The inability to utilize nitrogen sources from carrot agar may have resulted in immature ΔareA ascospores. The total nitrogen content of carrots agar is low, and the major nitrogen compounds

are nitrate and proteins, which ΔareA strains cannot use (Międzobrodzka et al., 1993; U.S. Department of Agriculture, 2010). When we supplemented carrot agar with 5 mM urea, the sexual development of ΔareA strains was restored to the level of the wild-type strain, suggesting that the deletion mutants exhausted all available nitrogen sources during early sexual development and therefore could not complete development. In conclusion, the global nitrogen regulator areA is required for nitrogen metabolism, virulence, secondary metabolism, vegetative Roscovitine growth, and sexual development in G. zeae. This study is the PI3K inhibitor first report to account for the functions of an areA orthologue in sexual development of filamentous fungi. The detailed mechanisms of how areA regulates fungal development with other regulators would be exciting topics for future studies of G. zeae. This work was supported by a grant (2012-0000575) by the National Research Foundation funded by the Korean government (MEST). “
“Plant pathogens usually promote pathogenesis

by secreting effector proteins into host plant cells. One of the secreted effectors of Pseudomonas syringae pv. phaseolicola, the causative agent of halo-blight disease in common bean (Phaseolus vulgaris), HopF1, activates effector-triggered immunity (ETI) in a bean cultivar containing R1 resistance gene, but displays

virulence function in a bean cultivar without the R1 gene. The virulence mechanism of the effector remained SPTLC1 unknown, although it was identified more than a decade ago. Here we demonstrated that HopF1 can inhibit pathogen-associated molecular pattern-triggered immunity (PTI) in a susceptible bean cultivar Tendergreen. HopF1 directly interacted with two RPM1-interacting protein 4 (RIN4) orthologs of bean, PvRIN4a and PvRIN4b. Like RIN4 in Arabidopsis, both PvRIN4 orthologs negatively regulated the PTI responses in bean. However, the virulence function of HopF1 was enhanced in Tendergreen silencing PvRIN4. Furthermore, silencing PvRIN4a compromised the avrβ1-induced hypersensitive response (HR), which previously was reported to be suppressed by HopF1. Together, these results demonstrated that PvRIN4 orthologs were not the virulence target of HopF1 for inhibiting PTI, but probably for interfering with ETI. Plant pathogens usually employ a type III secretion system to deliver type III secreted effectors (T3SEs) into plant cells, where they interact directly with host substrates to modulate defense pathways and promote disease. Plants rely on an elaborate immune system to counteract pathogens (Boller & He, 2009).