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YY1 Deletion Controls Condensin, Cohesin, and PcG Proteins DNA Recruitment, but Not Their Expression Levels

Undergraduate #9
Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology

Comfort Effi - Cheyney University of Pennsylvania
Co-Author(s): Arindam Basu and Michael Atchison, University of Pennsylvania, Philadelphia, PA



YY1 is a zinc finger containing DNA binding transcription factor that is known to regulate various cellular functions in development and disease. YY1 is essential for B cell development and function. Loss of YY1 arrests B cells at the pro-B cell like stage in the bone marrow and ex vivo loss of YY1 in spleens results in reduced class switch recombination (CSR). Various factors including YY1 have been implicated in long distance DNA interactions during immunoglobulin (Ig) locus rearrangement. We hypothesize that YY1 regulates these long-range DNA looping, probably by interactions with condensins, cohesins and Polycomb group (PcG) proteins. Our ChIP-seq studies indicate that during CSR to IgG1 YY1 binds to two regions on Igh locus (Eμ and 3’RR). But interestingly, we observe colocalization of YY1 with SMC4, Rad21 and EZH2 at hs4 (part of 3’RR) that is reduced upon loss of YY1. Western blot analyses are currently underway to determine whether reduced binding of these proteins is YY1-dependent and not due to decreased expression of these proteins upon the loss of YY1. Co-immunoprecipitatioin (co-IP) studies will also be performed to determine if YY1 physically interacts with these proteins to recruit them to hs4 in splenic B cells.

Funder Acknowledgement(s): National Heart Lung Blood Institute #5-R25-HL084664

Faculty Advisor: Arindam Basu,

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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