Abstract

Sugarcane mosaic virus (SCMV) causes substantial yield losses worldwide, yet the molecular basis underlying resistance and susceptibility in sugarcane remains incompletely understood. Here, we performed time-resolved transcriptome profiling of two contrasting sugarcane genotypes, the SCMV-susceptible cultivar Badila and its resistant somatic mutant FG1, across five infection stages. Absolute quantification revealed rapid viral RNA replication in Badila, whereas FG1 showed early suppression followed by SCMV clearance. Comparative transcriptomic analyses showed that FG1 mounted a rapid and sustained defence-associated transcriptional response, whereas Badila displayed delayed, predominantly repressive gene expression changes. Weighted gene co-expression network analysis identified gene modules strongly correlated with viral RNA levels and highlighted the small heat shock protein gene ScHSP17.5 as a central hub associated with susceptibility. Protein–protein interaction assays demonstrated that ScHSP17.5 and ScHSP17.9A specifically interact with the SCMV movement protein P3N-PIPO, but not with P3 or the coat protein. Functional assays in Nicotiana benthamiana further showed that overexpression of either ScHSP enhanced SCMV RNA replication, with co-expression producing a synergistic effect. Together, these results support a model in which SCMV exploits host small heat shock proteins via P3N-PIPO to promote viral accumulation, whereas early redox- and signalling-associated responses restrict infection in resistant sugarcane. This study provides mechanistic insight into SCMV–host interactions and identifies candidate targets for resistance breeding.