You are interested in studying the transcriptional regulation of the Gip1 promot

Question

You are interested in studying the transcriptional regulation of the Gip1 promoter. The Gip1 promoter contains a binding site for the Jk8 protein that overlaps with the binding site for the Pa5 protein. Jk8 and Pa5 cannot bind DNA at the same time, but both proteins are present at high levels in adult liver cells. The binding sites for Jk8 and Pa5 are shown in Figure Q8-33. Gip1 transcription start site Figure Q8-33 Jk8 binds to site A while Pa5 binds to site B. You create mutations that remove the nonoverlapping sequences of either binding site A or B, and examine Gip1 mRNA production in adult liver cells that contain these mutations. The data you obtain from these experiments are shown in Table Q8-33. experiment binding site Gip1 mRNA levels number B Table Q8-33 Reference: Figuro Q8-33 and Table Q8.33. You know that Gip1 is only expressed in adult liver cells and not in the liver of embryos. You also know that Jka and Pa5 behave similarly on other promoters in the embryo or in the adult, in terms of whether they act as repressors or gene activators. Given the data, use of which of the following mechanisms would make the most sense for regulating the Jk8 and Pa5 proteins:

Explanation / Answer

I would like to answer this question based on an assumption that both Jk8 and Pa5 proteins act in opposite fashion. Based on this assumption two scenarios can happen:

1. Jk8 acts as activator whereas Pa5 acts as repressor.

2. Jk8 acts as repressor whereas Pa5 acts as activator.

If you look into table 8-33, in two cases the expression of Gip-1 is higher. Incase of no mutations i.e. WT (experiment - 1) and if there is a mutation in binding site for B (experiment - 2) the expression is higher. This gives a conclusion that the binding site A is responsible for enhancing the Gip-1 expression after binding of Jk8. This further tells that Jk8 acts as activator. So, the scenario 1 can be taken into consideration. The scenario 1 is further proved in experiment 3, where a mutation in binding site for A leads to downregulation of Gip-1 expression.

Further, in the question it is stated that Gip-1 is expressed only in adult liver cells and not in embryonic liver. Based on this we can conclude that Jk8 activates the Gip-1 expression only in adult liver cells. This only happens if Jk8 expression is repressed during embryonic stages. In addition, the question also states that Jk8 and Pa5 behave in similar fashion on other genes during embryo or adult stages. Since we have already concluded that Pa5 acts as repressor, the hypothesis could be that Pa5 represses the expression of Jk8 during embryonic stages. Due to absence of Jk8 the expression of Gip-1 does not happen during adult stage.

Hence, based on the above conclusion the answer is C.

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