Keith Blackwell, MD, PhD

Keith Blackwell, MD, PhD

Joslin Diabetes Center
Harvard Medical School Department of Genetics
Keith Blackwell, MD, PhD

Using the model organism C. elegans, we study how regulatory pathways that are important in growth control influence stress defenses and aging, as well as relationships between stem cell function and aging.  We are particularly interested in understanding mechanisms through which aging is influenced by insulin/IGF-1 and TOR signaling, two pathways that are of critical importance in cellular growth, renewal, and differentiation.  We are also interested in elucidating mechanisms that influence aging of germline and somatic tissues, and in understanding a signaling pathway through which C. elegans germline stem cells communicate with their niche to modulate stress resistance and aging of the entire organism.


I received a B.S. in Chemistry from Duke University in 1978, then entered the Medical Scientist Training Program at Columbia University.  I graduated from Columbia with an M.D. in 1987, and a Ph.D. in Microbiology in 1988.  I did my thesis work with Dr. Frederick Alt, working on the mechanism and regulation of immunoglobulin gene assembly.  Upon graduating from medical school I decided to pursue a research career full time, and rejoined the Alt lab until 1989, when I began a postdoctoral fellowship with the late Dr. Harold Weintraub at the Fred Hutchinson Cancer Research Center in Seattle.  There I studied functions and DNA recognition properties of basic-helix-loop-helix protein transcription factors.  I started my own lab at the CBR Institute and Harvard Medical School in 1993.  At the beginning of 2004 I moved to Joslin Diabetes Center, as a Senior Investigator and Head of the Section on Developmental and Stem Cell Biology.  I am now Associate Research Director there and a Professor of Genetics at Harvard Medical School.  I became interested in the C. elegans system initially as a postdoctoral fellow, when I collaborated with Jim Priess to investigate whether the developmental regulator SKN-1 functions as a transcription factor.  This interest led me later to begin working with C. elegans in my own laboratory, so that now essentially all of my lab’s projects involve this model organism.  Our work on C. elegans oogenesis, early embryonic development, and relationships between stress and stem cell function led us into the stem cell field.

Research Interest(s)