Ontology highlight
ABSTRACT:
PROVIDER: PRJNA866153 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Worldwide, 20-25% of all harvested fruit and vegetables are lost annually in the field and throughout the postharvest supply handling chain due to spoilage by fungal pathogens. Most impactful postharvest pathogens exhibit necrotrophic lifestyles, resulting in rotting of the host tissues and complete loss of marketable commodities. Necrotrophic fungi can readily infect ripe fruit leading to the rapid establishment of disease symptoms. However, these pathogens generally fail to infect unripe fruit, or remain quiescent until host and environmental conditions stimulate a successful infection. Current research on necrotrophic infections of fruit was mainly focused on the host by characterizing genetic and physicochemical factors that inhibit or promote the disease. However, the pathogenicity and virulence strategies employed by necrotrophic pathogens in ripe and unripe fruit are mostly understudied. Here, we provide a first comparative transcriptomics study of fungal postharvest pathogens: Botrytis cinerea, Rhizopus stolonifer and Fusarium acuminatum, all of which display necrotrophic behavior when infecting fruit. We de novo assembled and annotated the transcriptomes of R. stolonifer, and F. acuminatum and performed a differential gene expression analysis comparing the three fungal transcriptomes during fruit infection with that of fungal in-vitro growth. Analysis of the differentially expressed genes for enrichment of functional annotations revealed shared strategies of the three fungi during infection of compatible (ripe fruit) and incompatible (unripe fruit) hosts. We furthermore selected candidate genes that are involved in these strategies to characterize their expression during infection of unripe and ripe-like fruit of the non-ripening (nor) tomato mutant, both of which are physiologically and biochemically similar to unripe wildtype fruit. By enabling a better understanding of fungal necrotrophic infection strategies, we move closer to generating accurate models of fruit diseases and development of early detection tools and effective management strategies.
2018-12-01 | GSE122555 | GEO
Project description:Postharvest fungal pathogens benefit from the increased host susceptibility that occurs during fruit ripening. In unripe fruit, pathogens often remain quiescent and unable to cause disease until ripening begins, emerging at this point into destructive necrotrophic lifestyles that quickly result in fruit decay. Here, we demonstrate that one such pathogen, Botrytis cinerea, actively induces ripening processes in order to facilitate infections and promote disease. Assessments of ripening progression revealed that B. cinerea accelerated external coloration, ethylene production, and softening in unripe fruit, while mRNA sequencing of inoculated unripe fruit confirmed the corresponding upregulation of host genes involved in ripening processes, such as ethylene biosynthesis and cell wall degradation. Furthermore, ELISA-based glycomics profiling of fruit cell wall polysaccharides revealed remarkable similarities in the cell wall polysaccharide changes caused by both infections of unripe fruit and ripening of healthy fruit, particularly in the increased accessibility of pectin polysaccharides. Virulence and additional ripening assessment experiments with B. cinerea knockout mutants showed that induction of ripening is dependent on the ability to infect the host and break down pectin. The B. cinerea double knockout Δbcpg1Δbcpg2 lacking two critical pectin degrading enzymes was found to be incapable of emerging from quiescence even long after the fruit had ripened at its own pace, suggesting that the failure to accelerate ripening severely inhibits fungal survival on unripe fruit. These findings demonstrate that active induction of ripening in unripe tomato fruit is an important infection strategy for B. cinerea.
2022-01-01 | GSE183836 | GEO
Project description:The increased susceptibility of ripe fruit to fungal pathogens poses a substantial threat to crop production and marketability. Here, we coupled transcriptomic analyses with mutant studies to uncover critical genes and processes governing ripening-associated susceptibility in tomato (Solanum lycopersicum) fruit. Using wild-type unripe and ripe fruit inoculated with three fungal pathogens—Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer—we identified common pathogen response genes reliant on chitinases, WRKY transcription factors, and reactive oxygen species detoxification. Interestingly, susceptible ripe fruit demonstrated a more extensive defense response than resistant unripe fruit, indicating that the magnitude and diversity of defense response does not significantly impact the interaction. To tease apart individual features of ripening that may be responsible for susceptibility, we utilized three tomato non-ripening mutants: Cnr, rin and nor. Fruit from these mutants displayed different patterns of susceptibility to fungal infection. Functional analysis of the genes altered during ripening in the susceptible genotypes revealed losses in the maintenance of cellular redox homeostasis. Moreover, jasmonic acid accumulation and signaling coincided with the activation of defenses in resistant fruit. Lastly, based on high gene expression in susceptible fruit, we identified and tested two candidate susceptibility factors, pectate lyase (PL) and polygalacturonase (PG2a). CRISPR-based knockouts of PL, but not PG2a, resulted in more than 50% decrease in the susceptibility of ripe fruit, demonstrating that PL is a major susceptibility factor. Ultimately, this study demonstrates that targeting specific genes that drive susceptibility is a viable strategy to improve resistance of tomato fruit against fungal pathogens.
