Significance: Members of the AT-HOOK MOTIF CONTAINING NUCLEAR LOCALIZED ( AHL ) family are involved in various plant biological processes. Our findings reveal a molecular model whereby the AHLs interact with each other via the plant and prokaryote conserved (PPC)/domain of unknown function #296 (DUF296) domain to form homo-/hetero-complexes, possibly trimers. The AHL complex also interacts with other nuclear proteins to form a macromolecular complex that modulates plant growth and development. The coordinated action of AHLs requires an AT-hook motif capable of binding AT-rich DNA, as well as a PPC/DUF296 domain containing a conserved six-amino-acid region. Our proposed model provides a better understanding of the roles of AHL genes in regulating plant growth and development, which may in turn lead to better seedling establishment and increased yield.

Plant pathogens degrade cell wall through secreted polygalacturonases (PGs) during infection. Plants counteract the PGs by producing PG-inhibiting proteins (PGIPs) for protection, reversibly binding fungal PGs, and mitigating their hydrolytic activities. To date, how fungal pathogens specifically overcome PGIP inhibition is unknown. Here, we report an effector, Sclerotinia sclerotiorum PGIP-INactivating Effector 1 (SsPINE1), which directly interacts with and functionally inactivates PGIP. S. sclerotiorum is a necrotrophic fungus that causes stem rot diseases on more than 600 plant species with tissue maceration being the most prominent symptom. SsPINE1 enhances S. sclerotiorum necrotrophic virulence by specifically interacting with host PGIPs to negate their polygalacturonase-inhibiting function via enhanced dissociation of PGIPs from PGs. Targeted deletion of SsPINE1 reduces the fungal virulence. Ectopic expression of SsPINE1 in plant reduces its resistance against S. sclerotiorum. Functional and genomic analyses reveal a conserved virulence mechanism of cognate PINE1 proteins in broad host range necrotrophic fungal pathogens.

The Arabidopsis thaliana hypocotyl is a robust system for studying the interplay of light and plant hormones, such as brassinosteroids (BRs), in the regulation of plant growth and development. Since BRs cannot be transported between plant tissues, their cellular levels must be appropriate for given developmental fates. BR homeostasis is maintained in part by transcriptional feedback-regulation loops that control the expression of key metabolic enzymes, including the BR-inactivation enzymes CYP734A1/CYP72B1/BAS1 and CYP72C1/SOB7. In this research, the NAC transcription factor (TF), ATAF2, is found to bind the promoters of BAS1 and SOB7 to suppress their expression. ATAF2 restricts the tissue-specific expression of BAS1 and SOB7 in planta. ATAF2 loss- and gain-of-function seedlings have opposite BR response phenotypes for hypocotyl elongation. ATAF2 modulates hypocotyl growth in a light-dependent manner, with the photoreceptor phytochrome A playing a major role. The photomorphogenic phenotypes of ATAF2 loss- and gain-of-function seedlings can be suppressed by treatment with the BR biosynthesis inhibitor brassinazole (BRZ). Moreover, the disruption of BAS1 and SOB7 abolishes the short-hypocotyl phenotype of ATAF2 loss-of-function seedlings in low-fluence-rate white light, which demonstrates an ATAF2-mediated connection between BR catabolism and photomorphogenesis. The expression of ATAF2 is suppressed by both BRs and light, which demonstrates the existence of an ATAF2-BAS1/SOB7-BR-ATAF2 feedback-regulation loop as well as a light-ATAF2-BAS1/SOB7-BR-photomorphogenesis pathway. ATAF2 also modulates root growth by regulating BR catabolism. Since ATAF2 was known to regulate plant defense and auxin biosynthesis, this TF acts as a central regulator of plant defense, hormone metabolism, and light-mediated seedling development.