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Tominello-Ramirez, C.

Publications and source records attributed to Tominello-Ramirez, C..

4 recordsLinked to original sources

Alternaria atra from distinct ecological roles share functional genomic repertoires

Fungi, particularly ascomycetes, exhibit diverse ecological lifestyles, including endophytism, pathogenicity, and saprotrophy. Species of the genus Alternaria are taxonomically and ecologically diverse, yet the genomic determinants underlying different lifestyles remain poorly understood. Here, we investigate lifestyle-associated genomic variation in Alternaria atra using two newly collected isolates obtained as plant endophytes. We confirm their taxonomic identity and generate draft genome assemblies for both isolates. We assess their phenotypic behaviour under laboratory conditions and examine their genomic features alongside those of a previously published A. atra isolate described as pathogenic. Despite differing isolation histories, the endophytic and pathogenic isolates exhibit similar behaviour under laboratory conditions and possess highly comparable genomic repertoires, including predicted effector proteins, carbohydrate-active enzymes, and biosynthetic gene clusters. We detect no clear genomic signatures distinguishing endophytic and pathogenic origins or lifestyles. These findings suggest that A. atra harbours a shared genomic repertoire compatible with multiple ecological strategies, supporting a model of lifestyle plasticity rather than fixed genomic specialization. Our results add to growing evidence that genome content alone does not reliably predict ecological roles in ascomycete fungi.

genomics↗

Co-optation of Transcription Factors Drives Evolution of Quantitative Disease Resistance Against a Necrotrophic Pathogen.

Wild relatives of crop species possess diverse levels of quantitative disease resistance (QDR) to biotic stresses, yet the genomic and regulatory mechanisms underlying these differences are poorly understood. In particular, how QDR against a generalist necrotrophic pathogen evolved and whether it is driven by conserved or species-specific regulatory networks remains unclear. Here, we examined the transcriptomic responses of five diverse wild tomato species that span a gradient of QDR. We initially hypothesised that conserved regulatory modules might control QDR. Instead, we use differential gene expression analysis and weighted gene co-expression network analysis (WGCNA) to find that species-specific regulatory features, encompassing both infection-induced and constitutively expressed genes, predominantly shape QDR levels. Although we identified an ethylene response factor among candidate genes for QDR-regulation, it did not fully account for the phenotypic variation. To further dissect the evolutionary basis of these regulatory patterns, we performed phylotranscriptomic analyses on gene regulatory networks. Notably, our findings reveal that the conserved NAC transcription factor 29 is pivotal in developing disease resistance only in S. pennellii. The differential regulation and altered downstream signalling pathways of NAC29 provide evidence for its co-option in the resistance mechanisms of S. pennellii. This finding highlights the species-specific rewiring of gene regulatory networks by repurposing a conserved regulatory element to enhance resistance against pathogens effectively. These results offer new insights into the evolutionary and regulatory complexity underlying QDR and emphasise the significance of species-specific gene regulation in shaping resistance against a cosmopolitan necrotrophic pathogen.

plant biology↗

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↗

Network analyses reveal D clade ethylene response factors as major regulators of jasmonic acid-mediated resistance to early blight disease complex in tomato

Resistance mechanisms to early blight disease complex (EBDC) in tomato remain obscure given its polygenic and quantitative nature. We investigated the early defense responses of Heinz 1706 tomato to EBDC using RNA-seq. We observed distinct transcriptional reprofiling upon exposure to two EBDC isolates and the PAMP chitin. Avirulent isolate CS046 (Alternaria alternata) elicited a vigorous defense response in the host, whilst the virulent isolate 1117-1 (Alternaria sect. Porri) showed subdued gene expression, suggesting a suppression of defense responses during compatible pathogenesis. We emphasize the specific roles of ETHYLENE RESPONSE FACTORs (ERFs) in defense against EBDC, with a particular focus on the D clade ERFs. Co-expression network analysis revealed the principal genes in early defense responses to EBDC are secondary metabolite biosynthesis genes, transcription factors, and hormone response genes. We constructed a gene regulatory network and predicted novel hub genes as putative global regulators of the defense response, including the D clade ERFs, WRKY, and NAC transcription factors. Our work highlights the failure of virulent EBDC pathogenesis to elicit hormone responses that suppress cell death. Additionally, we found a selective induction for specific ERFs that strongly influence the topology of the EBDC defense transcriptional network.

plant biology↗