Yongjie Xu
Wright State University, OH·Genetics
Each time a cell divides, it must copy its entire DNA. When copying runs into trouble, a safety system called the DNA replication checkpoint senses the problem.
- Fields
Genetics
Biochemistry
Biology
- Topics
DNA replication checkpoint
replication stress
replication fork protection
- Grants
- 1 known grant, through Jan 2027
What they work on
- 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.
- Uncover how the activated replication checkpoint regulates DNA polymerase epsilon on the leading strand, and identify other targets that protect replication forks under stress in fission yeast.
- Use an improved forward-genetic screen combined with biochemical analysis to identify replication proteins with conserved checkpoint functions, and reconstitute the checkpoint pathway in vitro from purified proteins.
- Evaluate whether checkpoint mechanisms found in fission yeast, such as those involving Rqh1, are conserved in human cells.
More about the research
It keeps the copying machinery, known as the replication fork, from stalling for good. Without it, cells can suffer genome damage and die, so the checkpoint acts as an important barrier against cancer. Many anticancer drugs work by disrupting DNA replication, so how well they work depends partly on a tumor's checkpoint status. Still, it is not fully understood how the checkpoint switches on at forks or how it protects them under stress.
Why it matters
Many cancer chemotherapies attack DNA replication, and their effectiveness depends on the replication checkpoint. A clearer picture of how this conserved checkpoint senses and protects stalled DNA copying could improve understanding of genome instability, how cancers arise, and why tumors respond to chemotherapy drugs differently.
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.
Fei Li
New York University, NY·Genetics
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.
Ke Reid
Wake Forest University, NC·Biochemistry
Test whether the distinct effects of losing Rpl27 paralogs, two gene copies of a large-subunit ribosomal protein, in fission yeast come from differences in protein sequence or in protein abundance.
The school
Wright State University: 2 labs on PI Pages, $23M a year on research, 28 research doctorates a year.
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