Downregulation of Tomato STEROL GLYCOSYLTRANSFERASE 1 Perturbs Plant Development and Facilitates Viroid Infection

Potato spindle tuber viroid (PSTVd) is a plant pathogen naturally infecting economically important crops such as tomato (Solanum lycopersicum). Here, we aimed to engineer tomato plants highly resistant to PSTVd and developed several S. lycopersicum lines expressing an artificial microRNA (amiRNA) ag...

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Detalles Bibliográficos
Autores: Cisneros, Adriana E., Lisón, Purificación, Campos, Laura, López-Tubau, Joan Manel, Altabella Artigas, Teresa, Ferrer i Prats, Albert, Daròs, José-Antonio, Carbonell, Alberto
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2022
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/193669
Acceso en línea:https://hdl.handle.net/2445/193669
Access Level:acceso abierto
Palabra clave:Tomàquets
Glucòsids
Enzims
Tomatoes
Glucosides
Enzymes
Descripción
Sumario:Potato spindle tuber viroid (PSTVd) is a plant pathogen naturally infecting economically important crops such as tomato (Solanum lycopersicum). Here, we aimed to engineer tomato plants highly resistant to PSTVd and developed several S. lycopersicum lines expressing an artificial microRNA (amiRNA) against PSTVd (amiR-PSTVd). Infectivity assays revealed that amiR-PSTVd-expressing lines were not resistant but rather hypersusceptible to the viroid. A combination of phenotypic, molecular and metabolic analyses of amiRNA-expressing lines non-inoculated with the viroid revealed that amiR-PSTVd was accidentally silencing the tomato STEROL GLYCOSYLTRANSFERASE 1 (SlSGT1) gene, which caused late developmental and reproductive defects such as leaf epinasty, dwarfism or reduced fruit size. Importantly, two independent transgenic tomato lines each expressing a different amiRNA specifically designed to target SlSGT1 were also hypersusceptible to PSTVd, thus confirming that downregulation of SlSGT1 was responsible for the viroid hypersusceptibility phenotype. Our results highlight the role of SGTs in proper plant development and indicate that the unbalance of sterol glycosylation levels favors viroid infection most likely by facilitating viroid movement.