Michael Greenberg

Laureate Profile

Michael Greenberg was born in Florida, but raised in Brooklyn, New York as the youngest of four children. Although no one in his family had previously worked in a science-related field, Greenberg became hooked on biochemistry and biophysics after his junior year in high school, when he participated in a National Science Foundation summer program at Roswell Park Memorial Institute in Buffalo New York. After graduating magna cum laude in 1976 from Wesleyan University with a degree in chemistry, Greenberg pursued his doctoral studies at The Rockefeller University where he received a PhD in biochemistry in 1982 for research carried out in the laboratory of biologist (and Nobel laureate) Gerald Edelman.  For his postdoctoral studies Greenberg worked in the New York University laboratory of molecular biologist Edward Ziff. In 1986, Greenberg accepted an assistant professorship at Harvard Medical School’s Department of Microbiology and Molecular Genetics, where he stayed until 1994, when he joined the neurology faculty at Children’s Hospital Boston, to direct the Division of Neuroscience. He returned to Harvard Medical School in 2008 to become the Chair of the Department of Neurobiology, a position he continues to hold. 

Greenberg has spent the last 30 years unlocking the mysteries of the molecular mechanisms that underlie the effects of experience on the brain thus elucidating how nature and nurture are intertwined during brain development. In 1984, he made the landmark discovery that growth factors send signals from the cell surface to the nucleus instructing cells to transcribe the c-fos gene. Since then Greenberg and other researchers demonstrated that this process is induced in neurons in response to neural activity, and have identified hundreds of genes in addition to c-fos that are activated in the brain in response to sensory stimuli. Greenberg has described in elegant detail the neural pathways of this transcription process, including how the “L-type” voltage-gated Ca2+ calcium channel leads to gene expression crucial for synapse development and for learning and memory. Working with cultured mouse neurons, Greenberg recently demonstrated that across the genome “enhancer regions” of DNA are not only activated by sensory stimuli, but also create strands of enhancer RNA (eRNA) that appear to play a role in the neuron’s response to an external stimulus   More recently, Greenberg has reported that the lack of the one crucial regulator of sensory-dependent gene expression, MeCP2, results in the disruption of the expression of long genes in the brain, a finding with profound implications for Rett syndrome and other neurobiological disorders.