HCS Colloquium: Double-Header!
Abstract: Grape and wine industries in colder regions such as Ohio have been expanding rapidly and demand for premium wine grapes has also increased. However, several popular cultivars are sensitive to freezing temperatures below -20°C. The objectives of this study are to: 1) evaluate freezing tolerance of wine grape cultivars new to Ohio, and 2) improve freezing tolerance of sensitive cultivars using exogenous ABA. Freezing tolerance (or LT50) of more than 20 cultivars will be evaluated between September and April in two locations for two seasons. In the ABA study, we will evaluate the effect of exogenous ABA on freezing tolerance of two cold sensitive cultivars, Vitis vinifera ‘Chardonnay’ and ‘Pinot gris’. Expected results are the existence of differences of LT50 among cultivars. Also, optimum timing of ABA application that leads to maximum freezing tolerance will be identified. Ultimately, the findings of this project are valuable to grape producers in Ohio and other cold regions.
Activation of the plant immune system by a potential pathogen elicits multiple signal transduction pathways leading to defense responses, including gene expression changes, changes in plant hormone levels, and cell wall fortification at the infection site. The signaling pathways comprise a robust signaling network that is resistant to suppression by pathogen-derived virulence factors. Successful pathogens utilize multiple virulence factors, including toxins and effector proteins, to target multiple pathways and thus overcome the network. Pseudomonas syrinagae pv. tomato (Pto) is a hemibiotrophic pathogen on tomato that causes bacterial speck on the leaf and fruit. Pto also induces disease symptoms in Arabidopsis thaliana. Coronatine is a Pseudomonas toxin that structurally and functionally mimics jasmonic acid (JA) and suppresses salicylic acid (SA) signaling important for defense response against biotrophic and hemibiotrophic pathogens. The type III effectors AvrE1and HopM1 make redundant contribution to suppressing plant defense, including suppression of SA-signaling and incorporation of callose into cell wall fortification. Our previous work showed that COR and HopM1 suppress callose deposition independent of inhibiting SA-signaling. COR was also shown to suppress the accumulation of an indoleglucosinolate (IG) that is downstream of ethylene (Et) signaling and required for callose deposition. Since one moiety of COR structurally mimics ACC, the precursor of Et, and several works have shown that COR perturbs Et homeostasis and other outputs of Et-signaling, we will examine if COR targets Et signaling by directly looking at COR’s effect on Et responses. We will also examine where in the network COR and the type III effectors target defense responses in plants with mutations disrupting one or more defense signaling pathways following challenge with Pto mutants of COR, HopM1, and/or AvrE1.