The Retromer Subunit CfVps29 Is Involved in the Growth, Development, and Pathogenicity of Colletotrichum fructicola

Abstract

Camellia oleifera is an edible oil tree species native to China. Anthracnose is a common disease of Ca. oleifera, which reduces the production of the trees and brings huge economic losses. We have previously identified the fungus Colletotrichum fructicola as the major pathogen of anthracnose in Ca. oleifera. The retromer complex participates in the intracellular retrograde transport of the cargos from the endosome to the trans-Golgi network in the eukaryotes. Vacuolar protein sorting 29 is a subunit of the retromer complex. Targeted CfVPS29 gene deletion revealed that CfVps29 is involved in growth, conidiation, and the response to cell wall stress. We further found that the ΔCfvps29 mutant was minimally pathogenic to Ca. oleifera leaves, as a result of its defect in appressorium formation. This study illustrated the crucial functions of CfVps29 in the development, cell wall stress response, and pathogenicity of C. fructicola and, therefore, identified it as a potential fungicide target for the control of anthracnose.

Endocytic dynamin deficiency impairs the host colonization of phytopathogenic fungi

“…During pathogen-host interactions, pathogens exploit the endolysosomal network to fine-tune intracellular homeostasis, thereby facilitating host colonization 9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30 . However, the complex interplay within the endolysosomal network and its potential in fungal disease control remain largely unknown.…”

“…Highlighting its importance, the endolysosomal network is associated with the pathogenesis of plant pathogenic fungi. Dysfunction of the endolysosomal network impairs the vegetative growth and infection-related development of various fungal pathogens 9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30 . Additionally, the endolysosomal network is required for effective modulation of autophagy process, which helps in adaptation to metabolic changes and environmental cues during pathogen-host interactions 21,26,27,28,29 .…”