Skip to main content
eScholarship
Open Access Publications from the University of California

UC Riverside

UC Riverside Electronic Theses and Dissertations bannerUC Riverside

The Role of Fungal Pathogen Small RNAs in Host-Microbe Interactions

Abstract

Botrytis cinerea is a necrotrophic fungal pathogen that causes gray mold disease on a broad range of plant species. Many pathogens secrete protein effectors into host cells to evade the host immune system; however, my dissertation project shows that B. cinerea small RNAs (Bc-sRNAs) act as a novel type of pathogen effector to silence host defense genes.

Small RNAs (sRNAs) are short non-coding RNAs that normally associate with Argonaute (AGO) protein and suppress the genes with complementary sequences. The role of host sRNAs in plant-pathogens interactions has been well characterized, and recent studies also revealed the function of pathogen sRNAs in infection processes. In the first chapter of this thesis, I will review the current progress of the role of both host sRNAs and microbial pathogen sRNAs during host-pathogen interactions.

Bc-sRNA effectors are induced during plant infection and trigger silencing of host plant genes. We identified and confirmed three Bc-sRNAs (Bc-siR3.1, Bc-siR3.2 and Bc-siR5) that can translocate into host cells and hijack host RNAi machinery to silence host immunity related target genes. The B. cinerea dcl1 dcl2 double mutant has lost Bc-siR3.1, Bc-siR3.2, and Bc-siR5, which significantly compromised its virulence. The second chapter will present these findings.

Chapter 3 will cover the identification and characterization of a new Bc-sRNA effector, Bc-siR37, which has multiple predicted target genes in both Arabidopsis and tomato (Solanum lycopersicum), and most are putatively related to plant defense. We further characterize three of these candidate targets, At-WRKY7, At-PMR6, and At-FEI2, and confirm that they are negatively correlated with Bc-siR37 and positively regulate plant immunity against B. cinerea.

Comparative analysis of Bc-sRNAs transcriptome in wild-type B. cinerea and the dcl1 dcl2 double mutant indicates that most retrotransposon region-derived Bc-sRNAs are DCL-dependent, and most predicted Bc-sRNA effectors are generated from retrotransposon regions. The compromised virulence of the B. cinerea dcl1 dcl2 double mutant is probably due to failure to produce many Bc-sRNA effectors. Finally, we successfully use host-induced gene silencing (HIGS) of B. cinerea DCL1 and DCL2 to enhance plant resistant against gray mold disease. The final chapter will focus on these results.

Main Content
For improved accessibility of PDF content, download the file to your device.
Current View