Degree

Doctor of Philosophy (PhD)

Department

Department of Biological Sciences

Document Type

Dissertation

Abstract

RNA interference (RNAi) triggered by virus produced dsRNA intermediate offers robust innate immunity against invading viruses in plants, insects and animals. Caenorhabditis elegans has been extensively used as a model organism to study host virus interaction. Recently, a forward genetic screen identified RNAi spreading deficient-6 (RSD-6), a Tudor domain protein, as a key component in antiviral RNAi pathway against Orsay virus in C. elegans but its contribution in the pathway remained unclear. Here, we generated a rsd-6 null allele using CRISPR-Cas9 genome editing, crossed it with other known RNAi mutants and analyzed Orsay virus replication in them and in combination with results from deep sequencing of small RNAs we show that abundant virus induced primary and secondary small RNAs are produced in rsd-6 mutant animals suggesting that RSD-6 acts downstream of secondary small RNA production in antiviral RNAi pathway in C. elegans. We also used various truncated versions of RSD-6 to rescue replication of FR1gfp in C. elegans and interestingly, our results show that Tudor domain of RSD-6 is not important in conferring antiviral RNAi in C. elegans. Finally, we show that the knock-down of RSD-6 in Caenorhabditis briggsae using feeding RNAi increases Santeuil virus replication suggesting that antiviral function RSD-6 is likely conserved among nematodes.

Date

7-28-2025

Committee Chair

Rui Lu

DOI

10.31390/gradschool_dissertations.6888

Available for download on Thursday, July 16, 2026

Included in

Biology Commons

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