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Latest Research from The Plant Cell
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The miR167-ARF8 Module Integrates HSFA1-HSFA2 and RVE4/8-ERF53/54 Transcriptional Cascades to Enhance Plant Thermotolerance
AbstractHeat stress (HS) is a major environmental factor limiting plant survival and crop productivity, prompting the evolution of adaptive responses driven by transcriptional reprogramming coordinated by Class A1 HS TRANSCRIPTION FACTORS (HSFA1s). Here, we demonstrate that the miR167–AUXIN RESPONSE FACTOR 8 (ARF8) module functions as a central regulatory hub, enhancing thermotolerance by integrating both HSFA1-dependent and HSFA1-independent signaling cascades. Under HS, the expression of ARF6 and ARF8 is repressed, while miR167 is induced. Disruption of ARF6/ARF8 or overexpression of miR167 significantly improves heat tolerance, whereas ARF8 overexpression increases HS sensitivity. ARF8 directly binds to the promoters of HSFA1 genes and heat shock protein (HSP) genes, repressing their transcription and thereby impairing the heat-responsive gene network. In addition, ARF8 physically interacts with HSFA1 proteins, further inhibiting their transactivation activity post-translationally. Notably, ARF8 also regulates HSFA2, a major amplifier of the HS response, through both HSFA1-dependent and HSFA1-independent mechanisms. Genetic evidence supports a model in which the HSFA1–HSFA2 axis functions downstream of the miR167–ARF8 module, but contributes only partially to the overall thermotolerance phenotype. Beyond the HSFA1–HSFA2 pathway, ARF8 also suppresses the RVE4/8–ERF53/54 transcriptional cascade, a circadian-regulated, HSFA1-independent module that promotes thermotolerance. This dual regulation allows ARF8 to fine-tune HS adaptation through integration of both canonical and noncanonical signaling routes. Together, these findings establish the miR167–ARF8 module as a central integrator of HS response pathways. This work not only reveals new mechanistic complexity in plant heat response networks but also identifies a conserved regulatory node with promising potential for genetic improvement of heat-resilient crops.Read moreSource: The Plant Cell Advance Publication Date: 2026-09-25
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The epigenetics of color swatches: histone deacetylation regulates green coloration in Chrysanthemum
Source: The Plant Cell Advance Publication Date: 2026-09-24
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When Fungi Knock, Nitrilases Unlock the Auxin Arsenal
Source: The Plant Cell Advance Publication Date: 2026-09-22
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Branching out or bearing fruit: how MADS-box transcription factors orchestrate maize ovule development
Source: The Plant Cell Advance Publication Date: 2026-09-22
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Timing it right: Dephosphorylation of a key transcription factor constrains the tapetal transcriptional cascade for timely pollen development
Source: The Plant Cell Advance Publication Date: 2026-09-22
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Single-cell epigenomics in plants
AbstractSingle-cell technologies enable epigenomics characterization at single-cell resolution, offering novel insights into gene expression regulation and a wide range of biological processes, including cell fate determination, developmental differentiation, and environmental adaptation. In recent years, plant single-cell epigenomics has witnessed rapid progress, empowering the construction of cell type–specific chromatin accessibility atlases, the identification of candidate cis-regulatory elements (CREs), the inference of gene regulatory networks, and the elucidation of regulatory mechanisms underlying plant development, stress responses, species evolution, and complex agronomic traits. Nevertheless, single-cell methodologies for profiling histone modifications, DNA methylation, three-dimensional genome organization, and spatial epigenomic states in plants are still in their infancy. In this review, we systematically elaborate the technological framework, bioinformatic workflows, key research advances, and existing challenges in the field of plant single-cell epigenomics, and highlight future perspectives for its in-depth development.Read moreSource: The Plant Cell Advance Publication Date: 2026-09-22
New ASPB journal Plant Direct

