Figure 4: A putative model showing possible mechanisms of JA regulated AAL toxin response in Solanum Lycopersicum.

The DE proteins caused by JA treatment and COI1 mutation during AAL toxin induced PCD were used to construct the model, and the impairment of COI1 induced protein changes were presented with the contrary change patterns. The identified proteins were assigned to different organelles or groups according to their subcellular localization and molecular functions. Up-regulated proteins are highlighted red and down-regulated proteins are colored green. Arrows and bars represent positive and negative regulation respectively. Red solid lines indicate that the pathways are up-regulated or promoted by JA during TA response, green solid lines with bars or arrows indicate that the pathways are down-regulated by JA during TA response, black solid lines with arrows links the proteins within the same pathway. TA induce PCD by inhibiting the synthesis of ceramide and inducing the overproduction of ROS, COI1-dependent JA pathway may promote this PCD progress by influencing the ROS production and scavenging, other hormone signaling pathways or some possible PCD regulators such as caspase-like proteins, autophagy and DNA repair related proteins. AAO, L-ascorbic acid oxidase; ABI1, ABA insensitive1; ACO1, 1-aminocyclopropane-1-carboxylate oxidase homolog 1-like; AHA, plasma membrane H⁺-ATPase; AOS, allene oxide synthase; ATG11, autophagy related protein 11; CHS, chalcone synthase; CPI, cysteine protease inhibitor; Cyt, Cytochrome; DAP-AT, probable n-succinyldiaminopimelate aminotransferase-like; DDB, DNA damage binding proteins; DDR, DNA damage response; DRA, DNA repair ATPase-related family protein; ER, endoplasmic reticulum; GST, glutathione S-transferase; Golgi, golgi complex; KTI1, kunitz trypsin inhibitor; MMR, DNA mismatch repair; NAT, nucleobase-ascorbate transporter 6-like; Prx, Peroxiredoxin; RNase E, Ribonuclase 2-Like; SBTs, subtilisin-like proteases; TF, transcription factor.