Physiological and transcriptomic analysis of Candidatus Phytoplasma pruni infection in Prunus persica

Authors: Wright, Alice; MOLNAR, CODY - Washington State University; SHIRES, MADALYN - Washington State University; BISHOP, GARRETT - Gs Long Company; HARPER, SCOTT - Washington State University

Submitted to: PhytoFrontiers
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/1/2022
Publication Date: 8/16/2023
Citation: Wright, A.A., Molnar, C., Shires, M.K., Bishop, G., Harper, S.J. 2023. Physiological and transcriptomic analysis of Candidatus Phytoplasma pruni infection in Prunus persica. PhytoFrontiers. Vol. 3, No.2. https://doi.org/10.1094/PHYTOFR-08-22-0083-R.
DOI: https://doi.org/10.1094/PHYTOFR-08-22-0083-R

Interpretive Summary: Phytoplasmas are plant bacteria that can cause disease in crops. In peaches the pathogen Candidatus phytoplasma pruni causes X-disease. Symptoms of X-disease include yellowing of leaves in July and August, shot-holing of leaves, and branch death. Trees die within four to five years of infection. It is unknown how infection by this pathogen causes these symptoms. In this study, we looked at changes to leaves and fruit and gene expression after infection. In branches with severe symptoms, pathogen count was high while counts were low where symptoms were not observed. Leaves with yellowing symptoms had less chlorophyll. Many genes showed changes in infected trees, including genes related to plant hormones, flowering time, and sugar. Genes that may be related to leaf yellowing and cell death were also identified. These data provide a clearer picture of symptom development in infected peach. This work also identifies additional areas of research for understanding how this phytoplasma interacts with peach.

Technical Abstract: Candidatus (Ca) Phytoplasma (P) pruni is the causative agent of X-disease in Prunus persica. Infected trees exhibit premature yellowing, leaf necrosis causing a shot-hole appearance, limb dieback, and eventual death. How pathogen infection leads to these symptoms is unknown. This study undertook a modern characterization of the disease by assessing the physiological and transcriptomic consequences of phytoplasma infection. Phytoplasma titer was high in the symptomatic tissues and undetected or at low titer in asymptomatic tissues. Symptomatic leaves had a significant decrease in chlorophyll a, chlorophyll b, and carotenoids. Transcriptomic analysis showed alterations in genes related to phytohormone synthesis and signaling, circadian rhythms, lignification, and sugar synthesis and transport. Several transcripts that may be related to symptom development were identified. Collectively these data give a much clearer picture of symptom development in Ca. P. pruni infected P. persica and provide several avenues of further research in determining how Ca. P. pruni interacts with its host to elicit the observed symptoms.