Gan Ai

Nonhost resistance (NHR) represents a durable phenomenon where plants resist nonadapted pathogens. While NHR holds substantial potential for engineering crops with broad-spectrum and durable resistance, its underlying molecular mechanism remains incompletely understood. The oomycete pathogen Phytophthora capsici is nonadapted to Nicotiana tabacum (Nt) but is virulent on the closely related Nicotiana benthamiana (Nb). Here, we demonstrated that both species encode the NLR Swordholder (Swh), which recognizes P. capsici AvrNt effector proteins. NtSwh restores NHR in ntswh mutants, whereas NbSwh confers only partial resistance. Mechanistically, NtSwh exhibits weaker autoinhibition mediated by its amino-terminal extension domains, enabling rapid immune signaling that prevent pathogen effector–mediated suppression; NbSwh’s stronger autoinhibition delays activation, permitting effector suppression. Heterologous expression of NtSwh in tomato enhances field resistance to P. capsici without yield penalty. These findings indicate that the kinetics of NLR can play a key role in defining NHR, in addition to the presence or absence of specific NLRs, providing insights into strategies for breeding durable crop immunity.

Clade A protein phosphatase 2Cs (PP2C-As) play crucial roles in plant stress responses. Although the ABA receptors PYLs inhibit PP2C-As in an ABA-dependent manner, other modulators of these phosphatases remain largely unknown. Here, we identify the FORKED-LIKE 7 (FL7) protein as a broad PP2C-A interactor that effectively suppresses PP2C activity through an ABA-independent, noncompetitive mechanism. By inhibiting PP2C-A activity, FL7 positively regulates osmotic tolerance and plant immunity in an ABA-independent manner. The N-terminal auxin canalisation (AC) domain of FL7 is required for its PP2C-As inhibitory activity. Further evolutionary analyses reveal that FL7 homologues containing an AC domain belong to an ancient family that emerged in a common ancestor of Klebsormidiophyceae algae and land plants. Genetic analyses indicate that algal FL7 homologues have a conserved function as PP2C-A inhibitors. Our study reveals an ABA-independent layer of PP2C-A modulation that regulates biotic and abiotic stress responses, which is likely conserved across a billion years of streptophyte evolution and predated the PYL-ABA regulation established in the common ancestor of land plants.

Nucleotide-binding leucine-rich repeat (NLR) proteins assemble into genetically linked pairs to mediate effector-triggered immunity (ETI) in plants. Here, we characterize the paired NLRs NRCX and NARY (NRCX adjacent resistance gene Y) in Nicotiana benthamiana. CRISPR/Cas9 knockout of NRCX caused severe dwarfism and constitutively activated immunity, marked by PR1 upregulation and enhanced resistance to Phytophthora capsici. Co-silencing or double knockout of the adjacent NLR NARY partially rescued the nrcx phenotype, revealing NARY as a compensatory regulator that modulates growth and immunity. Structural analysis revealed that NARY harbors non-canonical Walker B and MHD motifs, which lack autoactivation capacity despite their divergence from canonical NLR executors. Split-luciferase and co-immunoprecipitation assays showed that NRCX and NARY interact exclusively through their CC domains, forming a non-canonical regulatory complex. Notably, simultaneous silencing of NRC2/3 and NARY incompletely restored growth in nrcx mutants, implicating additional factors in immune modulation. Our findings establish NARY as a compensatory NLR partner of NRCX that fine-tunes immunity without triggering cell death, revealing a novel mechanism for balancing growth and defense in Solanaceae.

Plant diseases cause dramatic economic loss, posing a major challenge to modern agriculture. Plant pathogenic organisms secret effectors that utilize fascinating and intricate stratagems to facilitate infection. The consequences of plant-pathogen interactions are largely determined by effectors. The effector research has made great strides since its inception in the 1990s and the importance of effectors is increasingly noticed. Molecular investigation of effectors has provided critical insights into how plant pathogens manipulate their hosts to cause diseases. Thus far, numerous excellent reviews concerning effectors have focused on their targeting host pathways, recognition by host receptors, and evasion mechanisms, but few have ever summarized all known effector action modes. Here, we distinguish ten different stratagems of effector function from all types of pathogens, including damage, inhibition, hijacking, promotion, subversion, mimicry, reprogramming, evasion, decoying, and adaption. Furthermore, we discuss examples of these ten stratagems, refine the effector definition, and propose future directions of phytopathogenic effector research.

Background: The APETALA2 (AP2) transcription factor (TF) superfamily, one of the largest gene families in plants, plays an essential role in regulating plant growth and their stress responses. However, the role of AP2 in rice under pesticide stress remains unclear. To investigate the characteristics and functions of the rice AP2 gene family under pesticide stress, the expression of 105 AP2-coding genes and 26 AP2 differentially expressed genes (DEGs) were identified in mesotrione (MTR)-treated rice transcriptome datasets. Results: Three subfamilies of the AP2 gene family (AP2/ERF, RAV, and soloists) were identified using sequence alignment and phylogenetic analysis. Chromosome location analysis revealed that the 26 rice AP2 DEGs were unevenly distributed on 10 of the 12 rice chromosomes, and segmental duplication contributed to the expansion of Oryza sativa AP2 (OsAP2) gene family. Collinearity analyses demonstrated that rice AP2 genes displayed 16 orthologous gene pairs, and 12 and 26 orthologous gene pairs were shared of Arabidopsis and soybean, respectively. In addition, rice AP2 genes featured various gene structures, cis-elements, motif compositions, and conserved domains that allowed them to encode genes that elicit biotic and abiotic stress responses. An analysis of docking between MTR and six AP2 DEGs revealed amino acid residues involved in MTR binding. Quantitative reverse transcription–polymerase chain reaction verified that several AP2 genes were preferentially expressed during MTR-induced stress. The roles of OsAP2 proteins in MTR metabolism were further supported by protein–protein interaction network analysis, which illustrated how these proteins interact with target proteins. Conclusion: The initial findings of this study define the features of the OsAP2 superfamily and offer important tools for functional analyses of OsAP2 genes implicated in the metabolism of MTR. Graphical