Abstract
Salicylic acid (SA) and jasmonic acid (JA) are essential plant immune hormones, which could induce plant resistance to multiple pathogens. However, whether common components are employed by both SA and JA to induce defense is largely unknown. In this study, we found that the enhanced disease susceptibility 8 (EDS8) mutant was compromised in plant defenses to hemibiotrophic pathogen Pseudomonas syringae pv. maculicola ES4326 and necrotrophic pathogen Botrytis cinerea, and was deficient in plant responses to both SA and JA. The EDS8 was identified to be THO1, which encodes a subunit of the THO/TREX complex, by using mapping-by-sequencing. To check whether the EDS8 itself or the THO/TREX complex mediates SA and JA signaling, the mutant of another subunit of the THO/TREX complex, THO3, was tested. THO3 mutation reduced both SA and JA induced defenses, indicating that the THO/TREX complex is critical for plant responses to these two hormones. We further proved that the THO/TREX interacting protein SERRATE, a factor regulating alternative splicing (AS), was involved in plant responses to SA and JA. Thus, the AS events in the eds8 mutant after SA or JA treatment were determined, and we found that the SA and JA induced different alternative splicing events were majorly modulated by EDS8. In summary, our study proves that the THO/TREX complex active in AS is involved in both SA and JA induced plant defenses.
Highlights
Plants, as sessile organisms, have developed a multilayer immune system to cope with environmental pathogens
Previous studies suggest that both salicylic acid (SA) and jasmonic acid (JA) could induce plant resistance to multiple pathogens [16,41,42,43,44], while little is known about the common factors used by these two hormones
We found that enhanced disease susceptibility 8 (EDS8) mediated the plant response to both SA and JA
Summary
As sessile organisms, have developed a multilayer immune system to cope with environmental pathogens. JA isoleucine (JA-Ile), the active form of JA, is accumulated during pathogen infection and is perceived by its receptor coronatine insensitive 1 (COI1), which interacts with and promotes the degradation of jasmonate zim domain (JAZ) proteins to release the MYC transcription factors to trigger the expression of JA responsive genes, such as plant defensin 1.2 (PDF1.2) [9,10] As both SA and JA regulate plant immunity, their crosstalk has been widely studied. Whether common components or different players are recruited by SA and JA to induce defense is largely unknown To answer this question, we searched the published reports to check if mutants that may compromise in both SA and JA signaling could be identified, and the enhanced disease susceptibility 8 (EDS8) mutant aroused our interest.
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