Plant Communications最新文献

Optimization of plant architecture requires precise regulation of internode elongation; however, the post-translational mechanisms that integrate microRNA and phytohormone signaling remain poorly understood. Here, we describe a hierarchical miR164e-NAC32-DELLA regulatory network that controls stem development in maize. Genetic analyses demonstrate that ZmmiR164e negatively regulates its target gene ZmNAC32, with ZmmiR164e overexpression enhancing internode cell elongation and loss-of-function resulting in dwarfism. Notably, ZmNAC32 physically interacts with and stabilizes the DELLA protein ZmD8, as evidenced by increased ZmD8 protein levels in ZmNAC32-overexpressing plants compared with the wild type. Transcriptome profiling reveals that ZmNAC32-mediated regulation of plant height occurs primarily through post-translational stabilization rather than extensive transcriptional reprogramming, with downstream cell wall biosynthesis genes (EXP, XTH, and LAC) showing GA-responsive suppression. Structural analyses further reveal that ZmNAC32 binding stabilizes ZmD8 by shielding the key interaction residue K399, thereby suppressing its degradation. Together, these results identify a miRNA-NAC-DELLA module that governs post-translational protein stability during stem development and provides strategic targets for precision breeding of plant architecture.

Plant roots have evolved adaptive strategies mediated by transcriptional networks to cope with fluctuating nitrogen (N) forms and availability. However, the mechanisms linking root-foraging responses to N use efficiency (NUE) in crops remain poorly understood. Here, we show that rice exhibits enhanced root elongation under nitrate compared with ammonium, particularly under low N supply, suggesting a specific regulatory role for nitrate in root morphogenesis. We identify the transcription factor OsMADS61 as a key regulator of nitrate-dependent root morphological and physiological responses, as well as NUE, especially under N-limited conditions. OsMADS61 acts as a transcriptional activator of nitrate metabolism by directly binding to OsNRT2.1 and OsNR2 promoters. Nitric oxide produced via the nitrate reductase pathway, under the control of nitrate-responsive OsMADS61, precisely triggers cell proliferation in the root meristem. Moreover, single-nucleotide polymorphisms in the OsMADS61 promoter may be associated with differential root-foraging responses to nitrate availability. Therefore, enhancing N-adaptive root responses to optimize N uptake and assimilation represents a promising strategy for breeding crops with high NUE.

The infection cycle of Magnaporthe oryzae (M. oryzae) in rice typically involves initial invasion through penetration of the leaf epidermis, followed by expansion into neighboring cells. However, few studies have identified single genes that mediate defense against both invasion and expansion. In this study, we demonstrate that OsWRKY47 positively regulates resistance to both stages of M. oryzae infection. Mechanistic analyses indicate that OsWRKY47 transcriptionally activates OsMYB30 during the early stage, thereby enhancing lignin accumulation and strengthening physical barriers against fungal invasion. At later stages, OsWRKY47 represses OsWRKY39 expression, thereby inhibiting M. oryzae expansion. Knockout of OsWRKY39 leads to increased accumulation of stevioside, a metabolite that activates plant immune responses, representing a chemical defense strategy. Structure-function analyses further reveal that a region comprising amino acids 282-288 of OsWRKY47 is crucial for the positive regulation of OsMYB30, whereas the region comprising amino acids 303-333 is essential for repression of OsWRKY39. Collectively, these findings reveal an OsWRKY47-OsMYB30/OsWRKY39 regulatory module that confers resistance to M. oryzae by coordinating physical and chemical defenses to restrict pathogen invasion and expansion. Such coordinated activation of physical and chemical defenses may represent a widespread strategy in plant pathogen responses.

Maintaining a low sodium (Na⁺) concentration in shoots is a key determinant of salt tolerance in cereal crops. This process is largely mediated by Na⁺ transporters such as HKT1;5, which controls long-distance Na⁺ transport; however, the molecular mechanisms governing the transcriptional regulation of HKT1;5 under salt stress remain poorly understood. Here, we identify the rice transcription factor OsNAC10 and characterize its role as a transcriptional repressor of the high-affinity K⁺ transporter gene OsHKT1;5 under salt stress. OsNAC10 expression is predominantly root-localized and is rapidly downregulated in response to salt treatment. OsNAC10 knockout mutants exhibit enhanced salt tolerance, reduced shoot Na⁺ accumulation, and decreased root-to-shoot Na⁺ transport, whereas overexpression lines show increased Na⁺ accumulation and pronounced salt sensitivity. Subcellular localization and molecular interaction analyses reveal that OsNAC10 is a nuclear-localized transcription factor that directly and competitively binds to an ACGTA-core cis element within the OsHKT1;5 promoter. Consequently, OsHKT1;5 expression is markedly upregulated in nac10 mutants under salt stress. Genetic analysis further demonstrates that the enhanced salt tolerance of the nac10 mutant depends on OsHKT1;5, as the nac10hkt1;5 double mutant exhibits a salt-sensitive phenotype comparable to that of the hkt1;5 single mutant. Importantly, under saline soil conditions, OsNAC10 knockout lines maintain significantly higher grain yield than wild-type plants. Together, these findings uncover a novel transcriptional regulatory mechanism in which OsNAC10 negatively modulates rice salt tolerance by competitively inhibiting OsHKT1;5 expression, highlighting OsNAC10 as a promising target for breeding salt-tolerant crops.

Legumes engage in nitrogen-fixing symbiosis with rhizobia, in which host legumes supply dicarboxylates as a carbon source to rhizobia, while rhizobia reciprocate by providing ammonium to the host plants. Beyond this classical model, accumulating evidence suggests that amino acid exchange is also essential for legume-rhizobium symbiosis. However, it remains unclear whether amino acid transporters are present on the symbiosome membrane (SM) to mediate amino acid exchange during symbiotic nitrogen fixation (SNF). In this study, we identified three amino acid transporters in Medicago truncatula-MtCAT1a, MtCAT1b, and MtCAT1c-which belong to a clade of the plant Cationic Amino acid Transporter (CAT) family known to transport a wide range of amino acids. Notably, MtCAT1b and MtCAT1c are predominantly expressed in infected nodule cells and localize to the SM. Genetic analyses further demonstrate that both MtCAT1b and MtCAT1c are required for amino acid exchange at the SM, with additional evidence indicating that bacteroid metabolism is disturbed in the mutants. Transport assays show that both MtCAT1b and MtCAT1c exhibit broad substrate specificity. Collectively, these findings identify MtCAT1b and MtCAT1c as key mediators of cross-kingdom amino acid exchange, which is essential for maintaining efficient SNF in root nodules.