Citrus psorosis virus 24K protein interacts with citrus miRNA precursors, affects their processing and subsequent miRNA accumulation and target expression

REYES CA; OCOLOTOBICHE E; MARMISOLLÉ F; ROBLES LUNA G; BORNIEGO, MB; BAZZINI ARIEL A; ASURMENDI S; GARCIA ML

MOLECULAR PLANT PATHOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2016 vol. 17 p. 317 - 329

1464-6722

Sweet orange (Citrus sinensis) is one of the most important fruit crops worldwide. Disease symptoms caused by virus infections can interfere with cellular processes causing dramatic economic losses. Here we demonstrate that infection of sweet orange plants with two isolates of Citrus psorosis virus (CPsV) expressing different symptomatology alters accumulation of a set of microRNAs (miRNAs). miR156, miR167 and miR171 were the strongest down-regulated reaching levels of almost 3 folds reduction in infected samples and leading to a concomitant up-regulation of some of its targets: SPL9, SPL13 and SCL6. The most severe symptom, expressed as necrosis of young shoots (shock), showed the strongest decrease in miRNA levels, particularly miR156. Secondary structure of sweet orange pre-miR156 family of precursors (a to g) was predicted and analysis is consistent with a loop to base model of processing by DCL1. Pre-miR156 processing is affected in sweet orange by the virus as manifested by increment in the level of unprocessed pre-miR156 in relation to mature species. Co-immunoprecipitation of viral proteins and pre-miRNA, let us propose that processing alteration might be due to direct or indirect interaction of pre-miR156a with the viral 24K protein, coincident also with their nuclear localization. This work contributes to the understanding of how virus can alter host regulatory mechanisms, particularly miRNA biogenesis and function.