BBS Faculty Member - Mo Motamedi

Mo Motamedi

Department of Medicine
Department of Cell Biology

Massachusetts General Hospital
CNY 149 13th Street, Room 7-212
Charlestown, MA 02129
Tel: 617-726-0676
Fax: 617-724-9648
Email: mmotamedi@hms.harvard.edu
Visit my lab page here.



We are interested in the mechanisms by which cells regulate their gene expression patterns stably and heritably. Stable inheritance of distinct transcriptional states that persist through numerous cell divisions is critical for the formation of cellular identities during development. Several cis- and trans-acting factors govern this process. In eukaryotes, posttranslational modification (PTM) of histone tails, targeted by sequence-specific events to different regions of the chromosome, lead to alterations in chromatin structure and gene expression patterns, which can be inherited in cis following DNA replication. This process operates to create specialized chromosomal structures, such as those found at centromeres, telomeres and other repetitive DNA elements, which are maintained in a compact structure, called heterochromatin. Stability and heritability of heterochromatin is critical for the maintenance of genomic stability in eukaryotes. We use the fission yeast as a model for understanding the molecular mechanism of heterochromatin formation and its role in preventing spurious recombination among repetitive DNA elements. Graduate students in our lab can expect to use a wide range of genetic, biochemical, genomic and proteomic tools to ask fundamental questions about the underlying molecular mechanisms governing epigenetic pathways. Our goal is to uncover conserved mechanisms by which aberrations to epigenetic pathways contribute to the development of human diseases, especially cancers.



Last Update: 8/22/2013



Publications

For a complete listing of publications click here.

 


 

H. Li*, M. R. Motamedi*, C. Yip, Z. Wang, Thomas Walz, D. J. Patel, D. Moazed 2009. An alpha motif at Tas3 C terminus mediates RITS cis-spreading and promotes heterochromatic gene silencing. Mol Cell 34: 155-167. * co-authors **Previewed in Dev Cell 16: 630-632, 2009*

M. R. Motamedi, E. E. Hong, X. Li, S. Gerber, C. Denison, S. Gygi, D. Moazed 2008. HP1 proteins from distinct complexes and mediate heterochromatic gene silencing by non-overlapping mechanisms. Mol Cell 32: 778-790.

M. R. Motamedi*, A. Verdel*, S. Colmenares*, S. Gerber, S. Gygi, D. Moazed 2004. Two RNAi complexes, RDRC and RITS, physically interact and localize to non-coding centromeric RNAs. Cell 119: 789-802. * co-authors (Featured as the cover story for this issue of Cell).



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