Jung-Hyun Min
Baylor University, TX·Biochemistry
Every cell's DNA is damaged constantly, by ultraviolet (UV) light, cigarette smoke, fuel combustion, industrial pollutants and even some anti-cancer drugs. If the damage is not fixed, it can block DNA copying and gene reading and cause mutations.
- Fields
Biochemistry
Biophysics
Genetics
- Topics
nucleotide excision repair
DNA repair
DNA damage
- Grants
- 2 known grants, through Feb 2027
What they work on
- Determine how the yeast damage sensor Rad4-Rad23-Rad33 (equivalent to human XPC-RAD23B-CETN2) and the unwinding machine TFIIH together open DNA around a lesion, using cryo-electron microscopy and crosslinking/mass spectrometry.
- Test how torsional stress, the twisting strain in DNA, affects the start of nucleotide excision repair, using time-resolved fluorescence spectroscopy to follow changes in DNA shape.
- Define how the TFIIH-Rad4 complex begins unwinding DNA at genuine repair lesions, by combining cryo-EM 3D structures with fluorescence lifetime measurements of DNA shape changes.
- Reveal how full TFIIH is switched into repair mode by releasing TFIIK, a kinase module used in gene reading, using cryo-EM, crosslinking/mass spectrometry and yeast genetics.
- Capture how the TFIIH-Rad4 complex moves from opening the DNA to verifying the lesion, building a sequence of 3D structures of nucleotide excision repair initiation.
More about the research
Nucleotide excision repair (NER) is the cell's most versatile DNA repair pathway. It uses more than 30 proteins to cut out many kinds of damage that bend or distort the DNA double helix. NER works much the same way from yeast to humans. In people, broken NER genes cause xeroderma pigmentosum, a condition with extreme cancer risk, and Cockayne syndrome, which causes severe neurodevelopmental problems. NER also shapes where mutations cluster in many cancers. Even so, scientists still lack clear 3D pictures of how the repair machinery first grabs damaged DNA and pries it open. Two linked projects, one funded by NIH and one by NSF, aim to fill that gap using baker's yeast as a model.
Why it matters
Defects in NER cause xeroderma pigmentosum and Cockayne syndrome, and NER influences where mutations form in many cancers. NER has also been proposed as a target for anti-cancer therapy, because it repairs damage made by some cancer drugs. Detailed structures of how NER starts could help explain how specific disease-causing mutations act. Over time, they may also point to ways of adjusting this repair pathway to counter NER-linked diseases, including cancer.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ramiro Verdun
University of Miami, FL·Biochemistry
Determine how bypass of transcription-blocking DNA lesions by RNA Polymerase II, the enzyme that copies genes into RNA, disrupts the cellular response to ultraviolet radiation damage and disturbs normal cell function.
Christina Pacak
University of Minnesota, MN·Genetics
Optimize the capsid, or virus shell, and the promoter, the DNA switch controlling gene activity, of an AAV vector that delivers the ERCC5 (XPG) gene to improve treatment in Xpg-/- mice.
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.
The school
Baylor University: 5 labs on PI Pages, $135M a year on research, 280 research doctorates a year.
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