Abstract
Alternaria alternata f.sp. Lycopersici (AAL) toxin induces programmed cell death (PCD) in susceptible tomato (Solanum lycopersicum) leaves. Jasmonate (JA) promotes AAL toxin induced PCD in a COI1 (coronatine insensitive 1, JA receptor)-dependent manner by enhancement of reactive oxygen species (ROS) production. To further elucidate the underlying mechanisms of this process, we performed a comparative proteomic analysis using tomato jasmonic acid insensitive1 ( jai1), the receptor mutant of JA, and its wild type (WT) after AAL toxin treatment with or without JA treatment. A total of 10367 proteins were identified in tomato leaves using isobaric tags for relative and absolute quantitation (iTRAQ) quantitative proteomics approach. 2670 proteins were determined to be differentially expressed in response to AAL toxin and JA. Comparison between AAL toxin treated jai1 and its WT revealed the COI1-dependent JA pathway regulated proteins, including pathways related to redox response, ceramide synthesis, JA, ethylene (ET), salicylic acid (SA) and abscisic acid (ABA) signaling. Autophagy, PCD and DNA damage related proteins were also identified. Our data suggest that COI1-dependent JA pathway enhances AAL toxin induced PCD through regulating the redox status of the leaves, other phytohormone pathways and/or important PCD components.
Highlights
Fungi usually produce toxins to damage plant tissues, which are classified as host-selective or non-specific
Previous studies have shown that alternata f.sp. Lycopersici (AAL) toxin can inhibit ceramide biosynthetic enzymes and lead to programmed cell death (PCD) in sensitive asc/asc tomato species, due to the reduced sphingolipids and accumulated dihydrosphingosine (DHS) and 3-ketodihydrosphingosine (3-KDHS)[31,32]
Our research explored the potential pathways and regulators in AAL toxin induced PCD and the role of COI1-dependent JA signaling pathway in regulating the PCD process
Summary
Fungi usually produce toxins to damage plant tissues, which are classified as host-selective or non-specific. AAL toxin induced PCD process in Arabidopsis loh[2] mutant (a T-DNA knockout mutant of a homologue of the tomato Asc gene), ET-responsive genes were up-regulated within seven hours, but JA pathway related genes were unchanged, and there was no indication of JA accumulation[12]. Our previous study showed that JA and ET promoted AAL toxin induced cell death alone, and the receptor-dependent JA signaling promotes PCD through enhancing ET biosynthesis. The jai[1] mutant allows us to conduct an extensive study in the role of JA pathway in AAL toxin induced PCD. In Arabidopsis, the responses of the JA signaling mutants jar[1] and fad3/7/8 to O3 have indicated that JA could be an important factor involved in the ROS-dependent lesion propagation[16], it is quite interesting to investigate the relationship between ROS and JA pathway during AAL toxin induced PCD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: 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.
