Abstract
Potato cyst nematodes (PCN) are important pests in crop production, especially since they persist in the soil and may affect further potato production for many years. Little is known about putative resistance and susceptibility targets as well as the general signaling in potato after interactions with PCN. Here we characterize a new potato breeding clone, SW-1015, found to harbor resistance to Globodera rostochiensis pathotype Ro1/4, the main PCN pathotype present in Sweden. SW-1015 contains the H1 resistance gene. We then describe susceptible and resistant reactions of potato infested by G. rostochiensis Ro1/4 in a global potato RNA-seq analysis. Only the resistant clone reacted to PCN infection quickly (8 hpi), and the reaction included up-regulation of a TSRF1 transcription factor. 48 h after PCN infection, massive RNA reprograming was evident in both resistant and susceptible clones. In the resistant interaction, several genes were up-regulated including germins and a cysteine protease, as well as a laccase. In contrast, the susceptible interaction involved up-regulation of genes for auxin transport and homeobox binding. Enriched GO terms for kinase activity, calmodulin, and Ca2+ ion binding in susceptible potato might reflect the initiation of nematode feeding structures. A TIR receptor like protein member was induced in the susceptible interaction only, making this a putative susceptibility factor. The RNA data is deposited at ArrayExpress with the number E-MTAB-5215.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.