Developmentally Regulated Susceptibility of Tomato Fruit to Botrytis cinerea

Ripening is the terminal program of fruit development. The ripening is a collection of outcomes arising from a network of biochemical and physiological pathways, which render fruit attractive to seed dispersing organisms, edible and nutritious for humans, and valuable as agricultural commodities. In addition to these events, ripening is accompanied by a dramatic increase in susceptibility to necrotrophic pathogens, such as Botrytis cinerea ( Botrytis, henceforth). However, only particular aspects of the ripening syndrome are required to promote the susceptibility that accompanies the final stages of fruit development.;Ripening is regulated by multiple interacting, and in some cases, redundant, mechanisms (e.g., transcription factors, small RNAs, hormones) and occurs in an organized and developmentally timed manner (Chapter 1). Understanding how particular ripening-associated events are regulated is critical to distinguish between those that are required for normal ripening and those that are needed for susceptibility. Fruit softening is a ripening process that promotes fruit susceptibility to fungal pathogens (Chapters 2 and 3).;As an opportunistic pathogen, Botrytis modifies its infection strategy according to the ripening stage of the host (Chapters 2 and 5). The diverse and versatile infection mechanisms that Botrytis deploys on fruit help to define processes that the pathogen uses to hasten susceptibility but also demonstrate that Botrytis takes advantage of opportune ripening events that render its host vulnerable to aggressive infections.;Destruction of plant cell walls during infections is required for Botrytis' virulence (Chapters 3 and 4). Botrytis utilizes a large repertoire of enzymes that target multiple components of the cell walls of fruit (Chapter 4). Botrytis also induces the expression of fruit genes coding for endogenous cell wall degrading proteins to enhance, perhaps even initiate, the deconstruction of the fruit tissues (Chapter 5). The main objective of this PhD dissertation was to identify biological pathways that modulate susceptibility of tomato fruit to Botrytis using systems biology approaches. This was accomplished by: 1. Determining the patterns of expression of genes involved in plant hormone biosynthesis and signaling to infer the potential roles of stress hormones in tomato fruit-Botrytis interactions (Chapter 2). 2. Transcriptional profiling of Botrytis genes targeting plant cell walls during infections of different hosts to distinguish Botrytis cell wall degrading functions that are specific during fruit infections or are common among infections of different plant tissues. (Chapter 4). 3. Transcriptional profiling of genes of unripe and ripe tomato fruit in response to Botrytis infections to identify candidate tomato and Botrytis genes that are required for susceptibility (Chapter 5). 4. Characterizing the alterations in tomato fruit cell wall (i.e., "glycome") profiles that occur as a consequence of Botrytis infection of fruit and as healthy fruit ripen to detect changes in cell wall polysaccharides that are related to increased susceptibility of fruit (Chapter 5).;The results presented in this PhD. dissertation improve the understanding of the molecular basis of the tomato fruit's ripening-related susceptibility to Botrytis. The conclusions obtained can serve as a framework for the study of other pathosystems (e.g., fruit from other plant species and/or infected by different pathogens) and should help to resolve whether the same or similar mechanisms promote susceptibility in other plant versus pathogen situations. From an applied perspective, the identification of specific ripening events that promote susceptibility may facilitate the development of management strategies for diseases of ripened fruit and may guide breeding efforts to improve the shelf life and post- harvest qualities of fruit.