Fei Li
New York University, NY·Genetics
Every time a cell divides, it must give each daughter cell exactly one copy of every chromosome. Errors produce aneuploidy, meaning the wrong number of chromosomes, which is found in more than 90% of cancers and underlies conditions such as Down syndrome.
- Fields
Genetics
Biology
Biochemistry
- Topics
centromere
histone H3 variant
kinetochore
- Grants
- 1 known grant, through Aug 2029
What they work on
- Define how low-level transcription of centromeres into RNA is regulated in fission yeast and what role it plays in centromere function and chromosome segregation.
- Determine how tandem DNA repeats in heterochromatin, the silenced chromatin surrounding centromeres, are organized and how they contribute to assembling CENP-A chromatin, the histone variant that marks centromeres.
- Identify the regulatory mechanisms that position centromeres and heterochromatin in 3D space within the fission yeast nucleus, using genetics, genomics, cytology, biochemistry and structural biology.
More about the research
The key to accurate division is the centromere. This is a special region on each chromosome where the kinetochore assembles; the kinetochore is a protein machine that attaches chromosomes to the fibers that pull them apart. Centromeres are marked not by a DNA sequence but epigenetically, by CENP-A. CENP-A is a special version of histone H3, one of the proteins that DNA wraps around. How CENP-A gets placed at the right spot, and how this mark is inherited, is still poorly understood. When CENP-A ends up in the wrong place, chromosome separation fails, and this has been linked to many cancers.
Why it matters
Centromere failure gives cells abnormal chromosome numbers, a feature of more than 90% of cancers and of disorders such as Down syndrome. Understanding how centromeres are built and inherited could explain how disruptions in this process lead to cancer and other diseases. In the long run, it may suggest new ways to diagnose and treat them.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Songtao Jia
Columbia University, NY·Genetics
Determine how ubiquitylation of histone H3 at lysine 14 (H3K14ub) stimulates the H3K9 methyltransferase enzymes that create heterochromatin's key silencing mark in fission yeast.
Ajit Joglekar
University of Michigan, MI·Biology
Measure the rate at which a single unattached kinetochore generates the Spindle Assembly Checkpoint 'wait-anaphase' signal, using quantitative experimental data.
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
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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