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Mitzi Kuroda

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Mitzi Kuroda is a Professor of Genetics at Harvard Medical School and Brigham and Women’s Hospital.[1] She was an HHMI Investigator at Brigham and Women’s Hospital from 1993-2007.[2] She has identified many genes and enzymes involved in epigenetic regulation in the fruit fly. In addition, her research has shown the importance of epigenetics in cancer.  Her laboratory has identified chromatin remodeling signals and processes that predispose cells to be transformed into cancer cells.

Early life and education

Mitzi Kuroda was born in 1958 in Fayetteville AR where she attended elementary and junior high schools.[3]  She spent a year in Tokyo,Japan before returning to attend Fayetteville High School where she gradauated as valedictorian in 1977.[3]

Mitzi Kuroda said “When I learned about recombinant DNA in college, it captured my imagination. I had to toss aside all my plans to “save the world” because the ability to make specific DNA molecules for molecular genetic experiments was just too enticing.”[1]  Kuroda received her BS in Biology from Tulane University in 1981[3] and her PhD in Biological Sciences at Stanford University[3], working with mentor Charles Yanofsky.[1] Mitzi Kuroda’s work with Yanofsky involved collaboration with Iwona Stroynowski to reveal how a riboswitch mechanism called bacterial attenuation regulates operons for amino acid biosynthesis.[4]

Academic Research Career

After postdoctoral work at Stanford, Mitzi Kuroda became a faculty member at Baylor College of Medicine.[1]  Kuroda rose through the ranks at Baylor to full professor.[3] In 2003, she moved to Harvard Medical School.[1] Kuroda initially concentrated on regulation processes in the fruit fly. Her citation by the National Academy of Sciences upon her election said “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.” [5] She has developed an important technique in which epigenetic regulators and their targets are cross-linked, then analyzed via mass spectrometry. In 2017, her laboratory discovered a master regulatory complex for Drosophila development.[6]

Recently, she has begun studies of regulation in cancer cells. Kuroda’s laboratory has shown that BRD4-NUT regulator leads to cancer via causing histone modification changes that produce a cascade of remodleling in which domains are opened to allow inappropriate expression of genes by transcription of their RNA.[7]

Honors and Awards

1992 Searle Scholar

https://www.searlescholars.net/person/253[8]

2013 National Academy of Sciences[5]

National Academy of Arts and Sciences[1]

Personal Life

Kuroda is married to geneticist Stephen Elledge and they have two grown children.[9]

Selected Works

Alekseyenko AA, Walsh EM, Wang X, Grayson AR, Hsi PT, Kharchenko PV, Kuroda MI, French CA (2015). The oncogenic BRD4-NUT chromatin regulator drives aberrant transcription within large topological domains. Genes Dev 29, 1507–1523.

Kang HJ, McElroy KA, Jung YL, Alekseyenko AA, Zee BM, Park PJ, Kuroda MI (2015). Sex comb on midleg (Scm) is a functional link between PcG-repressive complexes in Drosophila. Genes Dev 29, 1136–1150.

Ho JWK, Jung YL, Liu T + ModEncode Consortium (2014). Comparative analysis of metazoan chromatin organization. Nature 512, 449–452.

Alekseyenko AA, Gorchakov AA, Zee BM, Fuchs SM, Kharchenko PV, Kuroda MI (2014). Heterochromatin-associated interactions of Drosophila HP1a with dADD1, HIPP1, and repetitive RNAs. Genes Dev 28, 1445–1460.

Ferrari F, Plachetka A, Alekseyenko AA, Jung YL, Ozsolak F, Kharchenko PV, Park PJ, and Kuroda MI (2013). “Jumpstart and gain” model for dosage compensation in Drosophila based on direct sequencing of nascent transcripts. Cell Rep 5, 629–636.

Larschan E, Bishop EP, Kharchenko PV, Core LJ, Lis JT, Park PJ, Kuroda MI (2011). X chromosome dosage compensation via enhanced transcriptional elongation in Drosophila. Nature 471, 115–118.

References

  1. ^ a b c d e f [(  https://www.abcam.com/epigenetics/scientist-of-the-month-mitzi-kuroda "Scientist of the month: Mitzi Kuroda"]. ABCAM. Retrieved December 1, 2018. {{cite web}}: Check |url= value (help); Cite has empty unknown parameter: |dead-url= (help); no-break space character in |url= at position 3 (help)
  2. ^ "Mitzi I Kuroda". HHMI. Retrieved December 1, 2018. {{cite web}}: Cite has empty unknown parameter: |dead-url= (help)
  3. ^ a b c d e "Mitzi Kuroda, Hall of Honor Album" (PDF). Fayetteville AR. Retrieved December 3, 2018. {{cite web}}: Cite has empty unknown parameter: |dead-url= (help)
  4. ^ I. Stroynowski, M. Kuroda, and C. Yanofsky (1983) "Transcription termination in vitro at the tryptophan operon attenuator is controlled by secondary structures in the leader transcript" Proc Natl Acad Sci U S A. 80(8): 2206–2210. PMCID: PMC393787 PMID: 6340118
  5. ^ a b "NAS Members: Mitzi Kuroda". National Academy of Sciences USA. Retrieved December 1, 2018. {{cite web}}: Cite has empty unknown parameter: |dead-url= (help)
  6. ^ Hyuckjoon Kang, Youngsook L. Jung, Kyle A. McElroy, Barry M. Zee, Heather A. Wallace, Jessica L. Woolnough, Peter J. Park, and Mitzi I. Kuroda.(2017) "Bivalent complexes of PRC1 with orthologs of BRD4 and MOZ/MORF target developmental genes in Drosophila." Genes & Development, 31 (19):1988-2002. DOI: 10.1101/gad.305987.117
  7. ^ A. Alekseyenko, E. Walsh, X. Wang, A. Grayson, P Hsi, P Kharchenko, M.I. Kuroda, and C. A. French. (2015) "The oncogenic BRD4-NUT chromatin regulator drives aberrant transcription within large topological domains." Genes Dev. 29(14):1507-23. doi: 10.1101/gad.267583.115.
  8. ^ "Mitzi Kuroda". Searle Scholars. Retrieved December 1, 2018. {{cite web}}: Cite has empty unknown parameter: |dead-url= (help)
  9. ^ "Stephen Elledge". Yale Gruber Award. Retrieved December 1, 2018. {{cite web}}: Cite has empty unknown parameter: |dead-url= (help)
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