Raymond C. Chan, Ph.D.

Assistant Professor of Human Genetics
Assistant Professor of Internal Medicine-MMG
Our laboratory studies genomic stability in germ cells. Proper organization of DNA is critical for the replication, repair and accurate segregation of genomic DNA. Specifically, we are focusing on the Structural Maintenance of Chromosomes (SMC) proteins, since SMC proteins are fundamental chromatin components that regulate higher-order chromosome organization. The combination of C. elegans genetics and cell biology provides powerful tools to dissect the in vivo functions of SMC protein complexes at both the molecular and cellular levels and their overall influence on the complex multicellular organism. Research in my laboratory has recently discovered a novel developmentally regulated function for a specific SMC protein complex in the germ cell lineage, where it serves an important role for maintaining genomic stability of germ cells and possibly in gametes. Ongoing efforts of my lab are focused on addressing the functional roles for SMC complexes in genomic stability, cell division and gametogenesis.
Rieseberg, L.H. , Choi, H., Chan, R., and Spore, C. 1993. Genomic map of a diploid hybrid species. Heredity 70: 285-293.
Min, H., Chan, R.C., and Black, D.L. 1995. The generally expressed hnRNP F is involved in a neural-specific pre-mRNA splicing event. Genes Dev. 9: 2659-2671.
Chan, R.C. and Black, D.L. 1995. Conserved intron elements repress splicing of a neuron-specific c-src exon in vitro. Mol. Cell. Biol. 15: 6377-6385.
Chan, R.C. and Black, D.L. 1997. The polypyrimidine tract binding protein binds upstream of neural cell-specific c-src exon N1 to repress the splicing of the intron downstream. Mol. Cell. Biol. 17: 4667-76.
Chu, D.S., Dawes, H.E., Lieb, J.D., Chan, R.C., Kuo, A.F., and Meyer, B.J. 2002. A molecular link between gene-specific and chromosome-wide transcriptional repression. Genes Dev. 16: 796-805.
Bickel, J.S., Kirkconnell, K.S., Faulkner, I.D., Verbrugghe, K.J., Bian, Y., and Chan, R.C. Redundancy in DNA replication stalling response contributes to cell-type-specific defects in C. elegans smc-5 and smc-6 mutants. Manuscript in preparation.