Regulation of Trx Flashcards
When lac operon on
low glucose, high lactose
lac operon genes
- lac operon repressor
2. enzymes used in lactose utilization
enzymes use din lactose utlizaion
beta galactosidase, permase, transacetylase
when repressor is bound
prevents trx of proteins, binds to operator and streakily blocks lac promoter/sigma subunit
allolactose
inducer that binds to repressor so can use lac operon
helix turn helix motif
proteins bind to palindromic sequences as dimers (lac repressor, trp repressor, and cap)
CAP
binds dna and cAMP -hunger signal
CAP-cAMP
positive regulatory factor that is resonsive to glucose levels
Lac repressor
CALLED LACI, negative reg factor resposnsive to lactose
+glucose/-lactose
CAP not bound to cAMP (adenyl cyclase off), repressor sits in operator, repressor mRNA synthesized (before the operator for the other proteins)
-glucose/+lactose
adenyl cyclase on, CAP binds to cAMP, CAP-cAMP bind to another cap binding site (promoter) and activate trx, allolactose binds to repressor to cause conformational change, and operator free, trx of three proteins occur
adenyl cyclase
turns off when no glucose-binds CAP to cAMP
+glucose/+lactose
adenyl cyclase off, CAP remains unbound, alloctose inhibits the repressor, but cap binding site is empty so no trx DRAW ALL 3 STATES
Binding sites
Cap binding site (promoter), repressor binding site
Repressor synthesis
always active
Agonists vs antagonists
Bind to hormone receptors, stimulate receptor activity/gene expression
vs
bind hormone receptors and block acceptor activity-repress gene expression
Structures of steroid receptors
ligand binding domian, DNA binding domain, activation domain
Zinc finger
Zn between cystine and histadine, and binds to DNA well
Gluccocorticoid/estrongen
17bps palindromic only difference is 4 nucleotides
- recruit bassal TRX factors, and unpack nucleosomes
activator specificity
1000’sbps away from TSS, dimeric protein=DNA binding domain, hormone binding domain, and DNA activation domain-unravels the promoter/gene from nucleosome which allows trx to occur
Chromatin remodeling
enhancer element binds to steroid hormone receptor, conformational change, recruits coactivator (affects histone tail or loosens up knot), gene will then be exposed
-signalled by hormones
Coactivator activity
Catalytic activity-Affect histeone tail-tightens or loosesns knot, or remodeling activity-ATP driven-loosen knot with small motor
Trx reg by sterooid hormone receptor
binding of steroid to receptor results in conformational change that uncovers zinc binding domain, Zn domain interacts with GRE complexes, which coupled with other coactivators and complexes bind to promoters and begin gene expression (creates loop)
Tamoxafin
binds to estrogen receptor, no conformaitonal change like estrogen makes receptor, not enhancing of trx
RNAi
decreases gene expression by resulting in degradation of mRNA
IRES
internal ribosome entry site
can have trx start from middle of mRNA
