Notes- February 23

Notes: Feb. 23, 3009
I. Interactions btwn transcriptional activators & enhancers (p.405 fig.11.25)
(fig. 11-25 in txt, p. 405- Transcriptional activation by recruitment)
*Transcriptional activator protein binds to enhancer on DNA- this leads to recruitment of other transcription factors.
Interaction of general transcription factors, specific transcription activators —> change in shape of DNA strand folded into allowing RNA polyermase to work.

II. Methylation of CpG motifs —> inactivation of genes
(i.e. methylated genes not transcribed)
in adult somatic cells, ~60 - 80% of genes are methylated
"somatic cells" is a term which here means diploid body cells (as opposed to haploid gamete cells)

*unmethylated genes in somatic cells
-genes specific to cell type
-"housekeeping genes" used by all cells, regardless of job
-all cells have active actin gene

III. Genomic imprinting
*Newly-replicated DNA not methylated after DNA replicated, the newly replicated strand is methylated in same pattern as strand it was copied off of.

a."Germ line"
*During gamete production, all methylation is erased, cells' DNA remethylated as fertilized egg divides, embryonic tissues differentiate

b. Differential imprinting of chromosome 15 in males & females in humans. (fig.11.32)
Chromosome 15: set of genes that we only need 1 copy of. So, genes on chromosome 15 methylated differently on mom's and on dad's chromosome 15.
i. Is there a post-male future? asks feminists
-No, you get full set of chromosomes still but get a double copy of one and none of the other
Prader-Willi syndrome
-is a complex genetic condition that effects many parts of the body
-common symptoms include
-weak muscle tone in newborns
-undescended testicles in the male infant
-delayed motor development
-slow mental development
-very small hands and feet
-rapid weight gain
-insatieable appetite, continuous eating
-almond-shaped eyes
-skeletal abnormalities
-most cases of Prader-Willi syndrome are not inherited. It is caused by a deletion in paternal chromosome 15 or by maternal uniparental disomy.

IV. RNA processing ss a means of gene regulation
a. mRNA stability - longer an mRNA persists in cell, more likely it will be translated to protein, so longer mRNA life span equal to more protein produces.
poly A tail added to mRNA increase stability so enzymes that remove poly A tail from mRNA lead to degradation of that mRNA.
i. deadenylation-dependent pathway- removal of poly A tail from mRNA from genes that are not to be expressed (to stop mRNA from being translated)
ii. nonesense-mediated decay- even on mRNA w/ poly A tail during round 1 of translation, enzymes still attached to sites where introns were removed. translation machinery coming across intron making protein then close stop codon that mRNA destroyed.
b. alternative splicing - introns being removed from different transcipts of genes resulting in alternate versions of proteins w/ different properties.

V.RNAi - cpmplete supression of expression of a particular genein response to dsRNA, transcript of gene leads to no translation of this mRNA

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