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Wounding activates HSFA1 to promote cellular reprogramming in Arabidopsis

ABSTRACT: Mechanical injury is a primary trigger for cellular reprogramming during organ regeneration, yet the transcriptional mechanisms that link wounding to reprogramming remain poorly understood. In this study we identify the HEAT SHOCK FACTOR A1 (HSFA1) class of transcription factors, key regulators of the heat stress response, as a central player in wound-induced callus formation and shoot regeneration in Arabidopsis. Loss of HSFA1 function in the hsfa1abd triple mutants severely impairs cellular reprogramming, reducing callus formation from wounded hypocotyls and shoot regeneration from explants. Conversely, overexpression of a gain-of-function HSFA1d variant markedly enhances regeneration. Time-series RNA-seq and ChIP-seq analyses revealed that HSFA1 directly activates key reprogramming regulators, WOUND-INDUCED DEDIFFERENTIATION 1 (WIND1), PLETHORA 3 (PLT3) and ZINC FINGER OF ARABIDOPSIS THALIANA 6 (ZAT6). Furthermore, we demonstrate that the HSFA1d activity is attenuated by SIZ1-mediated SUMOylation, linking post-translational modification to the regulation of wound responses. Our findings establish HSFA1 as an early transcriptional hub that integrates wound signals to activate a broad gene network that drives cellular reprogramming, thereby providing a mechanistic framework for understanding how stress-responsive transcription factors control regeneration.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE306295 | GEO | 2026/04/22

REPOSITORIES: GEO

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Project description:Short periods of heat (>37°C) are extremely damaging to non-acclimated plants and their capacity to acclimate to and recover from heat stress is a key parameter for their survival and longevity. To acclimate, the Heat Shock transcription Factor A1 (HSFA1) subfamily activates a transcriptional response that resolves the heat stress-induced protein damage. Importantly, HSFA1 activity is also critical for Arabidopsis to withstand sustained warmer periods of 28°C, a non-detrimental condition that triggers a thermomorphogenesis response. We find that SUMO, a protein modification whose adduct levels increase as a result of acute heat stress in eukaryotes, is also critical for plant longevity during warmer periods, in particular for shoot meristem development. The known E3 and E4 SUMO ligases (SIZ1, HPY1/MMS21, PIAL1/2) were not essential to endure these warmer periods, alone or in combination. Thermo-lethality was also not seen when plants lacked certain SUMO proteases (ESD4, OTS1/OTS2, SPF1/SPF2 combined) or when SUMO chain formation was blocked. Furthermore, SUMO thermo-resilience is not connected to the autoimmune phenotype found in the corresponding SUMO knockdown and a SIZ1 loss-of-function mutant. As acquired thermotolerance was normal in the SUMO knockdown mutant, we thus conclude that the role of SUMO in heat acclimation differs from that of HSFA1 and SIZ1. Combined, this study reveals that SUMO appears to be critical for shoot meristem integrity during warmer periods. This experiment we have examined how gene expression is affected in two SUMO mutants (siz1-2; sumo1 amiR-SUMO1 [aka. sumo1/2KD] ), and a HsfA1a,b,d triple mutant, when the plants are placed at 28C constant ambient temperature, which is a condition normally used to induce thermomorphogenesis. We used as control the pad1-4 background, as the siz1-2 and sumo1/2KD mutants normally suffer from constitutive defence signalling due hyperaccumulation of SA, which is suppressed by introgression of pad4 in these backgrounds.

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Wounding activates HSFA1 to promote cellular reprogramming in Arabidopsis

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