Welcome to Genetics at Harvard

Reflecting the breadth of the field itself, the Department of Genetics at Harvard Medical School houses a faculty working on diverse problems using a variety of approaches and model organisms, unified in their focus on the genome as an organizing principle for understanding biological phenomena. Genetics is not perceived simply as a subject, but rather as a way of viewing and approaching biological phenomena.

While the range of current efforts can best be appreciated by reading the research interests of individual faculty, the scope of the work conducted in the Department includes (but is by no means limited to) human genetics of both single gene disorders and complex traits, development of genomic technology, cancer biology, developmental biology, signal transduction, cell biological problems, stem cell biology, computational genetics, immunology, synthetic biology, epigenetics, evolutionary biology and plant biology.

The mission of our Department encompasses research and education while serving as a focal point for drawing together and integrating basic and clinical genetic efforts conducted across the University and its affiliated hospitals. The Department of Genetics is strongly committed to supporting its current community of faculty, postdoctoral fellows and graduate students and to securing the best new scientists, setting its sight on new research opportunities in the future.

In the News

Congratulations to Mitzi Kuroda, elected to the American Academy of Arts and Sciences

Mitzi Kuroda is a member of the 2012 class of international scholars, artists, scientists, writers and other professionals elected to the American Academy of Arts and Sciences. The Academy honors excellence in the Arts and Sciences. Members of the Academy provide independent, non-partisan research on the problems of American society.

more >>

Meet the Faculty

Christine Seidman, M.D.

Christine Seidman is interested in dominant-acting mutations in sarcomere protein genes that cause hypertrophic cardiomyopathy in humans. The Seidman lab has made a murine model of this disease and demonstrated that these mutations lead to altered Ca2+ concentrations in myocytes. Ca2+ channel blockers reduce the hypertrophic response to sarcomere protein gene mutations in mice.

more >>