Judd Christopher Rice, PhD

Associate Professor of Cancer Biology

Director, Biochemistry & Molecular Medicine Master's Degree Program

Culture and Engagement Champion

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Overview

Each human chromosome contains 50-250 x 10e6 base pairs of DNA that compacts into an orderly structure by interacting with chromosomal proteins. Together, the DNA and these chromosomal proteins are generically described as chromatin. In eukaryotic organisms, the ability to precisely regulate nuclear processes is hindered by the inherently repressive chromatin environment where DNA is tightly packaged with chromosomal proteins. The fundamental structural unit of chromatin is the nucleosome which consists of the core histone octamer (two each of histone proteins H2A, H2B, H3 and H4) and the associated 146 base pairs of DNA that wraps twice around them. The N-terminal “tails” of the histones protrude from the nucleosome to interact with the nuclear environment. The enzymatic addition or removal of various post-translational modifications on histones generates a “histone code” at specific genomic regions that directly function to regulate specific DNA-templated processes including transcription, replication, repair, recombination and chromosome structure. Importantly, the activities of chromatin-modifying proteins are frequently altered in many human pathologies including developmental and age-related diseases, such as cancer.

The overall goal of my lab is to elucidate the factors that establish and maintain the “histone code” and how their concerted functions regulate essential chromatin-dependent events including transcription, DNA replication and DNA repair. This is accomplished using a combination of conventional biochemical approaches and state-of-the-art technologies. Our long term goal is to translate these fundamental biological insights into novel epigenetic therapies for the treatment of human diseases.

Research Funding

  • Advancing an Innovative NGS Approach to Discover and Investigate Histone Tail Proteolysis
    NIH · R21HG012833 · Feb 17, 2023 – Jan 31, 2025 · Role: Principal Investigator
  • Histone Proteolysis as a Novel Regulator of Myogenic Activation
    NIH · R21AR074649 · Dec 1, 2018 – Nov 30, 2021 · Role: Principal Investigator
  • Molecular mechanisms of gene silencing by H4 methylation
    NIH · R01GM075094 · Aug 1, 2007 – Jul 31, 2012 · Role: Principal Investigator
  • Epigenetic silencing by histone methylation
    NIH · F32GM064279 · Jun 25, 2001 – Oct 31, 2003 · Role: Principal Investigator

Publications

  • Concerted activities of distinct H4K20 methyltransferases at DNA double-strand breaks regulate 53BP1 nucleation and NHEJ-directed repair. Cell Rep. 2014 Jul 24; 8(2):430-8.. View in PubMed
  • Bent bone dysplasia syndrome reveals nucleolar activity for FGFR2 in ribosomal DNA transcription. Hum Mol Genet. 2014 Nov 01; 23(21):5659-71.. View in PubMed
  • The PR-Set7 binding domain of Riz1 is required for the H4K20me1-H3K9me1 trans-tail ‘histone code’ and Riz1 tumor suppressor function. Nucleic Acids Res. 2014 Apr; 42(6):3580-9.. View in PubMed
  • Identification and characterization of functional risk variants for colorectal cancer mapping to chromosome 11q23.1. Hum Mol Genet. 2014 Apr 15; 23(8):2198-209.. View in PubMed
  • Proteomic and functional analyses reveal the role of chromatin reader SFMBT1 in regulating epigenetic silencing and the myogenic gene program. J Biol Chem. 2013 Mar 01; 288(9):6238-47.. View in PubMed
  • Hormone therapy and maximal eccentric exercise alters myostatin-related gene expression in postmenopausal women. J Strength Cond Res. 2012 May; 26(5):1374-82.. View in PubMed
  • Genome-wide evaluation of histone methylation changes associated with leaf senescence in Arabidopsis. PLoS One. 2012; 7(3):e33151.. View in PubMed
  • The UBC9 E2 SUMO conjugating enzyme binds the PR-Set7 histone methyltransferase to facilitate target gene repression. PLoS One. 2011; 6(7):e22785.. View in PubMed
  • A new regulator of the cell cycle: the PR-Set7 histone methyltransferase. Cell Cycle. 2011 Jan 01; 10(1):68-72.. View in PubMed
  • Genome-wide epigenetic analysis of human pluripotent stem cells by ChIP and ChIP-Seq. Methods Mol Biol. 2011; 767:253-67.. View in PubMed