The RNA Bioscience Initiative supports graduate students through its RNA Scholars Program. Applicants are selected (see application information) based on previous accomplishments and promise in RNA Research. The RNA Scholars are provided stipend support and a small discretionary fund.
2019-2020 RNA Scholars Application
Application details for next RNA Scholars Program coming Spring 2019.
2018-2019 RNA Scholars
My research is focused
on how the RNA helicase and viral sensor RIG-I responds to endogenous dsRNAs.
RIG-I is required to respond to certain types of viral infection by initiating
the production of type I interferon to combat infection. RIG-I must
discriminate between viral and self-RNA to prevent inappropriate interferon
production and the development of autoinflammatory and autoimmune disease. The
goal of my research is to understand how RNA cleavage and degradation during
cellular stress regulates RIG-I detection and activation by endogenous RNAs.
|My overall research goal is to understand the role of an angiogenic miRNA, miR-126, in the pathogenesis of a common and incurable pulmonary disease called emphysema. My hypothesis is that cigarette smoking (CS)-induced decrease of miR-126 mediates lung endothelial cell apoptosis and inhibits endothelial cell repair. I propose to utilize liposomes as a delivery tool to study the therapeutic effects of miR-126 restoration during in vivo CS exposure. Functional
outcomes of this study may provide basis for the development of a miRNA-based
drug to prevent cell death and enhance endothelial repair caused by smoking. |
focuses on RNA pseudoknot (PK) structures that are present in the 3’
untranslated regions (UTRs) of flaviviral genomes. These PKs are capable of
halting viral RNA degradation by a host exonuclease, Xrn1, and this activity
results in the formation of subgenomic flaviviral RNAs (sfRNAs) that are
necessary for viral pathogenicity. I have worked to biochemically characterize
these PKs from a variety of evolutionarily diverse flaviviruses and determined
that the structures are not only resistant to degradation by multiple
exonucleases, but that they also comprise more than one secondary structural
class of PKs. Additionally, I have adapted a genetically tractable infectious
clone system for Dengue wherein I can make specific mutations in the viral 3’UTR.
I have created a cassette of mutant viruses to interrogate the relationship
between the individual PK structures, the overall architecture of the viral
3’UTR, and the subsequent infection dynamics in both vertebrate host and mosquito
In eukaryotes, a subset of tRNAs contain introns that are
post-transcriptionally removed by a spliceosome-independent, enzyme-catalyzed
pathway. Essential genes in this pathway include the members of a conserved
endonuclease complex that excises tRNA introns, and an RNA ligase that rejoins
the resulting tRNA halves. Beyond tRNA splicing, these enzymes also play
additional intracellular roles. The tRNA ligase is required for the
non-canonical splicing of an mRNA encoding a key signaling molecule in the unfolded
protein response, and the tRNA splicing endonuclease has an additional
essential function that has yet to be identified. I am investigating the RNA
targets of this essential pathway to better understand how, when, and why cells
initiate RNA cleavage and repair.|