Robert G Roeder
Rockefeller University, NY·Biochemistry
Every cell in the body carries the same genes, yet a fat cell, a liver cell and a cancer cell switch on very different sets of them. That choice happens mostly at transcription, the step where RNA polymerase II (Pol II), the enzyme that copies protein-coding genes into RNA, is recruited to a gene and moves along it.
- Fields
Biochemistry
Genetics
Physiology
- Topics
transcription
RNA polymerase II
Pol II
- Grants
- 2 known grants, through Jun 2030
What they work on
- Determine how PPARγ, C/EBP pioneer factors and the Mediator complex cooperate at fat-cell enhancers (DNA control regions) to set white and brown fat identity, using in vitro transcription, cross-linking mass spectrometry, multiomics and rapid protein degradation.
- Define how interactions among ERRγ, the coactivator NCOA3 and Mediator specifically support the energy-burning function of brown and beige fat cells.
- Analyze how genes are activated in mature fat cells both when Mediator is recruited through MED1's receptor-binding NR boxes and when alternative routes operate. Examine why MED1 NR-box mutant mice resist harmful metabolic effects of obesity-inducing diets.
- Uncover how Mediator lifts Gdown1's block on transcription start by Pol II(G). The approach combines in vitro transcription, immobilized-template assays, and cross-linking mass spectrometry and cryo-EM structures of complexes with general factors and TFIIS.
- Test Gdown1's roles in Pol II pausing, pause release and processive elongation in liver cancer cells, using acute Gdown1 degradation with multiomics plus test-tube reconstitution on recombinant chromatin.
More about the research
The lab's two projects examine this machinery from two directions. One looks at how gene-switching proteins and their helpers set up the identity of fat cells. The other looks at an unusual form of Pol II that keeps specialized tissues working and helps cancer cells grow. Both projects center on the Mediator, a large multi-part protein complex that links gene-switching proteins to Pol II.
Why it matters
Faulty control of fat-cell genes underlies obesity, lipodystrophy, type 2 diabetes and cardiovascular disease. The finding that weakening MED1–receptor contacts benefits obese mice points to possible routes for designing metabolic therapies. Pol II(G) supports growth and lipid-gene expression in breast and liver cancer cells. Understanding how it works could suggest new therapeutic avenues for hepatocellular carcinoma and breast cancer.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Mechanisms of transcriptional control of adipocyte formation and function through nuclear receptor coactivators
NIH · Sep 2025 – Jun 2030
Mechanistic studies of transcription initiation and elongation functions of an RNA polymerase II variant, Pol II(G), that is implicated in development and cancer
NIH · Jul 2022 – Jun 2027
Closest labs
Jia Fei
Rutgers University-New Brunswick, NJ·Biochemistry
Characterize how NDF loosens nucleosomes, the protein spools that package DNA, and helps RNA Polymerase II move through them, using ultra-high-resolution optical tweezers and cryo-electron microscopy.
Motoki Takaku
University of North Dakota, ND·Genetics
Identify the nucleosome positions and shapes that let the pioneer factor GATA3 open chromatin and drive the mesenchymal-to-epithelial transition in triple-negative breast cancer cells, using high-resolution nucleosome mapping.
Hang Shi
Georgia State University, GA·Physiology
Test whether deleting or overexpressing Uhmk1, a gene that supports nerve-fiber growth, in mouse sympathetic neurons changes nerve supply to fat, brown/beige fat heat production and energy expenditure during cold exposure.
The school
Rockefeller University: 6 labs on PI Pages, $305M a year on research, 38 research doctorates a year.
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