Experiment URL: http://www.mhhe.com/biosci/genbio/tlw3/virtual_labs/lab7/overvie

Question

Experiment URL: http://www.mhhe.com/biosci/genbio/tlw3/virtual_labs/lab7/overview.pdf

1.) Why didn’t you use the intragenic deletion mutants (HLX3aHD and HLX3bHD) in this experiment examining the affects of mutations of LHX3’s ability to bind with protein partners?

2.) Can you predict what would have happened had you used the HLX3aHD and HLX3bHD mutants?

3.) The deletion mutation and the point mutation of the LHX3 gene have been shown to be associated with a severe form of CPHD. Based on the results of this experiment, would you expect a lack of binding with protein partners to be an underlying cause or contributor to this disorder? Why or why not?

4.) Do your results support or reject your hypothesis?

Explanation / Answer

1. The intragenic deletion mutants (HLX3aHD and HLX3bHD) lack the homeodomain which is required to bind the promoter region of target reporter gene.

2. We won't get DNA binding of these proteins on promoter region or in other words there would have been no promoter / reporter assay to analyze our results.

3. No, according to the results the point mutations don't disrupt the binding of LHX3 protein with protein partners as evident from Fig b. wherein binding of LHX3 with protein partners, NLI (red bars) and Pit-1 (blue bars) was reduced but not eliminated by the point mutations.

4. Our results do support our hypothesis that how the mutations disrupted normal LHX3 function.

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