Comparative expression analysis of resistant and susceptible Populus clones inoculated with Septoria musiva

Septoria musiva is a major pathogen of Populus and can cause leaf spots and stem cankers in susceptible clones. In order to investigate defense mechanisms of Populus in response to S. musiva, differential gene expression in leaf tissues of two resistant (DN34, P. deltoides×nigra; NM6, P. nigra×maximowiczii) and two susceptible clones (DN164, P. deltoides×nigra; NC11505, P. maximowiczii×trichocarpa) was analyzed by RNA-Seq. Of the 511 million reads obtained, 78% and 0.01% were successfully aligned to the genomes of P. trichocarpa and S. musiva, respectively. Functional annotation of differentially expressed genes based on comparisons between resistant and susceptible clones revealed that there were significant differences in the expression of genes involved in disease/stress resistance and oxidation-reduction in mock-inoculated leaves. Four days post inoculation with S. musiva, 36 differentially expressed genes were found to be regulated in the same direction in both resistant clones. The 22 up-regulated loci in resistant clones included genes involved in protein fate, cell wall structure, and responsiveness to various biotic and abiotic stresses. In particular, Potri.008G187100 locus encodes a putative multi antimicrobial extrusion protein and Potri.006G272600 encodes a family1 glycosyltransferase required for pathogen resistance. The differentially expressed loci with increased expression in the susceptible clones corresponded to NB-ARC domain-containing disease resistance protein, phospholipase A 2A, MutT/nudix family protein, and an elicitor-activated gene 3-1 product. The results from this study indicate that strong defense mechanisms involved in oxidation-reduction, protein fate, secondary metabolism, and accumulation of defense-related gene products may contribute to Septoria resistance in DN34 and NM6, while increased expression of hypersensitive response-loci, particularly those encoding NB-ARC domain-containing disease resistance proteins, may contribute to the susceptibility of DN164 and NC11505 through interaction with pathogen effectors.