Bioinformatic identification of cassava miRNAs differentially expressed in response to infection by Xanthomonas axonopodis pv. manihotis

This work addresses the role of miRNAs in the Manihot esculenta (cassava)-Xanthomonas axonopodis pv. manihotis (Xam) interaction. Next-generation sequencing was used for analyzing small RNA libraries from cassava tissue infected and non-infected with Xam. A full repertoire of cassava miRNAs was characterized, which included 56 conserved families and 12 novel cassava-specific families. Endogenous targets were predicted in the cassava genome for many miRNA families. Some miRNA families' expression was increased in response to bacterial infection, including miRNAs known to mediate defense by targeting auxin-responding factors as well as some cassava-specific miRNAs. Some bacteria-repressed miRNAs included families involved in copper regulation as well as families targeting disease resistance genes. Putative transcription factor binding sites (TFBS) were identified in the MIRNA genes promoter region and compared to promoter regions in miRNA target genes and protein coding genes, revealing differences between MIRNA gene transcriptional regulation and other genes.Taken together these results suggest that miRNAs in cassava play a role in defense against Xam, and that the mechanism is similar to what's known in Arabidopsis and involves some of the same families.Very succinctly plant-bacteria interactions can be thought as governed at molecular level mainly by three types of proteins: plant PRRs (pathogen recognition receptors), bacterial effectors and plant resistance proteins. PRRs are proteins recognizing highly conserved structures and molecules in microorganisms named MAMP (microbial-associated molecular patterns) and mediate MAMP-triggered immunity (MTI), which is efficient against non-adapted pathogens. Pathogens have developed effector proteins to suppress MTI. In turn, plants can counteract the action of effector by the specific recognition of effectors mediated by resistance proteins which will trigger a strong defence response known as ETI (effector-triggered immu