Nimrat Chatterjee
University of Vermont, VT·Biochemistry
Cells constantly accumulate DNA mutations and other genetic changes, a state called genome instability. It contributes to cancer, infectious diseases and neurodegenerative disorders.
- Fields
Biochemistry
Genetics
Biology
- Topics
translesion synthesis
DNA polymerase
genome instability
- Grants
- 1 known grant, through Jul 2028
What they work on
- Determine how the REV1 polymerase regulates autophagy and cellular metabolism, and how it steers cells toward autophagy or senescence after different types of DNA damage.
- Define the mechanism by which REV1 contributes to mitotic fidelity, the accurate division of chromosomes, through its direct regulation of mitosis proteins.
- Establish how REV1 controls replication stress through rereplication, in which DNA is copied more than once, and how this contributes to genome instability.
More about the research
One known source is translesion synthesis (TLS), a backup DNA-copying system. TLS uses sloppy polymerases, the enzymes that copy DNA, to copy past damaged DNA and to fill gaps, and it introduces mutations as it goes. REV1 is the polymerase that directs this process. The standard view is that REV1 matters because it makes mutations. Discoveries from this lab suggest REV1 does much more.
Why it matters
Genome instability underlies cancer, neurodegenerative disorders and other diseases. Showing how REV1 controls cell metabolism, accurate cell division and DNA rereplication could clarify how genetic damage drives these conditions. It could also point to new therapeutic opportunities that target REV1's newly recognized roles.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Aneel Aggarwal
Icahn School of Medicine at Mount Sinai, NY·Biochemistry
Determine how the CBASS anti-phage system, which signals through cyclic oligonucleotides, becomes allosterically activated to trigger abortive infection and protect a bacterial population.
Dale A Ramsden
University of North Carolina at Chapel Hill, NC·Biochemistry
Determine how Pol θ's interactions with the DNA-copying machinery, including the polymerase Pol δ and the DNA clamp PCNA, affect cells' need for Pol θ-mediated end joining.
Yongjie Xu
Wright State University, OH·Genetics
Determine how mutations in the Rad3-Rad26 complex, the RecQ helicase Rqh1, the Smc5/6 complex and RPA impair Rad3 (ATR) checkpoint signaling at stalled replication forks, using fission yeast mutants in vivo and in vitro.
The school
University of Vermont: 16 labs on PI Pages, $246M a year on research, 76 research doctorates a year.
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