bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.07.28.667131

New resistance to bacterial wilt in heat-stressed tomato is revealed by two-reference Genome Wide Association

Abstract

Bacterial wilt, caused by bacterial strains of the Ralstonia solanacearum species complex, is one of the most harmful diseases striking many crops including tomato. Its spread is dependent upon temperature and humidity, which are expected to fluctuate strongly due to climate change. Previous results have highlighted that temperature elevation led to an increase in disease severity in commercial cultivars, whose resistance is quantitative and mostly relies on the Quantitative Trait Loci (QTL) bwr-6 and bwr-12. In this study, we focused on temperature-dependent quantitative disease resistance (QDR) to bacterial wilt with the aim to unravel new resistance mechanisms that remain efficient at higher temperatures. For this purpose, a new panel of 189 accessions composed of tomato wild relatives, was assembled and sequenced thus creating a unique genomic resource. Its response to the Ralstonia pseudosolanacearum strain GMI1000 from three- to ten-days post-inoculation at 28{degrees}C and 32{degrees}C was explored. To discover the genetic basis underlying the responses of the panel, Genome-Wide Association (GWA) studies were conducted using the disease symptom scores recorded daily and monitored throughout the kinetics of the infection. To improve QTL detection, we have proposed a new approach using two reference genomes from within the panel. By correcting part of a single reference genome, especially when the only reference genome is a cultivar, this approach may be considered an alternative to pangenomic studies. As panel sequencing was highly resolutive, QTL positions allowed the identification of 44 candidate genes, which seemed to follow a temporal dynamic of activation after pathogen inoculation. Interestingly, no candidate genes were found to be common between the two phenotyping temperatures, highlighting the importance of the experimental design in addressing this type of question. Most of our quantitative disease resistance candidate genes belong to gene families described as being involved in immunity. Moreover, a significant proportion appears to be expressed in roots where bacterial infection occurs. Among them, two candidates are closely linked to the genomic positions of the bwr-6 and bwr-12 QTLs, the main QTLs of bacterial wilt Quantitative Disease Resistance (QDR) studied whose mechanisms of action are still unknown. Author summaryBacterial wilt is a plant disease that affects more than 200 crop species (including tomato, potato and banana) leading to high yield losses. The most efficient way to deal with this disease is still the use of genetic resistance. However, previous studies have shown that numerous sources of resistance are negatively affected when plants face heat stress, which is alarming in a context of global warming. In this study, we have developed a new approach for discovering candidate genes in tomato capable of conferring thermostable resistance to bacterial wilt. Forty-four genes were sequentially detected over time, reflecting different temporal dynamics of induction after inoculation. Even if none were found to be common between the two temperatures, available information on their transcriptional regulation in roots and their involvement in immune processes confirms their relevance. Finally, we provide a short list of the candidate genes identified, some of which are currently undergoing functional validation and will be used in breeding programs to help overcome epidemics in future years.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Belny, A., Desaint, H., Rigal, M., Carrere, S., Gouzy, J., Bonnet, G., Labourey, C., Albert, E., Grivet, L., Roux, F., Vailleau, F., Mary-Huard, T., Berthome, R.. 2025-07-31. New resistance to bacterial wilt in heat-stressed tomato is revealed by two-reference Genome Wide Association. https://doi.org/10.1101/2025.07.28.667131

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Pangenome Discoveries from Clinical Long-Read Genomes in Underrepresented Populations with Neurodevelopmental Disorders

Genetic diagnoses remain elusive for many individuals with neurodevelopmental disorders (NDDs), and the gap is wider in populations poorly represented in genomic reference resources. To demonstrate the equitable advantage of long-read whole genome sequencing (LR-WGS) and pangenomes in terms of clinical utility, we analyzed 211 NDD cases and 107 unaffected relatives from 24 populations, integrating their assemblies, resulting in a total of 1204 haplotypes with the Human Pangenome Reference Consortium Release 2 (HPRC_r2) and the Arab Pangenome Reference (APR) datasets. Clinical interpretation of small variants and structural variants (SVs) revealed pathogenic or likely pathogenic findings in 38.9% of the cases (82/211), and our workflow further detected pathogenic repeat expansions in 3.8% of the cases and runs of homozygosity (ROHs) exceeding 300 Mb in 4.7% of the cases, revealing substantial autozygosity suggestive of strong inbreeding. Beyond these clinical assessments, pangenome analysis revealed 3.9 million population-level novel small variants, 39,782 SVs and an average of 2.17 Mb of novel sequence per individual absent from linear references and global pangenomes. We identified 85.9 kb of case-unique nonreference sequences in exonic segments overlapping with curated NDD gene sets. Graph-based tertiary analysis further identified rare exonic complex homozygous rearrangements in the NDD associated genes for 2.4% of the cases. Together, these findings emphasize how diverse genome assemblies extend variant discovery beyond established linear reference-based clinical interpretation.

genetics↗

Integrated exome-transcriptome analysis of a schizophrenia case with an exceptionally low polygenic risk score

Schizophrenia liability reflects both common polygenic variation and rarer variants of larger effect. We investigated a post-mortem schizophrenia case (SZ07) with a schizophrenia polygenic risk score below the first percentile among ancestry-matched cases, asking whether individual-level genomic and transcriptomic analyses could help identify potentially novel schizophrenia-relevant variants. We used exome analysis with multiple variant-prediction tools to generate a panel of variants and corresponding candidate genes potentially implicated in the pathological process in SZ07. The prioritised variants were then assessed using RNA sequencing of three cortical regions. Of these, only an IZUMO4 splice-acceptor variant showed direct RNA-level support. Beyond variant-specific analyses, we characterised broader transcriptomic abnormalities in the SZ07 brain. Pathway analysis of gene-level expression deviations implicated innate immune processes, calcium signalling, synaptic biology, and axon remodelling. Notably, compared with conventional single-sample biological pathway analysis, the analysis we used showed only a weak association with neuronal specificity, suggesting their reduced sensitivity to the main axis of variation related to cellular composition in bulk brain tissue gene expression data. Although the candidate genes showed no significant pathway-level convergence, the broader transcriptomic profile revealed coherent biological alterations largely compatible with the documented history of cerebrovascular disease in SZ07. These results demonstrate how the integration of exome and transcriptome data at the individual level enables the formulation and constraint of hypotheses regarding patient-specific genetic features and their molecular consequences, while highlighting important limitations related to tissue composition, comorbidity, and the choice of reference cohort.

genetics↗

A genetic screen to identify host factors required for commensal bacterial adherence to the gut epithelia

Bacterial adherence to gut epithelial cells likely involves host genetic components. We isolated a gut commensal bacterium, Lelliottia jeotgali, that can robustly colonize C. elegans through attachment to intestinal epithelial cells. Here, we developed a novel screen in C. elegans to identify host genes required for microbiome bacterial colonization. Using transgenic L. jeotgali strain expressing tdTomato, we conducted forward genetic screens in C. elegans to select for mutants that completely lost colonization. We identified multiple allelic mutations in five different C. elegans genes, termed knockout of Lelliottia adherence (kola) mutants, with a near complete loss of adherence. Each of kola-1-5 is uncharacterized and predicted to encode for a secreted or membrane-bound protein. We also identified gly-5, a GalNAc transferase that initiates O-linked glycosylation. Overall, we describe the first C. elegans screen to identify host factors that control microbiome bacterial colonization in the gut.

genetics↗