Background
Piper nigrum L., or “black pepper”, is an economically important spice crop in tropical regions. Black pepper production is markedly affected by foot rot disease caused by Phytophthora capsici, and genetic improvement of black pepper is essential for combating foot rot diseases. However, little is known about the mechanism of anti- P. capsici in black pepper. The molecular mechanisms underlying foot rot susceptibility were studied by comparing transcriptome analysis between resistant (Piper flaviflorum) and susceptible (Piper nigrum cv. Reyin-1) black pepper species.Results116,432 unigenes were acquired from six libraries (three replicates of resistant and susceptible black pepper samples), which were integrated by applying BLAST similarity searches and noted by adopting Kyoto Encyclopaedia of Genes and Gene Ontology (GO) genome orthology identifiers. The reference transcriptome was mapped using two sets of digital gene expression data. Using GO enrichment analysis for the differentially expressed genes, the majority of the genes associated with the phenylpropanoid biosynthesis pathway were identified in P. flaviflorum. In addition, the expression of genes revealed that after susceptible and resistant species were inoculated with P. capsici, the majority of genes incorporated in the phenylpropanoid metabolism pathway were up-regulated in both species. Among various treatments and organs, all the genes were up-regulated to a relatively high degree in resistant species. Phenylalanine ammonia lyase and peroxidase enzyme activity increased in susceptible and resistant species after inoculation with P. capsici, and the resistant species increased faster. The resistant plants retain their vascular structure in lignin revealed by histochemical analysis.ConclusionsOur data provide critical information regarding target genes and a technological basis for future studies of black pepper genetic improvements, including transgenic breeding.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3155-7) contains supplementary material, which is available to authorized users.
