|MOYER, MICHELLE - Washington State University|
|GADOURY, DAVID - Cornell University - New York|
Submitted to: European Journal of Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/23/2015
Publication Date: 9/3/2015
Publication URL: http://DOI 10.1007/s10658-015-0745-1
Citation: Moyer, M., Londo, J.P., Gadoury, D., Cadle Davidson, L.E. 2015. Cold Stress-Induced Disease Resistance(SIDR): Indirect effects of low temperatures on host-pathogen interactions and disease progress in the grapevine powdery mildew pathosystem. European Journal of Plant Pathology. 2:5-8. doi: 10.1007/s10658-015-0745-1.
Interpretive Summary: Grape powdery mildew (GPM) cannot be cultured and grows on the surface of susceptible grape tissue. These features make GPM sensitive to environmental stresses, both directly and indirectly via the host responses. Directly, cold exposure kills sections of GPM colonies and delays sporulation. Indirectly after cold nights, grapevine leaves develop cold stress-induced disease resistance (SIDR). The effects of SIDR are even greater on older, more resistant leaves. Reserachers reviewed the biology of GPM cold responses and suggested opportunities for investigating the mechanistic basis of cold SIDR. While GPM is a challenging disease for research, its biology is fascinating.
Technical Abstract: Erysiphe necator is an obligate biotroph capable of infecting three genera within the Vitaceae (Vitis, Parthenocissus, and Ampelopsis). The pathogen inhabits a unique niche involving wholly external mycelial growth on the host epidermal cells. This growth habit coupled with its biotrophic reliance on the host makes it sensitive to both direct effects of abiotic stresses on the pathogen and indirect abiotic effects via the host responses. Directly, cold exposure of the developing pathogen results in in a protracted latent period in addition to death of hyphal segments. Indirectly, acute low temperature events are followed by a transient cold stress-induced disease resistance (SIDR) in leaves of Vitis vinifera. While the cold SIDR phenotype mimics the infection response observed on ontogenically-resistant leaves, the effects of SIDR and ontogenic resistance are additive. Sufficient tools are now available for investigating the mechanistic basis of cold SIDR. While pathosystems involving obligate biotrophs complicate research on direct and indirect environmental effects on the pathogen, this requisite interaction also creates interesting systems to understand how the condition of the host may influence subsequent disease development.