Publications
- Beck, S.A., O’Dor, E., Catching, A., Brock, H.W 2010. Cell cycle defects in polyhomeotic mutants are caused by abrogation of the DNA damage checkpoint. Dev. Biol. 339:320-328
- Fisher CL, Pineault N, Brookes C, Helgason CD, Ohta H, Bodner C, Hess JL, Humphries RK, Brock HW 2010. Loss-of-function Additional sex combs like 1 mutations disrupt hematopoiesis but do not cause severe myelodysplasia or leukemia. Blood 115:38-46
- Fisher, C.L. Lee, I., Komljenovic, I., Bozza, S., Pineault, N. ,Bloyer, S., Brookes, C., Chevalier, J., Dahl, A, Helgason, C., Hess, J.L., Humphries, R.K., and Brock, H.W 2010. Additional sex combs-like 1 belongs to the enhancer of trithorax and Polycomb Group and genetically interacts with Cbx2 in mice. Developmental Biology 337, 9-15
- Brock, H.W., Hodgson, J.W., Petruk, S., and Mazo, A 2009. Regulatory non-coding RNAs at Hox loci. Biochem. Cell Biol. 8,:27-34
- Sinclair, D.A.R., Syrzycka. M., Macauley, M. Rastgardani, T. , Komljenovic, I. , Vocadlo, D., Brock, H.W., Honda, B 2009. Drosophila O-GlcNAc transferase (OGT) is encoded by the Polycomb group (PcG) gene, super sex combs (sxc). Proc. Natl. Acad. Sci USA 106,13427-13432

Hugh W. Brock
Professor
Email:
Office phone: 604-822-2619
Lab phone: 604 822-4456
Research area: Cell and Developmental Biology
Lab Members: J. Hodgson, H. Jansen, T. Li
History: Director of the Genetics Graduate Program; B.Sc., U.B.C.; D.Phil., Oxford; EMBO Post-doctoral Fellow, Univ of Paris (1981); Jane Coffin Childs Fellow, Univ. of Washington (1981); Associate Member, Medical Genetics Dept., UBC; Associate Member, Biotechnology Lab., UBC; President of the Genetics Society of Canada 2002-2003.
For normal development, cells must pass on their gene expression patterns to their daughter cells. The DNA in different cells is the same. Therefore the mark that establishes which genes are on and which are off in a given cell must be epigenetic, and is probably a direct or indirect consequence of changes in chromatin structure. This epignetic mark must also be stable to mitosis. Despite 25 years of searching, we still don't have a clear idea what the epienetic mark is, how the it is established, and how the epigenetic mark is interpreted to regulate transcription. One clue comes from the observations that mutations in Polycomb group (PcG) genes fail to maintain gene expression patterns. PcG genes encode chromatin proteins, the modify histones, or change nucleosome positioning, or have unknown functions. My laboratory studies how PcG proteins are required for maintenance of gene expression in Drosophila. Our overall goal is to understand how Polycomb group proteins function at the molecular level in maintenance. Currently, we are attempting to develop new methods of establishing the details of how maintenance is established in homeotic genes during development. We are also examining the role of PcG proteins in the cell cycle. Trithorax group (trxG) proteins maintain gene activation. We study Asx, a protein that is required for both PcG and trxG activity.
Very recently we have discovered an unexpected connection between long non-coding RNAs and repression of homeotic genes. We are determining the molecular mechanism of RNA-mediated repression, and determining how this repression is integrated with PcG-dependent silencing.
Students coming to my lab are exposed to genetic, developmental, molecular, and biochemical approaches to studying questions in a developmental system. I encourage students to develop their own projects, to work independently, and to collaborate as necessary to maximize productivity.
Awards
2002
Killam Teaching Award
For Teaching
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