Gene Transcription Flashcards
Promotor Region
- Bound by General Transcrption factors and RNA pol II
- Defines Transcription Start Site
- Necessary for any transcription to occur
Enhancers and Silencers (regulatory elements)
Specific nucleotide sequence
Can be basically anywhere
bind to specific transcription factor
txn factor alters activity of promoters
–> How you get diversity
How can issues with Txn factors cause disease
- Irregular /hypo cell development essentially.
- i.e. atrial sepsis defect
Lineage determining factors
Bind to regulatory elements’ DNA and drive differentiation of cell type
i.e. GATA 4 in cardiomyocytes
3 Main Features of Transcription Factor Architecture
- DNA Binding Domain
- Transcription activating domains
- ->These activate proteins to alter chromatin structure
- ->Recruits General TXN factors
- ->Recruit Kinase to activate RNA Pol II - Dimerization/protein interaction domains
How do TF know where to bind?
Base order recognition and shape readout
–>Amino Acid substitutions affect ability of TXN factors to bind
Why do TXN Factors bind to themselves or other TXN Factors
Increase specificity
Mechanism of Transcription Activation
- GATA and TEX5 transcription factors recruit HATS and CRC (Histone acetyltransferase and Cromatin Remodeling Complex) to expose what genes you want expressed.
- TXN factors bring in General TXN Factors–>RNA POL II
- PTEF-4 brought in to phosphorylate RNA pol II
How do HATs and HDACs work?
Often acetyl group is added to Lysine (+ charge). This repulses DNA, Opening it up for txn.
De-acetylase removes acetyl group which causes DNA to tightly bind to histone,
Yomanaka Factors “master regulators”
Oct 3/4, Sox2, Klf4, c-MYC = proteins that can create stem cells
PAMPs, PRRS, in immune system?
Pathogen associated molecular paterns and Pathogen Recognition Receptors (TOL).
- PRRs recognize PAMP on bacteria which activates Nf kappa B
- Nf Kappa B goes to Nucleus
- TXN factors for inflammation activated
How are Gluccocorticoid anti-inflammatories related to Transcription?
- Gluccocorticoid receptor in cytoplasm. When signal binds to receptor it can now move into the nucleus.
- Now can bind to GRE (Glucocorticoid responsive element) in DNA as dimer
- activates assoc. genes (OR silencing of gene if it is in silencer region)
–> anti inflammatory because gluccocorticoid binds to Nf K b and inhibits it.
How to repress TXN:
- Block binding of General TXN factors
OR - Recruit HDAC
Prostate Cancer Risk
Elevated expression of RFX6 gene caused by SNP