2020-04-08 | GSE148217 | GEO
Project description:Members of the fungal genus Armillaria are necrotrophic pathogens with efficient plant biomass-degrading strategies. Armillaria species are some of the largest terrestrial organisms on Earth that cause tremendous losses in diverse ecosystems. Despite their global importance, how Armillaria evolved pathogenicity in a clade of dominantly non-pathogenic wood-degraders (Agaricales) remains elusive. Here, using new genomic data, we show that Armillaria species, in addition to widespread gene duplications and de novo gene origins, acquired at least 1,025 genes via 124 horizontal gene transfer (HGT) events, primarily from Ascomycota donors. Functional and expression data suggest that HGT might have affected plant biomass-degrading and virulence abilities of Armillaria, two pivotal traits in their lifestyle. HGT provides an explanation for their soft-rot like biomass degrading strategy, which is which is markedly different from the primarily white rot decay mechanism of related species. Combined multi-species expression data revealed extensive regulation of horizontally acquired and wood-decay related genes, putative virulence factors as well as novel conserved pathogenicity-induced small secreted proteins (PiSSPs), two of which were experimentally verified to induce necrosis in live plants. Overall, this study details how evolution knitted together horizontally and vertically inherited genes in complex adaptive traits, such as plant biomass degradation and pathogenicity in one of the most influential fungal pathogens of temperate forest ecosystems.
2023-06-20 | GSE233220 | GEO
Project description:Members of the fungal genus Armillaria are necrotrophic pathogens with efficient plant biomass-degrading strategies. Armillaria species are some of the largest terrestrial organisms on Earth that cause tremendous losses in diverse ecosystems. Despite their global importance, how Armillaria evolved pathogenicity in a clade of dominantly non-pathogenic wood-degraders (Agaricales) remains elusive. Here, using new genomic data, we show that Armillaria species, in addition to widespread gene duplications and de novo gene origins, appear to have acquired at least 1025 genes via 124 horizontal gene transfer (HGT) events, primarily from Ascomycota donors. Functional and expression data suggest that HGT might have affected plant biomass-degrading and virulence abilities of Armillaria, two pivotal traits in their lifestyle. HGT provides an explanation for their soft-rot like biomass degrading strategy too, which is markedly different from the primarily white rot decay mechanism of related species. Combined multi-species expression data revealed putative virulence factors, extensive regulation of horizontally acquired and wood-decay related genes as well as novel noserved pathogenicity-induced small secreted proteins (PiSSPs). Two PiSSPs induced necrosis in live plants, suggesting they are potential virulence effectors conserved across Armillaria. Overall, this study details how evolution knitted together horizontally and vertically inherited genes in complex adaptive traits, such as plant biomass degradation and pathogenicityin one of the most influential fungal pathogens of temperate forest ecosystems.
2023-06-23 | GSE235457 | GEO
Project description:Members of the fungal genus Armillaria are necrotrophic pathogens with efficient plant biomass-degrading strategies. Armillaria species are some of the largest terrestrial organisms on Earth that cause tremendous losses in diverse ecosystems. Despite their global importance, how Armillaria evolved pathogenicity in a clade of dominantly non-pathogenic wood-degraders (Agaricales) remains elusive. Here, using new genomic data, we show that Armillaria species, in addition to widespread gene duplications and de novo gene origins, appear to have acquired at least 1025 genes via 124 horizontal gene transfer (HGT) events, primarily from Ascomycota donors. Functional and expression data suggest that HGT might have affected plant biomass-degrading and virulence abilities of Armillaria, two pivotal traits in their lifestyle. HGT provides an explanation for their soft-rot like biomass degrading strategy too, which is markedly different from the primarily white rot decay mechanism of related species. Combined multi-species expression data revealed putative virulence factors, extensive regulation of horizontally acquired and wood-decay related genes as well as novel noserved pathogenicity-induced small secreted proteins (PiSSPs). Two PiSSPs induced necrosis in live plants, suggesting they are potential virulence effectors conserved across Armillaria. Overall, this study details how evolution knitted together horizontally and vertically inherited genes in complex adaptive traits, such as plant biomass degradation and pathogenicityin one of the most influential fungal pathogens of temperate forest ecosystems.
