Ph.D., Dartmouth Medical School, 2002
firstname.lastname@example.org | (516) 367-5207 (p)
As organisms develop, genes turn on and off with a precise order and timing, much like the order and duration of notes in a song. My group uses model organisms to understand the molecules that control the tempo of development. We also study how changes in the timing of gene expression contribute to diseases like cancer.
Christopher Hammell’s lab is interested in understanding gene regulatory processes that give rise to robust phenotypes associated with normal development in animals (specifically, how the timing of developmental processes is controlled) as well as the alterations in these pathways that give rise to diseases such as cancer (as in the alterations in mitogenic pathways in melanoma). Hammell and colleagues approach this elemental problem by using a variety of model organisms and patient-derived cancer cell lines. To directly identify the components that function in controlling normal developmental timing, they use the small nematode Caenorhabditis elegans, applying forward and reverse genetic approaches. In contrast to the extreme robustness of cell-fate lineage in C. elegans, in which specification of developmental programs is hard-wired, mutations that alter conserved signaling pathways in melanoma create relatively plastic developmental landscapes that allow these lesions to become aggressive tumors. Notably, the gene regulatory architecture of melanoma cells allows them to acquire resistance to therapeutic agents. Hammell’s team is interested in epigenetic mechanisms that contribute to resistance, specifically dramatic changes in gene expression patterns and intracellular signaling pathways. They are performing high-throughput screens to identify cellular factors that allow these re-wiring events to occur, with the idea that these components would make ideal therapeutic targets to complement existing clinical strategies.
Perales, R. and King, D. M. and Aguirre-Chen, C. and Hammell, C. M. (2014) LIN-42, the Caenorhabditis elegans PERIOD homolog, Negatively Regulates MicroRNA Transcription. PLoS Genetics, 10(7) pp. e1004486.
Zinovyeva, A. Y. and Bouasker, S. and Simard, M. J. and Hammell, C. M. and Ambros, V. (2014) Mutations in Conserved Residues of the C. elegans microRNA Argonaute ALG-1 Identify Separable Functions in ALG-1 miRISC Loading and Target Repression. PLoS Genetics, 10(4) pp. e1004286.
Hammell, C. M. and Hannon, G. J. (2012) Inducing RNAi in C. elegans by Feeding with dsRNA-expressing E. coli. Cold Spring Harb Protoc, 2012(12)
Hammell, C. M. and Karp, X. and Ambros, V. (2009) A feedback circuit involving let-7-family miRNAs and DAF-12 integrates environmental signals and developmental timing in Caenorhabditis elegans. Proc Natl Acad Sci U S A, 106(44) pp. 18668-73.
Hammell, C. M. and Lubin, I. and Boag, P. R. and Blackwell, T. K. and Ambros, V. (2009) nhl-2 Modulates microRNA activity in Caenorhabditis elegans. Cell, 136(5) pp. 926-38.Additional materials of the author at
CSHL Institutional Repository