Biology subjects

Barbacci, A.

Publications and source records attributed to Barbacci, A..

6 recordsLinked to original sources

bioRxiv2024

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↗

bioRxiv2024

High-resolution disease phenotyping reveals distinct resistance strategies of wild tomato crop wild relatives against Sclerotinia sclerotiorum

Besides the well-understood qualitative disease resistance, plants possess a more complex quantitative form of resistance: quantitative disease resistance (QDR). QDR is commonly defined as a partial but more durable form of resistance and, therefore, might display a valuable target for resistance breeding. The characterization of QDR phenotypes, especially of wild crop relatives, displays a major bottleneck in deciphering QDRs genomic and regulatory background. Moreover, the relationship between QDR parameters, such as infection frequency, lag phase duration, and lesion growth rate, remains elusive. High hurdles for applying modern phenotyping technology, such as the low availability of phenotyping facilities or complex data analysis, further dampen progress in understanding QDR. Here, we applied a low-cost phenotyping system to measure lesion growth dynamics of wild tomato species (e.g., S. pennellii or S. pimpinellifolium). We provide insight into QDR diversity of wild populations and derive specific QDR strategies and their crosstalk. We show how temporally continuous observations are required to dissect end-point severity into functional resistance strategies. The results of our study show how QDR can be maintained by facilitating different defense strategies during host-parasite interaction and that the capacity of the QDR toolbox highly depends on the hosts genetic context. We anticipate that the present findings display a valuable resource for more targeted functional characterization of the processes involved in QDR. Moreover, we show how modest phenotyping technology can be leveraged to help answer highly relevant biological questions.

plant biology↗

bioRxiv2024

"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↗

bioRxiv2021

Pathogen-derived mechanical cues regulate the spatio-temporal implementation of plant defense

How immune responses are activated and regulated is a central question in immunology. In addition to molecular signaling, recent work has shown that physical forces regulate the immune response of vertebrates by modifying transmembrane protein conformation and cell contact. Mechanical stress and strain produced by forces constitute physical cues perceived by cells instructing gene expression. Whether mechanical cues generated by pathogens during host colonization can trigger adaptive responses in plant cells remains elusive. We found that local and progressive variations of plant cell wall tension caused by fungal pathogen attacks are transmitted to neighboring healthy tissue around the infection site and trigger immunity in distal cells. This thigmoimmunity process requires the reorganization of cortical microtubules and contributes strongly to Arabidopsis disease resistance. One-Sentence SummaryActivation of plants immunity depends on fluctuations of mechanical tension caused by a fungal pathogen.

plant biology↗

bioRxiv2018

Rapid identification of an Arabidopsis NLR gene conferring susceptibility to Sclerotinia sclerotiorum using time-resolved automated phenotyping

The broad host range necrotrophic fungus Sclerotinia sclerotiorum is a devastating pathogen of many oil and vegetable crops. Plant genes conferring complete resistance against S. sclerotiorum have not been reported. Instead, plant populations challenged by S. sclerotiorum exhibit a continuum of partial resistance designated as quantitative disease resistance (QDR). Because of their complex interplay and their small phenotypic effect, the functional characterization of QDR genes remains limited. How broad host range necrotrophic fungi manipulate plant programmed cell death is for instance largely unknown. Here, we designed a time-resolved automated disease phenotyping pipeline and assessed the kinetics of disease symptoms caused by seven S. sclerotiorum isolates on six A. thaliana natural accessions with unprecedented resolution. We hypothesized that large effect polymorphisms common to the most resistant A. thaliana accessions, but absent from the most susceptible ones, would point towards disease susceptibility genes. This identified highly divergent alleles of the nucleotide-binding site leucine-rich repeat gene LAZ5 in the resistant accessions Rubenzhnoe and Lip-0. Two LAZ5-deficient mutant lines in the Col-0 genetic background showed enhanced QDR to S. sclerotiorum, whereas plants mutated in the closely related CSA1 gene responded like the wild type. These findings illustrate the value of time-resolved image-based phenotyping for unravelling the genetic bases of complex traits such as QDR. Our results suggest that S. sclerotiorum manipulates plant sphingolipid pathways guarded by LAZ5 to trigger programmed cell death and cause disease.

plant biology↗

bioRxiv2017

Shifts in diversification rates and host jump frequencies shaped the diversity of host range among Sclerotiniaceae fungal plant pathogens

The range of hosts that a parasite can infect in nature is a trait determined by its own evolutionary history and that of its potential hosts. However, knowledge on host range diversity and evolution at the family level is often lacking. Here, we investigate host range variation and diversification trends within the Sclerotiniaceae, a family of Ascomycete fungi. Using a phylogenetic framework, we associate diversification rates, the frequency of host jump events, and host range variation during the evolution of this family. Variations in diversification rate during the evolution of the Sclerotiniaceae define three major macro-evolutionary regimes with contrasted proportions of species infecting a broad range of hosts. Host-parasite co-phylogenetic analyses pointed towards parasite radiation on distant hosts long after host speciation (host jump or duplication events) as the dominant mode of association with plants in the Sclerotiniaceae. The intermediate macro-evolutionary regime showed a low diversification rate, high frequency of duplication events, and the highest proportion of broad host range species. Consistent with previous reports on oomycete parasites, our findings suggest that host jump and radiation, possibly combined with low speciation rates, could associate with the emergence of generalist pathogens. These results have important implications for our understanding of fungal parasites evolution and are of particular relevance for the durable management of disease epidemics.

evolutionary biology↗