteins o Chemical modification – add chemical groups o Processing – convert to active/inhibit form e.g. competitive inhibitor o Degradation – ubiquitin and proteasome or activate them by partial digestion o Chaperone – control how protein folds 3. Typical causes of cell death.  Lysosomes – digestive organelles (eating yourself)  Viruses – suicide (damaged, infected, don’t want to infect others and more beneficial to die)  Bad environment (toxins, temperatures)  Cannot support itself due to surface area and volume ratio 4. Mechanism of plasmid toxin/antitoxin system as a possible origin for cell death genes.  Plasmids carry a long half-life toxin gene but short half-life of antitoxin o Cell without plasmid will die because it doesn’t have antitoxin  Protease digest toxins and antitoxins  Sometimes antitoxin gene can be on chromosome during recombination o Host control making of antitoxin o Plasmids make new toxin and antitoxin (arms race)  Cells took over and put under developmental control of when to die  Endosymbiosis early life took up mitochondria & programmed cell death o Why apoptosis and mitochondria relate 5. Irreversible programmed cell death cascade in C. elegans (nematode)  Outside developmental signal  receptor  inhibit CED – 9 (associated with mitochondria)  CED – 4 release  activate and bind CED 3 (caspase)  active protease, nuclease o Cut a peptide off a protein and it becomes active  Other ways to activate a protein o Cofactor or change its shape to activate proteins o Add/remove chemical group (acetylate and methylate them) o Change its flexibility o Binding 6. Bacterial plasmids (parasites - infectious) can code for their own transfer  Experiments in silicon (on a computer)  Cells don’t like plasmids and try to get rid of them o Cell might divide and daughter cell might not have it by luck, see #4 for more details 7. Main stages in Drosophila embryonic development.  Attractive model sy
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