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Plant–pathogen interactions and elevated CO(2): morphological changes in favour of pathogens

Crop losses caused by pests and weeds have been estimated at 42% worldwide, with plant pathogens responsible for almost $10 billion worth of damage in the USA in 1994 alone. Elevated carbon dioxide [ECO(2)] and associated climate change have the potential to accelerate plant pathogen evolution, whic...

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Detalles Bibliográficos
Autores principales: Lake, Janice Ann, Wade, Ruth Nicola
Formato: Texto
Lenguaje:English
Publicado: Oxford University Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2718216/
https://www.ncbi.nlm.nih.gov/pubmed/19470658
http://dx.doi.org/10.1093/jxb/erp147
Descripción
Sumario:Crop losses caused by pests and weeds have been estimated at 42% worldwide, with plant pathogens responsible for almost $10 billion worth of damage in the USA in 1994 alone. Elevated carbon dioxide [ECO(2)] and associated climate change have the potential to accelerate plant pathogen evolution, which may, in turn, affect virulence. Plant–pathogen interactions under increasing CO(2) concentrations have the potential to disrupt both agricultural and natural systems severely, yet the lack of experimental data and the subsequent ability to predict future outcomes constitutes a fundamental knowledge gap. Furthermore, nothing is known about the mechanistic bases of increasing pathogen agressiveness. In the absence of information on crop species, it is shown here that plant pathogen (Erysiphe cichoracearum) aggressiveness is increased under ECO(2), together with changes in the leaf epidermal characteristics of the model plant Arabidopsis thaliana L. Stomatal density, guard cell length, and trichome numbers on leaves developing post-infection are increased under ECO(2) in direct contrast to non-infected responses. As many plant pathogens utilize epidermal features for successful infection, these responses provide a positive feedback mechanism facilitating an enhanced susceptibility of newly developed leaves to further pathogen attack. Furthermore, a screen of resistant and susceptible ecotypes suggest inherent differences in epidermal responses to ECO(2).