Adam Norris
University of California-Riverside, CA·Genetics
Some RNA binding proteins (RBPs), which control how genetic messages are edited, stabilized and positioned in a cell, are made in nearly every cell. Yet when they fail, only certain cells are damaged.
- Fields
Genetics
Biology
Neuroscience
- Topics
RNA binding proteins
alternative splicing
RNA processing
- Grants
- 1 known grant, through May 2029
What they work on
- Determine how the broadly expressed RNA binding protein MEC-8/RBPMS produces cell-specific outcomes by identifying its physiologically relevant RNA targets in different C. elegans cell and tissue types.
- Investigate why loss of SMN-1, the worm counterpart of the spinal muscular atrophy protein, causes cell-specific defects, and which of its targets drive these phenotypes in C. elegans.
- Dissect cell-specific formation of circular RNAs made by back-splicing, rather than standard forward splicing, in C. elegans tissues.
- Examine alternative splicing of exons whose lengths are not multiples of three nucleotides and its consequences, including amino acid recoding, altered protein ends and regulated RNA degradation.
More about the research
In spinal muscular atrophy (SMA), for example, the widely made protein SMN1 is mutated, but mainly motor neurons degenerate. Similar RBP problems underlie ALS and frontotemporal dementia. Why do broadly expressed RBPs have such cell-specific effects? Which of an RBP's many target RNAs cause a given defect? Do the important targets differ from tissue to tissue?
Why it matters
Diseases such as spinal muscular atrophy and ALS/FTD arise when RNA binding proteins are mutated or misregulated, yet the damage strikes specific cell types. Learning why, and which RNA targets matter in each tissue, could help explain why motor neurons are vulnerable. It could also point toward the key targets involved in these disorders.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Charlotte Sumner
Johns Hopkins University, MD·Neuroscience
Dissect how levels of SMN protein, which declines sharply around birth in SMA, are regulated during development and during treatment with SMN-inducing drugs, using patient data, mice and iPSC-derived motor neurons.
Daniel Dominguez
University of North Carolina at Chapel Hill, NC·Biochemistry
Define the mechanisms by which intrinsically disordered low-complexity domains (LCDs) of RNA binding proteins recognize structured RNA, such as RNA G-quadruplexes, using biochemical and computational approaches.
Gemma Carvill
Northwestern University, IL·Genetics
Identify the RNA-binding proteins that cause extra splicing-in of an SCN1A poison exon in people with epilepsy, using splice reporters and proteomics, and test whether antisense oligonucleotides correct it in patient iPSC-derived neurons.
The school
University of California-Riverside: 21 labs on PI Pages, $232M a year on research, 328 research doctorates a year.
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