SeqCode Logo SeqCode Registry
cognitis nomina
  • About
  • Search
  • •
  • Login
  • Register
Authors Harper

JSON
See as cards

Harper, S. J.


Publications
4

CitationNamesAbstract
Differences in ‘ Candidatus Phytoplasma pruni’ Gene Expression When Infecting Sweet Cherry Versus Leafhoppers Harper et al. (2026). PhytoFrontiers™ 6 (1) Ca. Phytoplasma pruni
Text
First Report of a ‘ Candidatus Phytoplasma pruni’-Related Strain Associated with Chlorosis and Decline of Artemisia tridentata in Washington State Shires et al. (2026). Plant Disease 110 (2) Ca. Phytoplasma pruni
Alternative Hosts of ‘Candidatus Phytoplasma pruni’ Identified Through Surveys and Vector Gut Content Analysis Shires et al. (2025). Plant Health Progress 26 (2) Ca. Phytoplasma pruni
Text
Titer and Distribution of ‘Candidatus Phytoplasma pruni’ in Prunus avium Wright et al. (2022). Phytopathology® 112 (7) Ca. Phytoplasma pruni
Text

Differences in ‘ Candidatus Phytoplasma pruni’ Gene Expression When Infecting Sweet Cherry Versus Leafhoppers
The X-disease phytoplasma (‘ Candidatus Phytoplasma pruni’) is an obligate pathogen that is capable of infection, persistence, and pathogenicity in both its major plant host ( Prunus spp.) and leafhopper vector ( Colladonus spp.) species. How ‘ Ca. P. pruni’ interacts with its plant and insect hosts, and how it alters its gene expression to do so, is unknown. Therefore, in this study, we conducted comparative RNA sequencing and differential gene expression analysis on ‘ Ca. P. pruni’-infected Prunus avium and Colladonus reductus samples. We found that the phytoplasma altered the expression of approximately 32% of its annotated protein-coding and pseudogenes, including intercellular transporters, proteolytic activity, and membrane structure, as well as upregulating genes associated with potential mobile units when in insect tissues versus in plant tissues. Most notably, differential expression was observed in genes that were identified by in silico analysis as being putative secreted effectors that may play a role in allowing phytoplasma infection and survival in these two very different host systems, as well as inducing X-disease in Prunus spp., which offers targets for control of this damaging pathogen by disrupting phytoplasma–host interactions. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
Alternative Hosts of ‘Candidatus Phytoplasma pruni’ Identified Through Surveys and Vector Gut Content Analysis
The ongoing spread of X-disease, which is associated with ‘ Candidatus Phytoplasma pruni’, has resulted in severe economic losses for cherry and stone fruit growers in the U.S. Pacific Northwest in the last decade. Given that this pathogen is transmitted by polyphagous leafhopper species, primarily Colladonus montanus ssp. reductus and C. geminatus in the Pacific Northwest, alternative plant hosts present a significant management concern. Here, we surveyed phytoplasma incidence in non- Prunus plants found in and around stone fruit orchard borders and compared these results to the leafhopper feeding patterns through gut content analysis. We confirmed ‘ Ca. P. pruni’ infection in 21 plant species from 15 families. Of these, 15 species were commonly found in the diets of phytoplasma-carrying leafhoppers. Due to the abundance of common plant species, including Taraxacum, Malva, and Trifolium spp., alternative hosts were found across all growing seasons, although ‘ Ca. P. pruni’ titer was low (<102 cells) in most of these hosts. No geographic patterns were identified; instead, phytoplasma incidence and spread at individual orchards was related to the management of annual and biennial host species, thus removing preferred leafhopper feeding hosts. These data suggest that alternative host removal, along with the removal of infected trees, is an effective means of slowing disease spread.
Titer and Distribution of ‘Candidatus Phytoplasma pruni’ in Prunus avium
‘Candidatus Phytoplasma pruni’ infection in cherries causes small, misshapen fruit with poor color and taste, rendering the fruit unmarketable. However, this is a disease with a long development cycle and a scattered, nonuniform symptom distribution in the early stages. To better understand the biology as well as the relationship between pathogen titer and disease expression, we carried out seasonal, spatial, and temporal examinations of ‘Ca. P. pruni’ titer and distribution in infected orchard-grown trees. Sequential sampling of heavily infected trees revealed marked seasonal patterns, with differential accumulation in woody stem and leaf tissues and, most notably, within fruit in the early stages of development from bloom to pit hardening. Furthermore, mapping phytoplasma distribution and titer in trees at different stages of infection indicated that infection proceeds through a series of stages. Initially, infection spreads basipetally and accumulates in the roots before populating aerial parts of the trees from the trunk upward, with infection of specific tissues and limbs followed by an increasing phytoplasma titer. Finally, we observed a correlation between phytoplasma titer and symptom severity, with severe symptom onset associated with three to four orders of magnitude more phytoplasma than mild symptoms. Cumulatively, these data aid in accurate sampling and management decision-making and furthers our understanding of disease development.
Search