Shahab Uddin, Kris John Silvano, Rupak Chakraborty, Donah Mary Macoy, Gyeong Ryul Ryu, Rakhimov Abdurakhim Ramazon Ugli, Gyeongik Ahn, Hamad Khan, Joon-Yung Cha, Woe-Yeon Kim, Min Gab Kim
Homozygous genetic background is more favorable for epidemic outbreak in a short period of time in comparison with the population of multiple genetic background. Since this complex genetic background disturbs the infectious cycle of the pathogen. So that a variety or a hybrid which developed from multiple parental lines are notable for their durable resistance than the monogenic resistance variety.
TEX1 contributes to mRNA export and SA-mediated defense while modulating ABA-driven susceptibility, linking RNA processing to immune regulation in Arabidopsis TEX1, a subunit of the multi-protein THO/TREX complex conserved in eukaryotes, facilitates the synthesis, splicing, and nuclear-cytoplasmic export of mRNAs. However, its mechanism in plants remains to be thoroughly established, particularly its contribution to plant immunity and the mRNA export mechanism in response to pathogen challenges. Here, we showed that TEX1 contributes to mRNA export and hormonal signaling during pathogen infection. The TEX1 mutant was impaired in plant resistance to the Pseudomonas syringae pv. tomato DC3000 and exhibited a compromised salicylic acid (SA) accumulation and reduced expression of SA-regulated genes. Moreover, we show that the pattern-triggered immunity (PTI) response was compromised in the tex1-4 mutant, as it contributes to a reduced defense phenotype upon flg22, leading to reduced flg22-induced defense responses. TEX1 also positively regulates effector-triggered immunity (ETI) against Pto carrying AvrRpm1 and AvrRpt2. Epistasis analysis revealed that TEX1-mediated resistance is SA-dependent. The tex1-4 mutant accumulated elevated abscisic acid (ABA) levels and increased ABA-mediated susceptibility, accompanied by enhanced ABA biosynthesis and reduced expression of catabolic genes. Analysis with sid2-2 further indicated that ABA-induced susceptibility depends on SA signaling, supporting SA-ABA antagonism. Furthermore, the tex1-4 mutation exhibited defective bulk nuclear mRNA export to the cytoplasm upon pathogen infection, as observed by in situ hybridization using 48-mer fluorescein-labeled oligo(dT) probe. Thus, our findings suggest that mRNA export is a crucial component of plant immune activation, with TEX1 serving as a contributing factor that mechanistically links mRNA export with hormone-regulated immune signaling to promote effective plant defense.