ABSTRACT
Verticillium nonalfalfae, a soilborne vascular phytopathogenic fungus, causes wilt disease in several crop species. Of great concern are outbreaks of highly aggressive V. nonalfalfae strains, which cause a devastating wilt disease in European hops. We report here the genome sequence and annotation of V. nonalfalfae strain T2, providing genomic information that will allow better understanding of the molecular mechanisms underlying the development of highly aggressive strains.
ABSTRACT
Plant-pathogenic microbes secrete effector molecules to establish themselves on their hosts, whereas plants use immune receptors to try and intercept such effectors in order to prevent pathogen colonization. The tomato cell surface-localized receptor Ve1 confers race-specific resistance against race 1 strains of the soil-borne vascular wilt fungus Verticillium dahliae which secrete the Ave1 effector. Here, we describe the cloning and characterization of Ve1 homologues from tobacco (Nicotiana glutinosa), potato (Solanum tuberosum), wild eggplant (Solanum torvum) and hop (Humulus lupulus), and demonstrate that particular Ve1 homologues govern resistance against V. dahliae race 1 strains through the recognition of the Ave1 effector. Phylogenetic analysis shows that Ve1 homologues are widely distributed in land plants. Thus, our study suggests an ancient origin of the Ve1 immune receptor in the plant kingdom.
Subject(s)
Disease Resistance/genetics , Evolution, Molecular , Genes, Plant , Plant Diseases/genetics , Plant Diseases/microbiology , Plant Proteins/metabolism , Solanum lycopersicum/microbiology , Verticillium/physiology , Amino Acid Sequence , Arabidopsis/genetics , Arabidopsis/immunology , Arabidopsis/microbiology , Cloning, Molecular , Fungal Proteins/metabolism , Solanum lycopersicum/genetics , Phylogeny , Plant Proteins/genetics , Plants, Genetically Modified , Receptors, Immunologic/genetics , Receptors, Immunologic/metabolism , Sequence Homology, Amino Acid , Solanum/microbiology , Solanum tuberosum/microbiology , Nicotiana/immunology , Nicotiana/microbiologyABSTRACT
Prion protein (Prp(c)) is involved in the etiology of prion neurodegenerative diseases in mammals. The biological functions of Prp(c) are still largely unknown despite many studies in recent years. Different studies have shown impairment in locomotion, emotional/social behaviors, sleep disorders and memory impairment in mice lacking the prion gene Prnp (Prnp(-/-)) but its exact functions in the brain are still unclear. In the present study, Zurich I Prnp(-/-) and their littermate wild type (WT) control male mice were behaviorally characterized for offensive aggressive behavior in a resident-intruder paradigm with the aim to establish the possible function of Prp(c) in the regulation of offensive aggressive behavior. Prnp(-/-) mice showed reduced latencies to the first attack and bite, higher percentage of mice biting and higher frequencies of attacks of stimulus males. These results show that Prnp(-/-) mice exhibit altered aggressive behavior in comparison to their WT controls and therefore suggest that lack of the Prnp either directly or indirectly affects brain circuitry responsible for the regulation of offensive aggressive behavior.
