Phosphorylation of an ethylene response factor by MPK3/MPK6 mediates negative feedback regulation of pathogen-induced ethylene biosynthesis in Arabidopsis

Plants under pathogen attack produce high levels of the gaseous phytohormone ethylene to induce plant defense responses via the ethylene signaling pathway.The 1-aminocyclopropane-1-carboxylate synthase(ACS)is a critical rate-limiting enzyme of ethylene biosynthesis.Transcriptional and post-translational upregulation of ACS2 and ACS6 by the mitogen-activated protein kinases MPK3 and MPK6 are previously shown to be crucial for pathogen-induced ethylene biosynthesis in Arabidopsis.Here,we report that the fungal pathogen Botrytis cinerea-induced ethylene biosynthesis in Arabidopsis is under the negative feedback regulation by ethylene signaling pathway.The ethylene response factor ERF1 A is further found to act downstream of ethylene signaling to negatively regulate the B.cinerea-induced ethylene biosynthesis via indirectly suppressing the expression of ACS2 and ACS6.Interestingly,ERF1 A is shown to also upregulate defensin genes directly and therefore promote Arabidopsis resistance to B.cinerea.Furthermore,ERF1 A is identified to be a substrate of MPK3 and MPK6,which phosphoactivate ERF1 A to enhance its functions in suppressing ethylene biosynthesis and inducing defensin gene expression.Taken together,our data reveal that ERF1 A and its phosphorylation by MPK3/MPK6 not only mediate the negativefeedback regulation of the B.cinerea-induced ethylene biosynthesis,but also upregulate defensin gene expression to increase Arabidopsis resistance to B.cinerea.

Abscisic Acid Antagonizes Ethylene Production through the ABI4-Mediated Transcriptional Repression of ACS4 and ACS8 in Arabidopsis

Increasing evidence has revealed that abscisic acid （ABA） negatively modulates ethylene biosynthesis, although the underlying mechanism remains unclear. To identify the factors involved, we conducted a screen for ABA-insensitive mutants with altered ethylene production in Arabidopsis. A dominant allele of ABI4, abi4-152, which produces a putative protein with a 16-amino-acid truncation at the C-terminus of ABI4, reduces ethylene production. By contrast, two recessive knockout alleles of ABI4, abi4-102 and abi4-103, result in increased ethylene evolution, indicating that ABI4 negatively regulates ethylene produc- tion. Further analyses showed that expression of the ethylene biosynthesis genes ACS4, ACSS, and AC02 was significantly decreased in abi4-152 but increased in the knockout mutants, with partial dependence on ABA. Chromatin immunoprecipitation-quantitative PCR assays showed that ABI4 directly binds the pro- moters of these ethylene biosynthesis genes and that ABA enhances this interaction. A fusion protein containing the truncated ABI4-152 peptide accumulated to higher levels than its full-length counterpart in transgenic plants, suggesting that ABI4 is destabilized by its C terminus. Therefore, our results demon- strate that ABA negatively regulates ethylene production through ABI4-mediated transcriptional repression of the ethylene biosynthesis genes ACS4 and ACS8 in Arabidopsis.

Dual and opposing roles of EIN3 reveal a generation conflict during seed growth

Seed size critically affects grain yield of crops and hence represents a key breeding target.The develop-ment of embryo-nourishing endosperm is a key driver of seed expansion.We here report unexpected dual roles of the transcription factor EIN3 in regulating seed size.These EIN3 functions have remained largely undiscovered because they oppose each other.Capitalizing on the analysis of multiple ethylene biosynthesis mutants,we demonstrate that EIN3 represses endosperm and seed development in a pathway regulated by ethylene.We,in addition,provide evidence that EIN3-mediated synergid nucleus disintegration promotes endosperm expansion.Interestingly,synergid nucleus disintegration is not affected in various ethylene biosynthesis mutants,suggesting that this promoting function of EIN3 is inde-pendent of ethylene.Whereas the growth-inhibitory ethylene-dependent EIN3 action appears to be encoded by sporophytic tissue,the growth-promoting role of EIN3 is induced by fertilization,revealing a generation conflict that converges toward the key signaling component EIN3.