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ARS Home » Pacific West Area » Kimberly, Idaho » Northwest Irrigation and Soils Research » Research » Publications at this Location » Publication #426307
Research Project: Decipher Molecular Mechanisms for Genetic Variations in Agronomically Important Traits to Improve Sugar Beet Disease Resistance and Yield

Location: Northwest Irrigation and Soils Research

Title: Small RNA mediated regulation of cross-kingdom gene expression in sugar beet genotypes resistant and susceptible to rhizomania disease

Author
item Long, Evan
item Majumdar, Rajtilak
item Strausbaugh, Carl
item EUJAYL, IMAD - Retired ARS Employee

Submitted to: Journal of General Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/17/2025
Publication Date: N/A
Citation: N/A

Interpretive Summary: Sugar beet is highly susceptible to rhizomania which significantly reduces sugar yield worldwide. Typical symptoms of rhizomania are characterized by innumerous lateral rootlets on the main tap root accompanied by browning of vascular tissues, yellow erect leaves, and plant wilting in poorly drained soils. Resistance to rhizomania in commercial cultivars is primarily dependent upon the presence of Rz1 and Rz2 resistant genes, which have recently shown some compromise causing yield reduction. In this study we demonstrate new resistance mechanisms involving small non-coding RNAs in a rhizomania resistant mutant sugar beet breeding line developed at the USDA-ARS facility in Kimberly, ID. The information provided here will be useful to develop new sugar beet varieties with improved rhizomania resistance in the future.

Technical Abstract: Rhizomania in sugar beet causes significant yield and sucrose loss worldwide. The disease is caused by Beet necrotic yellow vein virus (BNYVV) vectored by the plasmodiophorid, Polymyxa betae. Resistance to rhizomania in commercial cultivars is dependent upon the presence of Rz1 and Rz2 resistant genes in commercial cultivars. We have developed an ethyl methanesulfonate (EMS) mutant breeding line (KEMS12; PI672570) highly resistant to rhizomania. Using the rhizomania resistant (R) and susceptible (S) lines, natural infection, and comprehensive RNA sequencing we demonstrate regulatory roles of sncRNAs in resistance and/or susceptibility. Examples of target genes of differentially expressed sugar beet miRNAs in the roots at early and late infection stages included Bevul.9G209500 (cytoplasm related catalytic activity), Bevul.2G095700 (potassium transporter) and Bevul.9G160600 (zinc finger), that were up-regulated in the R line (vs. S). Pathway enrichment analysis of miRNA target sugar beet genes showed enrichment of genes associated with ribosome, alanine, aspartate, glutamate, proteasome metabolism etc. Viral derived sncRNAs predominantly originated from RNA1 and RNA2 and targeted a subset of 69 sugar beet genes whose overall expression showed a strong negative correlation with higher sncRNA abundance. Sugar beet miRNAs putatively targeted viral genes namely RNA-dependent RNA polymerase, 42 kDa transport protein and showed up-regulation of those miRNAs in the R line (vs. S lines). Peptidome analysis of infected roots identified small peptides originating from BNYVV. The results presented here for the first time demonstrate putative roles of sugar beet miRNAs in rhizomania resistance, and BNYVV derived sncRNAs and small peptides as potential pathogenicity factors.