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Carvalho-Silva, P.

Publications and source records attributed to Carvalho-Silva, P..

2 recordsLinked to original sources

Acclimation to high daily thermal amplitude converts a defense response regulator into susceptibility factor

Acclimation enables plants to adapt to immediate environmental fluctuations, supporting biodiversity and ecosystem services. However, global changes are altering conditions for plant disease outbreaks, increasing the risk of infections by pathogenic fungi and oomycetes, and often undermining plant immune responses. Understanding the molecular basis of plant acclimation is crucial for predicting climate change impacts on ecosystems and improving crop resilience. Here, we investigated how Arabidopsis thaliana quantitative immune responses acclimates to daily temperature fluctuations. We analyzed responses to the fungal pathogen Sclerotinia sclerotiorum following three acclimation regimes that reflect the distribution areas of both species. Mediterranean acclimation, characterized by broad diurnal temperature amplitudes, resulted in a loss of disease resistance in three natural A. thaliana accessions. Global gene expression analyses revealed that acclimation altered nearly half of the pathogen-responsive genes, many of which were down-regulated by inoculation and associated with disease susceptibility. Phenotypic analysis of A. thaliana mutants identified novel components of quantitative disease resistance following temperate acclimation. Several of these mutants were however more resistant than wild type following Mediterranean acclimation. Notably, mutant lines in the NAC42-like transcription factor did not show a loss of resistance under Mediterranean acclimation. This resistance was linked to an acclimation-mediated switch in the repertoire of NAC42-like targets differentially regulated by inoculation. These findings reveal the rewiring of immune gene regulatory networks by acclimation and suggest new strategies to maintain plant immune function in a warming climate.

plant biology↗

"Out of sight, out of mind". The antagonistic role of the transcriptional memory associated with repeated acoustic stimuli on the priming of plant defense.

BackgroundPriming plant immunity offers a powerful and sustainable strategy for crop protection, enabling plants to respond faster and more efficiently to threats. This increased readiness is driven by transcriptional memory--molecular mechanisms that store and recall stress responses, including protein accumulation, transcription factor activity, and epigenetic modifications. However, the interplay among transcriptional stress memory, its stability, and its broader impact on plant resistance remain poorly understood. ResultsHere, we reveal a tight link between transcriptional memory and defense priming in Arabidopsis thaliana exposed to repeated acoustic stimulations. Using a combination of experiments and computational modeling, we show that enhanced resistance to Sclerotinia sclerotiorum after three stimulations arises from three key mechanisms: (1) preemptive activation of defense pathways in noninoculated plants, (2) increased diversification of defense-related genes, and (3) gene priming. This heightened defense state is sustained by transcriptional stress memory across thousands of genes, which is likely orchestrated by transcription factor cascades. Challenging the conventional view that priming involves stepwise activation of distinct pathways, our findings suggest that priming instead results from the simultaneous modulation of a broad spectrum of defense pathways. This built-in redundancy enhances resilience, shielding primed plants from the genetic variability-driven resistance loss observed in naive plants. However, this same redundancy imposes strict limits on further enhancing the resistance. More frequent acoustic stimulations did not amplify the protective effect, and transcriptional memory faded within 1.5 days after stimulation ceased. ConclusionsBy integrating experimental and computational approaches, we present a genome-scale quantitative model of stress-induced gene regulation. Our results highlight the trade-offs inherent in transcriptional memory-driven priming, revealing both its potential and its limitations in optimizing plant immunity.

plant biology↗