Chris Hsiung
University of California-San Francisco, CA·Genetics·Early-career
Cells can switch genes off and keep them off long after the original signal is gone. This project asks how that kind of lasting "off" state is set up, and whether it can be installed on purpose in human cells.
- Fields
Genetics
Biochemistry
Biomedical Engineering
- Topics
epigenetics
epigenetic memory
chromatin
- Grants
- 1 known grant, through Jul 2028
What they work on
- Build CRISPR/Cas-based tools that can deliver many combinations of chromatin signals at once, overcoming the limited combinatorial capacity of existing systems for manipulating gene regulation in human cells.
- Test which combinations of regulatory elements, chromatin-modifying protein complexes and covalent chromatin marks are needed to trigger silencing that persists after the synthetic trigger is removed.
- Map how well memorized silencing generalizes across different genomic locations, comparing promoters that sit at the start of genes with enhancers that act from a distance.
- Use high-throughput functional genomics screens with single-cell readouts of gene expression to score silencing and its durability across engineered conditions in human cells.
More about the research
The motivation is practical: catalogues of disease-linked DNA variants keep growing, but turning those annotations into treatments is hard. Gene editing with CRISPR/Cas, a bacterial system repurposed to cut or bind chosen DNA sequences, can change the genome permanently, yet it carries risks of cutting at unintended sites and works less well on regulatory switches, the stretches of DNA that tune when and where a gene is used. Those switches are where most disease-associated variants actually sit. An alternative is a brief "hit-and-run" treatment that leaves the DNA sequence untouched but leaves behind a memory of silencing.
Why it matters
Many DNA variants tied to disease fall in regulatory regions that are difficult to address with conventional gene editing. Tools that silence a chosen promoter or enhancer with a short-lived synthetic treatment, and have that silencing persist, could widen the part of the genome open to therapy while avoiding permanent cuts to DNA and long-term expression of foreign editing proteins. The work may inform future epigenetic therapies targeted to specific cell types and disease mechanisms.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michael Joseph Buck
University at Buffalo, NY·Genetics
Determine how transcription factors recognize binding sites wrapped on a nucleosome, the DNA spool unit, using the in vitro Pioneer-seq assay to compare sites at every nucleosome position and across sequence variants.
Venkatesan Sundaresan
University of California-Davis, CA·Plant Science & Agriculture
Generate diploid, unrecombined gametes in maize by editing multiple genes required for cell division and meiosis, testing whether cis-regulatory elements are conserved between meiosis and mitosis.
Anat Kreimer
Rutgers University-New Brunswick, NJ·Genetics
Develop methods that integrate massively parallel reporter assay (MPRA) data, which test thousands of DNA sequences at once, with other genomic assays and deep learning to reconstruct cell-type-specific gene regulatory networks and their condition-specific regulators.
The school
University of California-San Francisco: 89 labs on PI Pages, $2.1B a year on research, 164 research doctorates a year.
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