Biochem Abnormal Amnio Gene Regulation2

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name 3 ways to regulate gene expression post-transcriptionally: - poly a(primary trancript has two or more but only one can be functional)
- splicing (primary transcript contains two or more splice sites)
- partially processed mRNA may be fully processed to matur mRNA or aborted and hydrolyzed
Once processed, what other post translational control can occur and what is it called list an example: RNA EDITING - modifications of bases in mRNA

ex) production of apoB(component of blood lipoproteins)
RNA editing c gets deaminated to u creating a stop codon UAA, that way in some mRNA's you get apoB48 and some apoB100
selective protection of globin mRNA in reticulocyte, post translational, translational, transcriptional, post transcriptional control?: TRANSCRIPTIONAL CONTROL, during the final four or so cell divisions
conservation of globin mRNA and specific destruction of all other mRNA's
this has to do with mRNA half life's and the relative rates of degredation (AUBF)
cytokines oncogene products and transcriptional activators have a half life of?: 10-30min
what is a reccurent motif in rapidly degraded mRNA species?: AUUUA pentamer in 3' untranslated tail region (UTR),
trans factor AUBF (adenosine urosine binding factor) may recog motif and target for degradation
Note the similarities between this and ubiquitinylation protein degredation
What other elements affect mRNA stability: Transcriptional control?
3' terminal stem loop

Iron responsive elements: transferrin receptor gene with lots of stem loops, iron responsive elements bind and stabalize region in levels of low fe
If heme decreases, what happens to translation of hemoglobin mRNA? how does this happen: also decreases

heme controlled inhibitor (HCI) catalyses phosphorylation of elf2(alpha subunit, translation initiation factor), this inactivates it
what is RNAi?: dsRNA from viral infection triggers RNA interference(RNAi)
how does a cell silence RNA's when a viral dsDNA is introduced?: RNAase DICER hydrolyzes dsRNA into olig's ~ 21-24nt's long. these are called siRNA

siRNA complexes with RISC (RNA induced silencing complex), it hybridizes with a complementary seq and targets mRNA's for degradation
siRNA's are transcriptional post transcriptional translational post translational: post transcriptional regulation
Since euk dont have operons, what do they have that is similar: gene clusters
when does the selection of X-chrom for inactivation begin?: blastocyst stage ~ 20 cell stage
XIST where located encodeS? How does it silence?: X-inactivation-specific transcript, on Xq13 in the XIC(Xinactivator center)

encodes an RNA product, NOT a protein
RNA inactivates one X through methylation of cytosine
non random X chrom inactivation is affected by?: mutations, if you inactivate the non-mutated chromosome, and the mutation is lethal, those cells will die, only the cells in which the mutated X is inactivated survive
Defect in X chrom inactivation process: nonrandom methylation, have a mutated XIST
Histone deacetylation/acetylation: acetylation via HATS -loosens DNA/nucleosome interaction
histone dependent activation: activator proteins bind the H4 tail(N region) of a histone complex and cause disruption to expose the TATA box and coding region
What is the classical dbl standed helical structure of DNA?: BDNA
What is Z-DNA: alternating pur/pyr bases (usually G-C), transition from B to Z is reversible

increase Z DNA and increase transcription, ZDNA segments are part of enhancer element
what is SV 40?: an enhancer
two domains(A and B)
B domain: contains two elements of potential Z DNA forming seq's within a 72bp repeat
A) and another just upstream of B
what is transition vs transversion what affects SV40 the most?: transition pur-> pur
transversion pur-> pyr

transversion
what happens when you alter the pur/pyr sequence in Z DNA?: the enhancer effect is lost and the virus can't replicate
silencers -: cis, repress transcription using orientation, distance indep-ish
have been found in immunoglobulin
what is five-azacytidine: a cytidine analog that inhibits DNA methyltransferases, therefore inducing some genes
how does methylation work?: methylate cytosine in the 5'CG3' seq,
believed that hypomethylated regions are functionally active.
describe methylation of a daughter strand: methylation of a daughter strand in replication is carried out by methylase and acts exclusively on hemi-methylated 5'meCG3' sites. It requires sam
what is gene amplification?: ability to replicate specific genes in preference to the entire genome. Increase numbers of a gene.
unequal sister chromatid exchange is used to explain this occurence
sister chromatids misalign in mitosis and recombination results in one with a deletion and one with a duplication
advantages and clinical disadvantages of gene amplification: advantage -

clinical disadvantage - underlying cause of drug resistance in vivo, and probably others, resistance to methotrexate (anti-cancer) due to amplification of DHF reductase
is gene amplification normal or abnormal in proc/yeast/dros/vertebrates: abnormal
what are HSR's: homogenously staining regions, ie regions of gene amplification, duplications are only double copies, amplification can be a lot
what are DM's: double minutes
are small fragments of extrachromosomal DNA, which have been observed in a large number of human tumors including breast, lung, ovary and colon. They are a manifestation of gene amplification during the development of tumors, which give the cells selective advantages for growth and survival. Unlike typical chromosomes, they are composed of circular fragments of DNA, up to only a few million base pairs in size and contain no centromere or telomere.
Other model for gene amplification: unscheduled non-S DNA rep, onion skin, genes further from the center will be less amplified

makes HSR's DM's and Translocations
immunoglobulin formation requires: bringing C and V regions close together in the DNA
heavy chain C's make what type of Ab's? Cdelta Cgamma Cmu C: Cdelta = igD
Cgamma - IgG
Cmu- IgM
C - IgA
heavy chain immunoglobulin rearragment: V 50
D 30
J 6
C 9

D is chosen first D-->J rearrangement (exonuclease)

V is chosen V-->DJ rearrangement (exonuclease)

TRanscription RNA splicing (C chosen, gamma delta mu etc, j is also chosen)
Light chain rearrangement: V chosen V-->J rearrangement

J chosen (DNA rearrangement)

RNA splicing (only one C so doesnt matter)
transposon: goes to target sequence which gets mutliplied in the process of transpotition, random, IR and transposase gene, can carry genes inbetween two transposons
two types of transposition: dircet transposition and replicative transposition

retrotransposon
two types or retrotransposons: those with long terminal repeats (like retroviruses only cant move cell to cell) and those without

nonLTR - ex in humans is LINEs, have caused diseases in humans

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