Genome editing of NPR3 confers potato resistance to zebra chip disease

Monday, August 4, 2025

12:30 PM - 12:45 PM HST

Location: Room 313 C

Presenting Author(s)

MR

Manikandan Ramasamy, PhD (he/him/his)

Research Scientist
Texas A&M AgriLife Research and Extension Center
Weslaco, Texas, United States

Author(s)

MR

Mohan Singh Rajkumar

Assistant Research Scientist
Texas A&M AgriLife Research and Extension Center
Weslaco, Texas, United States
SI

Sonia Irigoyen

Research Scientist
Texas A&M AgriLife Research and Extension Center
Weslaco, Texas, United States
RB

Renesh Bedre

Texas A&M AgriLife Research and Extension Center
Weslaco, Texas, United States
KF

Katherine Berg- Falloure

Department of Plant Pathology and Microbiology, Texas A& M University
College Station, Texas, United States
MK

Michael V. Kolomiets

Department of Plant Pathology and Microbiology, Texas A& M University
College Station, Texas, United States
KM

Kranthi K. Mandadi

Professor
Texas A&M AgriLife Research and Extension Center
Weslaco, TX, USA

Abstract Text: Zebra chip (ZC) disease in potatoes (Solanum tuberosum) is caused by the phloem-limited, fastidious pathogen Candidatus Liberibacter solanacearum (CLso). This pathogen, transmitted by potato psyllids (Bactericera cockerelli Šulc.), is notoriously difficult to culture and leads to significant yield losses in affected potato crops. In plant immunity, systemic acquired resistance (SAR) response is mediated by NON-EXPRESSOR OF PATHOGENESIS RELATED (NPR) proteins, which serve as transcriptional co-factors and receptors of the salicylic acid (SA) defense hormone. While NPR1 is an activator of SAR in Arabidopsis, its homolog, NPR3, functions as a negative SAR regulator. In this study, CRISPR-CAS9 technology was used to edit an NPR3 ortholog in potatoes. ZC disease challenges with CLso-carrying psyllids showed a significant reduction of CLso accumulation and attenuation of disease symptoms on the NPR3-edited plants compared to Cas9-alone controls. LC-MS/MS-based metabolite quantification showed a significant accumulation of SA in the NPR3-edited lines and correlated with increased expression of PR genes. Furthermore, transcriptome analysis identified resistance-associated transcription factors and their co-expressed gene networks perturbed in the NPR3-edited lines. Together, the results demonstrated that activating SA-mediated defenses by CRISPR-CAS9-mediated editing of NPR3 can confer ZC disease resistance in potatoes, offering a promising strategy for managing this devastating pathogen.