Department of Plant Pathology

Powdery mildew is one of the most significant diseases affecting grape (Vitis vinifera) production around the world. The disease is caused by the hyaline ascomycete, Erysiphe necator, a pathogen capable of rapid proliferation under optimal environmental conditions. Disease onset begins in the spring with the release of ascospores from over-wintering chasmothecia (Gubler and Hirschfelt 1992). Once initial colonies are established, the fungus can asexually propagate via large numbers of conidia that disperse and re-infect additional leaves and developing fruits. Powdery mildew effects on the host include reduction in berry mass, potential cracking of berries, and increased susceptibility to berry rots (Gubler and Hirschfelt 1992, Calonnec et al. 2004, Gadoury et al. 2007). Economically, the disease may be damaging to California’s grape industry because of lost yield, a shortened shelf life for table grapes, and alterations in wine flavor (Gubler and Hirschfelt 1992, Gadoury et al. 2007).

In California, powdery mildew is principally controlled via periodic application of foliar fungicides, including sulfur and synthetic materials such as demethylase inhibitors and strobilurins (California Department of Pesticide Regulation 2004). A wide range of materials show at least some reduction in disease levels under field conditions (Janousek et al. 2007, Adaskaveg et al. 2008). We continued our annual powdery mildew trials during 2008 to evaluate the efficacy of various fungicide products, including registered synthetic materials of varied chemical classes, oils, and biocontrol products. We present the results of five trials conducted in a Chardonnay vineyard at Herzog Ranch in Sacramento County, California.

Cysteine-rich receptor-like kinases (CRKs) are a large subfamily of plant receptor-like kinases that play a critical role in disease resistance in plants. However, knowledge about the CRK gene family in cotton and its function against Verticillium wilt (VW), a destructive disease caused by Verticillium dahliae that significantly reduces cotton yields is lacking. In this study, we identified a total of 30 typical CRKs in a Gossypium barbadense genome (GbCRKs). Eleven of these (>30%) are located on the A06 and D06 chromosomes, and 18 consisted of 9 paralogous pairs encoded in the A and D subgenomes. Phylogenetic analysis showed that the GbCRKs could be classified into four broad groups, the expansion of which has probably been driven by tandem duplication. Gene expression profiling of the GbCRKs in resistant and susceptible cotton cultivars revealed that a phylogenetic cluster of nine of the GbCRK genes were up-regulated in response to V. dahliae infection. Virus-induced gene silencing of each of these nine GbCRKs independently revealed that the silencing of GbCRK18 was sufficient to compromise VW resistance in G. barbadense. GbCRK18 expression could be induced by V. dahliae infection or jasmonic acid, and displayed plasma membrane localization. Therefore, our expression analyses indicated that the CRK gene family is differentially regulated in response to Verticillium infection, while gene silencing experiments revealed that GbCRK18 in particular confers VW resistance in G. barbadense.

The Sigatoka disease complex, caused by the closely-related Dothideomycete fungi Pseudocercospora musae (yellow sigatoka), Pseudocercospora eumusae (eumusae leaf spot), and Pseudocercospora fijiensis (black sigatoka), is currently the most devastating disease on banana worldwide. The three species emerged on bananas from a recent common ancestor and show clear differences in virulence, with P. eumusae and P. fijiensis considered the most aggressive. In order to understand the genomic modifications associated with shifts in the species virulence spectra after speciation, and to identify their pathogenic core that can be exploited in disease management programs, we have sequenced and analyzed the genomes of P. eumusae and P. musae and compared them with the available genome sequence of P. fijiensis. Comparative analysis of genome architectures revealed significant differences in genome size, mainly due to different rates of LTR retrotransposon proliferation. Still, gene counts remained relatively equal and in the range of other Dothideomycetes. Phylogenetic reconstruction based on a set of 46 conserved single-copy genes strongly supported an earlier evolutionary radiation of P. fijiensis from P. musae and P. eumusae. However, pairwise analyses of gene content indicated that the more virulent P. eumusae and P. fijiensis share complementary patterns of expansions and contractions in core gene families related to metabolism and enzymatic degradation of plant cell walls, suggesting that the evolution of virulence in these two pathogens has, to some extent, been facilitated by convergent changes in metabolic pathways associated with nutrient acquisition and assimilation. In spite of their common ancestry and shared host-specificity, the three species retain fairly dissimilar repertoires of effector proteins, suggesting that they likely evolved different strategies for manipulating the host immune system. Finally, 234 gene families, including seven putative effectors, were exclusively present in the three Sigatoka species, and could thus be related to adaptation to the banana host.

Background

Scope and conclusion