Class Notes (837,447)
Canada (510,273)
Biology (6,824)
Biology 1002B (1,346)
Lecture 17

Lecture 17.docx

2 Pages
118 Views
Unlock Document

Department
Biology
Course
Biology 1002B
Professor
Denis Maxwell
Semester
Winter

Description
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
More Less

Related notes for Biology 1002B

Log In


OR

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.


Submit