YY1 Control of AID-Dependent Lymphomagenesis
Annual rept. 1 Jul 2014-30 Jun 2015
PENNSYLVANIA UNIV PHILADELPHIA
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We hypothesize that YY1 levels control AID nuclear accumulation, AID mutation rates, and subsequent AIDmediated B cell lymphomagenesis. We are testing this hypothesis by exploring the impact of YY1 overexpression, or deletion, in mouse lines that spontaneously develop AID-dependent B cell lymphoma. In the initial granting period this year, we have bred the mice that spontaneously develop B cell lymphoma and have initiated YY1- overexpression studies. Our results are still preliminary but suggest that overexpression of YY1 leads to higher mortality. Second, we have bred the yy1 ff and gamma1-CRE alleles onto the background of the mice that spontaneously develop AID-dependent B cell lymphoma. These mice will enable us to test in the coming year if YY1 knock-out reduces B cell lymphoma. Finally, we have demonstrated that knock-out of YY1 results in reduced AID-mediated mutagenesis, supporting our main hypothesis. In the coming year we anticipate being able to complete experiments to test the role of YY1 in controlling AID-dependent lymphoma.
- Genetic Engineering and Molecular Biology
- Medicine and Medical Research