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Adaptation of necrotrophic infection strategies by Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer as a function of tomato fruit ripening

ABSTRACT: Adaptation of necrotrophic infection strategies by Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer as a function of tomato fruit ripening

PROVIDER: PRJNA505650 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8191350.fastq.gz	Fastqsanger.gz
	SRR8191360.fastq.gz	Fastqsanger.gz
	SRR8191370.fastq.gz	Fastqsanger.gz
	SRR8191380.fastq.gz	Fastqsanger.gz
	SRR8191390.fastq.gz	Fastqsanger.gz

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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.

Project description:Worldwide, 20-25% of all harvested fruit and vegetables are lost annually in the field and throughout the postharvest supply chain due to rotting by fungal pathogens. Most postharvest pathogens exhibit necrotrophic or saprotrophic lifestyles, resulting in decomposition of the host tissues and 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 conditions stimulate a successful infection. Previous research on infections of fruit has mainly been focused on the host's genetic and physicochemical factors that inhibit or promote disease. Here, we investigated if fruit pathogens can modify their own infection strategies in response to the ripening stage of the host. To test this hypothesis, we profiled global gene expression of three fungal pathogens that display necrotrophic behavior-Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer-during interactions with unripe and ripe tomato fruit. We assembled and functionally annotated the transcriptomes of F. acuminatum and R. stolonifer as no genomic resources were available. Then, we conducted differential gene expression analysis to compare each pathogen during inoculations versus in vitro conditions. Through characterizing patterns of overrepresented pathogenicity and virulence functions (e.g., phytotoxin production, cell wall degradation, and proteolysis) among the differentially expressed genes, we were able to determine shared strategies among the three fungi during infections of compatible (ripe) and incompatible (unripe) fruit tissues. Though each pathogen's strategy differed in the details, interactions with unripe fruit were commonly characterized by an emphasis on the degradation of cell wall components, particularly pectin, while colonization of ripe fruit featured more heavily redox processes, proteolysis, metabolism of simple sugars, and chitin biosynthesis. Furthermore, we determined that the three fungi were unable to infect fruit from the non-ripening (nor) tomato mutant, confirming that to cause disease, these pathogens require the host tissues to undergo specific ripening processes. By enabling a better understanding of fungal necrotrophic infection strategies, we move closer to generating accurate models of fruit diseases and the development of early detection tools and effective management strategies.

Dataset Information

Adaptation of necrotrophic infection strategies by Botrytis cinerea, Fusarium acuminatum, and Rhizopus stolonifer as a function of tomato fruit ripening

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