Plant Communications最新文献

The convergence of high-resolution multi-omics technologies with computational systems biology is transforming plant physiology by enabling predictive, mechanistic, and field-relevant insights into crop performance, adaptation, and resilience. This review presents an integrative and forward-looking synthesis spanning genomics, transcriptomics, proteomics, metabolomics, epigenomics, phenomics, and the rapidly emerging fields of single-cell and spatial omics, highlighting how these complementary layers can be computationally unified to achieve cell-type-resolved and tissue-specific insights into plant function. We discuss integrative analytical frameworks that combine gene regulatory network inference, machine learning, and explainable artificial intelligence (XAI), illustrating how these approaches accelerate the identification of key regulators, improve genotype-environment interaction modeling, and advance multiscale phenotypic prediction. Representative case studies demonstrate how multi-omics integration-ranging from single-cell transcriptomic atlases in Arabidopsis to nitrogen-use-efficiency modeling and omics-guided genome editing in cereals-bridges laboratory-scale discovery with field-level validation. We further propose a translational roadmap that links persistent bottlenecks, including data heterogeneity, limited spatiotemporal resolution, and the underrepresentation of non-model species, with actionable solutions such as FAIR-compliant data infrastructures, high-resolution spatiotemporal omics, hybrid mechanistic artificial intelligence (AI) modeling, and digital twin frameworks. By connecting molecular mechanisms to ecosystem-level performance, this review articulates a coherent vision for predictive, design-driven, and climate-resilient agriculture grounded in systems-level plant biology.

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.

Mitochondrial biogenesis requires the import of more than a thousand proteins encoded by nuclear DNA. The translocase of the outer mitochondrial membrane (TOM) complex serves as the primary gateway for specific recognition of precursor proteins, which are synthesized in the cytosol. Little is known about the regulation of the abundance of the TOM complex. Using forward genetics, we identified key 26S proteasome subunits, including REGULATORY PARTICLE NON-ATPASE1A (RPN1A), that affect the abundance of TOM-complex subunits through the ubiquitin-proteasome pathway. Loss of proteasome function through rpn1a mutation or MG132 treatment increased the abundance of TOM20 isoforms and induced mitochondrial stress marker genes. By contrast, overexpression of ANAC017, an endoplasmic reticulum-anchored transcription factor that activates mitochondrial retrograde signaling under stress, lowered TOM20 abundance and reduced mitochondrial protein import. The rates of mitochondrial protein import and respiratory activity were also altered. Genetic analyses placed the proteasome downstream of ANAC017, since the reduction in TOM20 required the RPN1a subunit. Transcriptome profiling after antimycin A treatment showed broad ANAC017-dependent reprogramming of ubiquitin-proteasome system genes. A second tier formed by ANAC053- and ANAC078-bound promoters of proteasome subunits, including RPN1a, is required to restrain TOM20 accumulation. These findings establish a two-step transcriptional circuit that engages the ubiquitin-proteasome system to tune TOM abundance and coordinate protein import with organelle function.

The phytohormone abscisic acid (ABA) governs plant stress responses through dynamic control of its cellular distribution by ABA transporters, yet the mechanisms controlling ABA transporter activity remain poorly understood. Here, we identify a phosphorylation-dependent regulatory mechanism that modulates cellular ABA levels and root growth responses in Arabidopsis. We show that ABA alters the subcellular distribution of its transporter ATP-binding cassette G16 (ABCG16), which functions as a negative regulator of ABA-induced root growth inhibition. In contrast to ABCG16, the receptor-like kinases BARELY ANY MERISTEM 1 and 2 (BAM1/2) are essential for proper root responses to ABA. BAM1/2 physically interact with ABCG16 and phosphorylate it at threonine 45. Relative intensity analyses and cell-free degradation assays reveal enhanced ABCG16 accumulation in the bam1;+/-bam2 mutant, indicating that ABCG16 protein stability is at least partially dependent on BAM1/2. ABA transport and root growth assays further show that the non-phosphorylated ABCG16 variant promotes ABA efflux and restores ABA-induced root growth inhibition similar to the wild-type protein, whereas the phospho-mimic ABCG16 variant impairs cytosolic ABA efflux and fails to restore root growth under ABA treatment. Consistently, the bam1;+/-bam2 mutant shows constitutively elevated ABA efflux activity compared with wild-type landsberg erecta (Ler), supporting the notion that BAM1/2-mediated phosphorylation dampens ABCG16 transport activity. The abcg16 bam1 and abcg16 bam2 double mutants phenocopy the abcg16 single mutant, showing ABA hypersensitivity in root growth. Together, these findings demonstrate that BAM1/2-mediated phosphorylation of ABCG16 reduces its stability and ABA export activity, thereby maintaining cellular ABA levels required for root growth inhibition.

Despite their ecological and biotechnological importance, the extent to which microalgae are regulated by epigenetic mechanisms has remained poorly understood. In the model industrial microalga Nannochloropsis oceanica, by comprehensive, multi-dimensional epigenomic analyses, this study uncovers an epigenetic regulatory network responsive to CO₂ levels. This network involves intricate interactions among DNA methylation, histone modifications, dynamic nucleosome positioning, and three-dimensional chromatin organization during adaptation to low-CO₂ conditions. Although DNA methylation is minimal, histone modifications-such as lysine acetylation, crotonylation, and methylation-are associated with active chromatin states and linked to 43.1% of differentially expressed genes. Notably, histone H3K4 di-methylation (H3K4me2) displays a distinct dual-peak profile around the transcription start site and is correlated with chromatin compartment dynamics. Knockout of NO24G02310, a putative H3K4 methyltransferase gene, caused genome-wide shifts in H3K4me2 peaks and decreased H3K4me1 levels, accompanied by direct or indirect downregulation of NoHINT and NoPMA2 expression, slower algal growth, and reduced photosynthetic efficiency (indicated by Fv/Fm), specifically under low-CO₂ conditions. Deletion and overexpression of genes encoding the histidine triad nucleotide-binding protein NoHINT and the plasma membrane H⁺-ATPase NoPMA2 confirmed their roles in growth and photosynthetic efficiency under low CO₂; NoHINT influences growth and NoPMA2 affects photosynthesis. As a previously unrecognized low-CO₂ adaptation mechanism, NO24G02310 likely coordinates the regulation of NoHINT and NoPMA2 through H3K4 modifications. These findings provide a foundation for enhancing microalgal productivity through targeted epigenetic engineering.