2023-06-23 | GSE235456 | GEO
Project description:Members of the fungal genus Armillaria are necrotrophic pathogens with efficient plant biomass-degrading strategies. Armillaria species are some of the largest terrestrial organisms on Earth that cause tremendous losses in diverse ecosystems. Despite their global importance, how Armillaria evolved pathogenicity in a clade of dominantly non-pathogenic wood-degraders (Agaricales) remains elusive. Here, using new genomic data, we show that Armillaria species, in addition to widespread gene duplications and de novo gene origins, appear to have acquired at least 1025 genes via 124 horizontal gene transfer (HGT) events, primarily from Ascomycota donors. Functional and expression data suggest that HGT might have affected plant biomass-degrading and virulence abilities of Armillaria, two pivotal traits in their lifestyle. HGT provides an explanation for their soft-rot like biomass degrading strategy too, which is markedly different from the primarily white rot decay mechanism of related species. Combined multi-species expression data revealed putative virulence factors, extensive regulation of horizontally acquired and wood-decay related genes as well as novel noserved pathogenicity-induced small secreted proteins (PiSSPs). Two PiSSPs induced necrosis in live plants, suggesting they are potential virulence effectors conserved across Armillaria. Overall, this study details how evolution knitted together horizontally and vertically inherited genes in complex adaptive traits, such as plant biomass degradation and pathogenicityin one of the most influential fungal pathogens of temperate forest ecosystems.
2023-06-23 | GSE235454 | GEO
Project description:Soft rot or Rhizopus rot, caused by the fungal pathogen Rhizopus stolonifer, is an aggressive postharvest disease that affects many fruit and vegetables. We proposed that R. stolonifer displays a necrotrophic behavior when infecting fruit, actively killing the host tissues to complete its life cycle. We tested this hypothesis by identifying R. stolonifer infection strategies when interacting with four fruit hosts (tomato, grape, strawberry, and plum). First, we generated a complete and highly contiguous genome assembly for R. stolonifer using PacBio sequencing, of 45.02 Mb in size, an N50 of 2.87Mb, and 12,644 predicted loci with protein-coding genes. We then performed a transcriptomic analysis to identify genes preferentially used by R. stolonifer when growing in fruit versus culture media, and then classified these host-related genes into clusters according to their expression patterns across four time points. Based on the expression data, we determined that R. stolonifer deploys infection mechanisms characteristic of necrotrophs, including a suite of oxidases, proteases, and cell wall degrading enzymes, when it is actively breaking down tissues of all four fruit hosts. Better understanding R. stolonifer – fruit host interactions can support better diagnostic tools and efficient management strategies in postharvest.
2024-11-01 | GSE232735 | GEO
Project description:Tomato fruit ripening is associated with a dramatic increase in susceptibility to the fungal pathogen Botrytis cinerea, the causal agent of gray mold. Mature green fruit, prior to ripening, are largely resistant to B. cinerea, whereas red fruit, at the end of ripening, are susceptible to B. cinerea infection. We used microarrays to detail the gene expression changes that are induced by B. cinerea when tomato fruit at unripe and ripe stages are infected. Keywords: plant responses to pathogens
2009-05-22 | GSE14637 | GEO
Project description:Infections by the fungus Monilinia laxa, the main cause of brown rot in Europe, result in considerable losses of stone fruit. Herein, we present a comprehensive transcriptomic approach to unravel strategies deployed by nectarine fruit and M. laxa during their interaction. We used M. laxa-inoculated immature and mature fruit, which were resistant and susceptible to brown rot, respectively, to perform a dual RNA-seq analysis. In immature fruit, host responses, pathogen biomass, and pathogen transcriptional activity peaked at 14 – 24 hours post inoculation (hpi), at which point M. laxa appeared to switch its transcriptional response to either quiescence or death. Mature fruit experienced an exponential increase in host and pathogen activity beginning at 6 hpi. Functional analyses in both host and pathogen highlighted differences in stage-dependent strategies. For example, in immature fruit, M. laxa unsuccessfully employed carbohydrate-active enzymes (CAZymes) for penetration, which the fruit was able to combat with tightly regulated hormone responses and an oxidative burst that challenged the pathogen’s survival at later time points. In contrast, in mature fruit, M. laxa was more dependent on proteolytic effectors than CAZymes and was able to invest in filamentous growth early during the interaction. Hormone analyses of mature fruit infected with M. laxa indicated that, while jasmonic acid activity was likely useful for defense, high ethylene activity may have promoted susceptibility through induction of ripening processes. Lastly, we identified M. laxa genes that were highly induced in both quiescent and active infections and may serve as targets for control of brown rot.
2020-08-01 | GSE146293 | GEO