Regulation Of Eukaryotic Gene Expression Flashcards
role of histone acetylases
favor gene expression by actetylating certain lysyl residues …decreasing the positive charge ….weakening the interaction with DNA
what are enhancers and silencers
enhancers in the DNA are the binding site for activator proteins.
silencers in the DNA are the binding site for repressor proteins.
where are enhancers located
may be located upstream, downstream , or within an intron of the gene they control.
what are the 2 domains present on transcription factors
- DNA binding domain
2. activation domain
name some common DNA binding domains of transcription factors
ZINC FINGERS::steroid hormone receptor
LEUCINE ZIPPERS::cAMP dep TF
HELIX- LOOP -HELIX
HELIX -TURN -HELIX::homeodomain proteins encoded by homeotic/ homeobox genes
role of activation domain
bind to other TFs and coregulators
interacy with RNA pol2 to stabilise the formation of initiation complex
recruit chromatin modifying proteins such as histone acetylases / deacetylases
homeodomain proteins
TFs that bind to DNA and regulate gene expression during development
helix turn helix– DNA binding domain
steroid receptors
these are TFs that binds to HRE response element on DNA and induce steroid response.
DNA binding domain – Zn fingers
whivh TFs have Zinc fingers as DNA binding domain
steroid receptors
peroxisome proliferator activated receptors PPARs
fxn of PPARs (TFs)
- regulaye multiple aspects of lipid metabolism
2. activated by fibrates and thiozolidenediones
NFkappaB role
TF which regulates expression of many genes in immune system
Rel domains
cAMP response element binding (CREB)protein fxn
TFs which bind to CRE and response to cAMP
leucine zipper
general and specific TFs
GENERAL TFs–:
bind to promoter to allow RNAP II to bind and form initiation complex at the start site for trancription.
eg:TFIID, SP-1, NF-1
SPECIFIC TFs–:
bind to enhancer regions or in some cases silencers and modulate the formation of initiation complex, this regulating the rate of initiation of transcription.
eg:steroid, PPARs, NFkB, homeodomain
PPARs activated by
fatty acids
PG derivatives
fibrates
thiozolidenediones
Zellweger syndrome defect
genetic ds caused by a mutation in any one of the several gene(locus heterogeneity) involved in peroxisome biogenesis.
accum of long chain f.a. and abnormal f.a.
aka hepatocerbrorenal syn
eg of how response elements effect metabolism
pathway of gluconeogenesis.
activated by glucagon and cortisol
GLUCAGON: memb ass receptor that increase cAMP ..activate protein kinase A..CREB
CORTISOL:binds to intracellular receptor which binds DNA via Zn fingers(permissive action)
both lead to transcription of PEPCK(phosphoenol pyruvate carboxykinase)
which is the rate limiting step in gluconeogensis.
klein waardennburg syndrome
dvelopmental disorder resulting from a mutation in PAX(paired box) gene.
HOX and POX genes are req proper tissue and cell differentiation during embryonic period.
features of klein waardenburg syndrome
K-looks like X so mutation in PAX3 L-limb abnormalities E-eyes coloured(heterochromia of iris) I-inner canthus displaced laterally N-neural crest cells mutated
W-white blaze of frontal hair A-abnormal upper limbs A-altered pigmentation R-root of nose depressed D-deafness
what is the cause of holoprosencephaly HPE
haploinsufficiency of SHH(sonic hedgehog)
develpmental anomaly of forebraina nd face where there is failure of separation of cerebral hemisphere
major exceptions to the rule of codominance
barr body
in the Ig heavy and light chain loci(ensuring that only one B cell makes only one type of Antibody)
in the T cell reveptor loci.
