• Dr. Bo-Ruei Chen received PhD degree at Case Western Reserve University with Dr. Kurt Runge. His graduate work focused on the molecular mechanism of aging and telomere maintenance using yeast a a model system. He later joined Dr. Barry Sleckman's laboratory at Washington University in St. Louis and Weill Cornell Medicine as postdoctoral fellow to study DNA damage response, mechanism of DNA double strand repair and genetic regulation of genome stability. He joined University of Alabama at Birmingham as an assistant professor of Medicine in Division of Hematology and Oncology in 2020.
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2022 DNA-PK promotes DNA end resection at DNA double strand breaks in G0 cellseLife.  11. 2022
    2022 A Whole Genome CRISPR/Cas9 Screening Approach for Identifying Genes Encoding DNA End-Processing ProteinsMethods in Molecular Biology.  2444:15-27. 2022
    2021 The RNF8 and RNF168 Ubiquitin Ligases Regulate Pro- and Anti-Resection Activities at Broken DNA Ends During Non-Homologous End JoiningDNA Repair.  108. 2021
    2021 DNA-PK Promotes DNA End Resection at DNA Double Strand Breaks in G0 cells 2021
    2021 LIN37-DREAM prevents DNA end resection and homologous recombination at DNA double-strand breaks in quiescent cellseLife.  10. 2021
    2021 Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) activity is required for V(D)J recombinationJournal of Experimental Medicine.  218. 2021
    2021 LIN37-DREAM Prevents DNA End Resection and Homologous Recombination at DNA Double Strand Breaks in Quiescent Cells 2021
    2020 Loss of H3K36 Methyltransferase SETD2 Impairs V(D)J Recombination during Lymphoid DevelopmentiScience.  23. 2020
    2019 XLF and H2AX function in series to promote replication fork stability 2019
    2018 MRI Is a DNA Damage Response Adaptor during Classical Non-homologous End JoiningMolecular Cell.  71:332-342.e8. 2018
    2017 Deficiency of XLF and PAXX prevents DNA double-strand break repair by non-homologous end joining in lymphocytesCell Cycle.  16:286-295. 2017
    2016 RAG-mediated DNA double-strand breaks activate a cell type-specific checkpoint to inhibit pre-B cell receptor signalsJournal of Experimental Medicine.  213:209-223. 2016
    2014 HCoDES Reveals Chromosomal DNA End Structures with Single-Nucleotide ResolutionMolecular Cell.  56:808-818. 2014
    2013 Identification of a lifespan extending mutation in the Schizosaccharomyces pombe cyclin gene clg1+ by direct selection of long-lived mutants.PLoS One.  8:e69084. 2013
    2012 Mec1p associates with functionally compromised telomeres. 2012
    2012 Generation and analysis of a barcode-tagged insertion mutant library in the fission yeast Schizosaccharomyces pombe.BMC Genomics.  13:161. 2012
    2009 A new Schizosaccharomyces pombe chronological lifespan assay reveals that caloric restriction promotes efficient cell cycle exit and extends longevity.Experimental Gerontology.  44:493-502. 2009
    2009 The yeast Cdc8 exhibits both deoxythymidine monophosphate and diphosphate kinase activities.FEBS Letters.  583:2281-2286. 2009
    2007 Tel1p preferentially associates with short telomeres to stimulate their elongation.Molecular Cell.  27:851-858. 2007
    2003 Identification of a novel cell cycle regulated gene, HURP, overexpressed in human hepatocellular carcinoma.Oncogene.  22:298-307. 2003

    Research Overview

  • My broad research is the genetic regulation of DNA double strand break (DSB) repair and its impact on genome stability. One one hand, the generation of DNA DSBs is genetically programed and is involved in critical physiological processes such as the assembly and diversification of antigen receptors that ultimately lead to the production of antibodies and T cell receptors. On the other hand, DNA DSBs can be induced by exposure to genotoxic agents such as irradiation and chemotherapeutics.

    Non-homologous end joining (NHEJ) and homologous recombination (HR) are the two major DSB repair pathways in cells. NHEJ is the only major DSB repair pathway available in G1 phase and is essential for V(D)J recombination, the assembly of antigen receptor genes. We have a long standing interest in elucidating the function of novel factors or genetic interactions in the repair of DNA DSBs generated during V(D)J recombination. These findings not only advance our understanding of V(D)J recombination and lymphocyte development, but also help uncover novel DSB repair genes that function in NHEJ.

    The major determining factor of the choice or NHEJ and HR is the processing of DNA DSB ends by the process termed DNA end resection. We have begun addressing the spatial and temporal regulation DNA end processing so that cells can choose the proper and optimal DSB repair activities. To this end, we have recently conducted genome-wide CRISPR/Cas9 screens for genes that promote or inhibit DNA end resection. Our screens have uncovered novel genes in both categories. While our current focus is on the molecular function of these genes on DNA end processing, we have started to look into how manipulation of these genes can alter the activities of HR and NHEJ that will be beneficial for gene targeting and efficacy of cancer therapy involving chemotherapeutics and irradiation.
  • Education And Training

  • Doctor of Philosophy in Genetics, Case Western Reserve University 2011
  • Full Name

  • Bo-Ruei Chen