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Lecture 17

Biology 1002B Lecture Notes - Lecture 17: Cell Nucleus, Helix-Turn-Helix, Gene Duplication


Department
Biology
Course Code
BIOL 1002B
Professor
Denis Maxwell
Lecture
17

Page:
of 2
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 system because it is small and sentient
Fertilized egg 2n nucleus divides but not cell nuclei to edge, grow cell membranes individual cells
blastoderm development embryo into segments specialize
Makes 2 organisms through cell death of larval tissue; larva fly
How could you discover the genes involved in development?
o Mutational studies on development
o Comparative genomics
Genes tell embryo which way is up and down (polarity)
o Bicoid mutant anterior head posterior tail mutant
o Gurken mutant mix up dorsal back and ventral belly
Maternal bicoid mRNA and protein gradients
o Mother packs egg with information (proteins,
untranslated mRNA) for after fertilization
How to pack mRNA that is not translated until fertilization?
o Lots of Bicoid mRNA masked means it is the head
o Gradient bicoid proteins made at head and less at end
Nanos gradient at butt so they can tell where they are in the embryo, know which genes to turn on
8. Main role of maternal effect, segmentation and homeotic genes in Drosophila development.
Maternal effect genes determine polarity of embryo
o Bicoid, gurken, nano gene is expressed in the mother and packed into the eggs
Segementation genes divide embryo into segments switched on by maternal effect
o Each segment turn on segment specific homeotic genes
9. Structure/function of the "homeobox" in homeotic genes
Segment homeotic genes (transcription factors) turned on by segmentation determine structures
Sometimes they are mutated and structures and body parts grow in wrong places or duplication
o Bithorax wings grow in wrong segment
Homeobox (helix turn helix binding domain)
o Sequence in protein that binds the DNA
o Master switches that control elaboration of structures
o Want proteins, put under control of same transcription factor unlike prokaryotes with operons
Gene duplication give rise to multiple homeotic genes
o Function is able to diverge and give rise to increase in complexity
o So different segments can regulate and turn on/off different genes and give different structures
o Ancient common ancestor has hox genes are evolutionary conserved
We used them to make different structures
Homeotic genes expressed in the same order in chromosome as they appear from head to butt
10. Role of programmed cell death in Drosophila development
Imaginal discs, pouches of cell in larvae wait until larvae pupa ecdysome death signal hormone
Destroy larval tissues by program cell death similar to C. elegans
Cells die when grim and reaper (killing cells) activated
Reaper is the master switch
o Upstream of it is ecdysome binding site that
sometimes turns reaper on or off
P53 detect DNA damage, tell reaper to kill cell
Hox genes (homeotic genes) control which cell to
live and die or if you are needed (then it will die)
One gene is in control of all the different cellular signals
o Hormones
o Environmental and developmental signals (all control whether cells live or die)