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In female mice, both the glucocorticoid (cortisol) receptor and the estrogen receptor are expressed in liver cells (hepatocytes). The control element to which the glucocorticoid receptor binds is a short-strip of DNA that can accommodate the binding of the glucocorticoid receptor dimer. This control element is called a glucocorticoid response element (GRE). It is located1000 bp downstream from the poly-A site for the PEPCK gene. When this gene is activated by cortisol, it helps the hepatocyte to release glucose into the blood. When the GRE is experimentally moved upstream to -500 bp from the PEPCK gene transcription start site, cortisol is still able to activate transcription of the PEPCK gene In the same mice, the estrogen receptor (when activated by estrogen) binds to a control element (the estrogen response element, ERE) -75 bp upstream from the transcription start site of the albumin gene. If the ERE is moved upstream to -100 bp upstream from the albumin gene start site, estrogen is no longer able to activate albumin synthesis. When either the estrogen receptor or the glucocorticoid receptor bind to their respective hormones (ie, ligands), they become activated and bind to their response elements (ERE or the GRE, respectively). Importantly, in both cases, the first protein these receptors recruit after binding is a HAT protein The motif that allows the glucocorticoid receptor to dimerize is a 1 zinc finger 2 leucine zipper 3 omega loop 4 coiled-coil 5 four-helix bundle

Given the information in the Background and Question 2, the glucocorticoid receptor would be considered a and HAT would be a O 1. enhancer, activator 2.activator, co-activator 3. repressor, silencer O 4.activator, proximal control element 5.code-reader, code-writer

Given the above information, the ERE could be considered what type of control element? 1.Activator 2. Proximal control element O3. Enhancer O 4. Silencer 5. Dimeric

Lets suppose you experimentally took the GRE and reversed it i.e, the coding strand sequence that was AAGT became TGAA, note that the non-coding strand would also have to be reversed to remain complementary). What would happen to the expression of PEPCK if you added cortisol to the hepatocytes compared to control hepatocytes that received no cortisol? 1.Albumin expression would go down 2.PEPCK expression would go down 3. Albumin expression would go up 4 PEPCK expression would not change 5. PEPCK expression would go up

Consider the following scenario. You create a new line of hepatocytes that no longer expresses a normal (wild-type) glucocorticoid receptor. Instead, you now remove the portion of the glucocorticoid receptor that codes for its DNA-binding domain (in an expression plasmid that allows you to express the protein of your choice in hepatocytes). That domain is replaced by the DNA sequence coding for the DNA-binding domain of the estrogen receptor. This procedure is done in such a way that the cortisol (ligand) recognition region of the protein coded for by this plasmid is unaffected (i.e., it will still respond to the cortisol ligand). What would be the effect on hepatocytes of introducing (transfecting) them with this chimeric protein (i.e., a composite of two different genes) into hepatocytes? More specifically, what would happen if the hepatocytes were now treated with cortisol compared to controls (no cortisol or estrogen 1.Albumin gene expression will not change 2. Albumin gene expression will increase O 3. PEPCK gene expression will increase 4. PEPCK gene expression will not change 5.Answers (B) and (D)

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