To overcome pathogen infection, plants deploy a highly efficient innate immune system, which often uses hydrogen peroxide (H₂O₂), a versatile reactive oxygen species, to activate downstream defense responses. H₂O₂ is a potential substrate of aquaporins (AQPs), the membrane channels that facilitate the transport of small compounds across plasma membranes or organelle membranes. To date, however, the functional relationship between AQPs and H₂O₂ in plant immunity is largely undissected. Here, we report that the rice (Oryza sativa) AQP OsPIP2;2 transports pathogen-induced apoplastic H₂O₂ into the cytoplasm to intensify rice resistance against various pathogens. OsPIP2;2-transported H₂O₂ is required for microbial molecular pattern flg22 to activate the MAPK cascade and to induce the downstream defense responses. In response to flg22, OsPIP2;2 is phosphorylated at the serine residue S125, and therefore gains the ability to transport H₂O₂. Phosphorylated OsPIP2;2 also triggers the translocation of OsmaMYB, a membrane-anchored MYB transcription factor, into the plant cell nucleus to impart flg22-induced defense responses against pathogen infection. On the contrary, if OsPIP2;2 is not phosphorylated, OsmaMYB remains associated with the plasma membrane, and plant defense responses are no longer induced. These results suggest that OsPIP2;2 positively regulates plant innate immunity by mediating H₂O₂ transport into the plant cell and mediating the translocation of OsmaMYB from plasma membrane to nucleus.

EDS1 (Enhanced Disease Susceptibility 1) plays a crucial role in both effector‐triggered immunity activation and plant basal defence. However, whether pathogen effectors can target EDS1 or an EDS1‐related pathway to manipulate immunity is rarely reported. In this study, we identified a Phytophthora capsici Avirulence Homolog (Avh) RxLR (Arg‐any amino acid‐Leu‐Arg) effector PcAvh103 that interacts with EDS1. We demonstrated that PcAvh103 can facilitate P. capsici infection and is required for pathogen virulence. Furthermore, genetic evidence showed that PcAvh103 contributes to virulence through targeting EDS1. Finally, PcAvh103 specifically interacts with the lipase domain of EDS1 and can promote the disassociation of EDS1–PAD4 (Phytoalexin Deficient 4) complex in planta. Together, our results revealed that the P. capsici RxLR effector PcAvh103 targets host EDS1 to suppress plant immunity, probably through disrupting the EDS1–PAD4 immune signalling pathway.

The plant signaling pathway that regulates pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) involves mitogen-activated protein kinase (MAPK) cascades that comprise sequential activation of several protein kinases and the ensuing phosphorylation of MAPKs, which activate transcription factors (TFs) to promote downstream defense responses. To identify plant TFs that regulate MAPKs, we investigated TF-defective mutants of Arabidopsis thaliana and identified MYB44 as an essential constituent of the PTI pathway. MYB44 confers resistance against the bacterial pathogen Pseudomonas syringae by cooperating with MPK3 and MPK6. Under PAMP treatment, MYB44 binds to the promoters of MPK3 and MPK6 to activate their expression, leading to phosphorylation of MPK3 and MPK6 proteins. In turn, phosphorylated MPK3 and MPK6 phosphorylate MYB44 in a functionally redundant manner, thus enabling MYB44 to activate MPK3 and MPK6 expression and further activate downstream defense responses. Activation of defense responses has also been attributed to activation of EIN2 transcription by MYB44, which has previously been shown to affect PAMP recognition and PTI development. AtMYB44 thus functions as an integral component of the PTI pathway by connecting transcriptional and posttranscriptional regulation of the MPK3/6 cascade.