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Heads of Laboratories

C. David Allis, Ph.D.

Tri-Institutional Professor
Joy and Jack Fishman Professor
Laboratory of Chromatin Biology and Epigenetics

Research Lab Members Publications In the News

Faculty Bio

C. David Allis

Dr. Allis studies the DNA-histone protein complex called chromatin, which packages genetic information within each cell. Chromatin can facilitate or restrict access to specific genes, enabling the cell to efficiently manage expression of its genome and serving as a means of gene regulation outside of DNA — the basis of epigenetics.

Chromatin is the physiological template of the human genome. The histone proteins within chromatin, their posttranslational modifications, and the enzyme systems responsible for generating them are highly conserved through evolution. Meanwhile, elaborate mechanisms have evolved to introduce meaningful variation into chromatin to alter gene expression and other important biological processes.
One such mechanism involves the addition or loss of chemical groups, and the Allis lab is currently investigating these covalent modifications to histones and their biological roles in a variety of unicellular and multicellular eukaryotic models. Through such enzymatic processes as acetylation, methylation, phosphorylation, and ubiquitylation, histones are believed to function like master on/off switches and determine whether particular genes are active or inactive. Knowing how to turn particular genes on or off could reduce the risk of certain diseases.
The frequent, high-density posttranslational modifications (PTMs) in histone proteins has led members of the Allis laboratory to hypothesize that PTMs are located strategically along the histone tail as a way for the cell to deal, reversibly, with gene silencing or activation. The lab has been a front-runner in deciphering elaborate interactions within the same histone tails (cis) or across distinct histone tails (trans). These combinatorial changes appear to govern chromatin function in a variety of processes and have been described as the “histone or epigenetic code” — a widely cited and influential hypothesis.

More recently, researchers in the Allis lab proposed that the mammalian genome is indexed by H3 variants so as to control whether genes are constitutively expressed or remain silent. The Allis lab produced the first genome-wide maps of H3.3 localization, first in mammalian embryonic stem cells and then again after the cells had differentiated to become neurons. Biochemical approaches have led to chaperone complexes that engage H3.3 selectively, depositing it into distinct regions of the genome. One of these chaperone systems is mutated in a significant fraction of patients who suffer from pancreatic neuroendocrine tumors, and H3.3 mutations are also highly specific to pediatric gliomas. Dr. Allis and his colleagues hypothesize these mutations can alter the recruitment and activity of histone modifying complexes and therefore alter the epigenetic landscape and dysregulate gene expression. Given the restricted distribution of H3.3 mutations to pediatric gliomas, they further hypothesize that cell lineage–specific cellular context is crucial for the ability of these mutations to mediate oncogenesis. Active investigations are under way to test these hypotheses with collaborators in more clinically relevant settings, including human patients.


Dr. Allis received his Ph.D. in 1978 from Indiana University and performed postdoctoral work with Martin Gorovsky at the University of Rochester. Before he joined Rockefeller in 2003 as the Joy and Jack Fishman Professor and head of laboratory, Dr. Allis held several academic positions, including ones at the Baylor College of Medicine and the University of Virginia Health System.
Dr. Allis is a member of the National Academy of Sciences and the American Academy of Arts and Sciences. Among his many honors are the 2015 Breakthrough Prize, the 2014 Japan Prize, the 2011 Lewis S. Rosenstiel Award for Distinguished Work in Basic Medical Science, the 2008 ASBMB-Merck Award, the 2007 Gairdner Foundation International Award, the 2004 Wiley Prize in Biomedical Sciences, the 2003 MAssry Prize and the 2002 Dickson Prize in Biomedical Sciences.

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