Furthermore, low levels of aldicarb suppress the movement and growth defects of these mutants

a new pathotype into U.S. pathogen populations has resulted in a loss of this resistance. While minimal knowledge of the genetic variation within Ps. cubensis exists – specifically related to virulence, pathogenicity, and host specificity among physiological races – the genetic basis of these processes, and the underlying mechanism associated with infection have not been elucidated. To date, analyses of the Ps. cubensis-C. sativus interaction have been limited to the identification of the LY341495 aforementioned physiological races, and have largely focused on the utilization of variation in host specificity for the identification and classification of pathotypes. To this end, six physiological pathotypes, or races, have been identified within populations in the U.S., Israel, and Japan, as well as additional races throughout Europe. In the U.S., increased disease pressure on cucumber production since 2004 is hypothesized to be the result of the introduction of a new, more virulent pathotype, capable of overcoming the downy mildew resistance gene dm-1, that has been 21164513 widely incorporated into commercial cucumber varieties since the 1940’s. While genetic analyses such as Amplified Fragment Length Polymorphism have been used to differentiate these physiological races and some effort has been made to refine the species within Pseudoperonospora, there is limited information available about pathogenicity or 23692283 virulence genes in Ps. cubensis or the moleculargenetic basis of resistance to this pathogen in the cucurbits. 1 mRNA-seq Analysis of Cucurbit Downy Mildew Recent work generated the first sequence assembly of the Ps. cubensis genome and subsequent in silico analysis has identified candidate effector proteins that may have either virulence or avirulence roles in Ps. cubensis infection. Structurally, oomycete effector proteins display a modular organization, consisting of a N-terminal signal peptide, a conserved RXLR translocation motif, followed by a variable C-terminal effector domain. In short, it is the function and activity of the variable C-terminal effector domain that drives the activity of these molecules. A set of 61 candidate effectors were identified in the first draft of the Ps. cubensis genome and included a large class of variants with sequence similarity to the canonical RXLR motif. Specifically, the function of a QXLR-containing effector, designated PcQNE, was characterized and shown to be a member of a large family of Ps. cubensis QXLR nuclear-localized effectors, which was up-regulated during infection of cucumber. Additionally, internalization of PcQNE into the host cell was shown to require the QXLR-EER motif, thereby establishing a basic functional homology with the well-characterized Phytophthora spp. effector proteins. While this work serves as a substantial development in understanding the genetic basis for pathogenicity in Ps. cubensis, additional work is needed to identify and characterize additional effectors and other proteins involved in establishment of infection and pathogen proliferation. The accessibility of oomycete pathogen genome sequences, combined with gene expression data from both pathogen and host throughout the course of infection, can serve as a basis for identification and curation of genes that may have important roles in both virulence and avirulence. To date, oomycete RXLR effectors have been demonstrated to suppress basal host resistance, as well as to activate effector-triggered immunity . In addition