Exploring the functional effects of Leukemia-promoting natural mutations in the tumor suppressor protein, BCL11B Public

http://ir.library.oregonstate.edu/concern/honors_college_theses/gt54kp831

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  • Thymocytes, cells of the thymus gland, undergo developmental steps that enable them to properly mature into T-cells. Errors in gene expression may lead to improper maturation and potentially mass proliferation of dysfunctional thymocytes, a hallmark of leukemia or lymphoma. BCL11B is a tumor suppressor and transcriptional regulatory protein that is required for thymocyte development. The partial loss of BCL11B leads to T-ALL in humans and lymphoma in mice. Functionally, BCL11B suppresses certain genes associated with blood cell cancers. This thesis focuses on characterizing the effect of leukemia-associated BCL11B point mutations on gene expression in thymocytes. We have two parallel hypotheses: first, we hypothesize that BCL11B expression levels or post-translational modifications will be different or modified in leukemia cells compared to normal thymocytes. Second, we hypothesize that BCL11B leukemia-associated point mutants will have altered capacity to regulate transcription of target genes relative to normal BCL11B.For these studies, we will create a site-directed mutant construct of Flag-tagged BCL11B containing a leukemia-associated mutation, Glycine592 to Serine, in a mammalian expression vector. Key Words: LOUCY cells, T-ALL, transcription factor, thymocytes
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