Mitzi I. Kuroda is a Professor of Genetics and a Professor of Medicine at Harvard Medical School & Brigham & Women’s Hospital. She is a molecular biologist recognized for her work on mechanisms of gene regulation in the model organism, Drosophila melanogaster. She is known particularly for her analyses of the mechanism of dosage compensation, in which expression of the X chromosome in males is increased to match the output of both X chromosomes in females. Kuroda was born in Fayetteville, Arkansas in 1958, graduated from Tulane University in 1981 with a degree in Biology, and received her doctorate from Stanford University in 1987. She was on the faculty of Baylor College of Medicine in Houston, Texas, before joining Harvard Medical School in 2003. Kuroda was previously an NSF Presidential Young Investigator, Searle Scholar, and Investigator of the Howard Hughes Medical Institute. She has served as a member of the Board of Directors of the Genetics Society of America and of the North American Drosophila Board, and is a Fellow of the American Academy of Arts & Sciences.

Research Interests

Kuroda and her laboratory have utilized dosage compensation in Drosophila as a model for understanding how genomes are organized into chromatin. Her lab identified the MSL ribonucleoprotein complex, and discovered that it assembles and spreads from sites of non-coding roX RNA synthesis to regulate genes specifically on the fruitfly male X chromosome. Furthermore, they dissected the sex-specific regulation of this process, and the molecular mechanism by which the MSL complex influences transcriptional elongation. Recently, Kuroda has expanded her studies of chromatin through biochemical and genomic analyses of additional epigenetic regulators, such as the Polycomb group in fruitflies and in human cells. One approach is to use cross-linking followed by mass spectrometry to identify the components of epigenetic complexes within their chromatin context. Long-term interests include deciphering the role of aberrant chromatin organization in specific cancer models.

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Primary Section

Section 26: Genetics