Ke Reid
Wake Forest University, NC·Biochemistry
Ribosomes are the machines that build every protein in a cell. They are often treated as identical, but cells can assemble them from different versions of their parts.
- Fields
Biochemistry
Genetics
Biology
- Topics
ribosome
ribosomal proteins
paralogs
- Grants
- 1 known grant, through Sep 2027
What they work on
- 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.
- Determine how the two nearly identical Rps19 paralogs differ in regulatory elements and expression, especially under heat stress, in Schizosaccharomyces pombe.
- Test whether ribosomes built with different Rpl27 or Rps19 paralogs differ in which mRNAs they translate, or work differently under stress.
More about the research
Many ribosomal proteins are encoded by paralogs, two similar gene copies. Losing one copy or the other can produce different effects. That might mean ribosomes are specialized to translate particular messages. Or it might just mean cells make abnormal numbers of ribosomes. Settling this question is relevant to Diamond-Blackfan anemia (DBA), a rare disease that often appears in the first year of life. In DBA, the bone marrow cannot make enough red blood cells, possibly because of ribosome problems.
Why it matters
Mutations affecting ribosomal proteins are tied to Diamond-Blackfan anemia, a disease of young children whose bone marrow cannot make enough red blood cells. Learning whether different versions of ribosomal proteins control which proteins a cell makes could reveal new regulatory mechanisms in protein synthesis. In the long run, this could help guide new treatments for DBA.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
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
Wake Forest University: 27 labs on PI Pages, $345M a year on research, 54 research doctorates a year.
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