|Hogan, Clifford -|
|Mole, Beth -|
|Grant, Sarah -|
|Charkowski, Amy -|
Submitted to: PLoS One
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 30, 2013
Publication Date: June 3, 2013
Repository URL: http://handle.nal.usda.gov/10113/56862
Citation: Hogan, C.S., Mole, B.M., Grant, S.R., Willis, D.K., Charkowski, A.0. 2013. The type III secreted effector DspE is required early in Solanum tuberosum leaf infection by Pectobacterium carotovorum to elicit cell death, and requires Wx(3-6)D/E motifs. PLoS One. Available: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0065534. Interpretive Summary: Pectobacterium carotovorum subsp. carotovorum (P. carotovorum) is an economically important pathogen of potato causing soft rot in the field and in storage. We found that this pathogen appears to secrete a protein called DspE that is required for disease on potato. We found that this protein causes plant cell death and is required for the expression of several bacterial genes required for disease on plants. Our results provide a target for developing potato varieties that contains novel resistance to this important disease. Inhibition of the expression of this gene is expected render potato resistant to bacterial soft rot.
Technical Abstract: Pectobacterium species are enterobacterial plant-pathogens that cause soft rot disease in diverse plant species. Unlike hemi-biotrophic plant pathogenic bacteria, the type III secretion system (T3SS) of Pectobacterium carotovorum subsp. carotovorum (P. carotovorum) appears to secrete only one effector protein, DspE. We have previously shown that HrpL, the T3SS regulator, and DspE are required for pathogenesis on leaves. In this work, we identified genes up-regulated by HrpL, visualized expression of hrpL in planta, and established that DspE causes host cell death. DspE required its full length, and WxxxE-like motifs, which are characteristic of the AvrE-family effectors, for host cell death. We also examined expression in plant leaves and showed that hrpL is required for the expression of dspE and hrpN, as well as the genes ffh, gyrA, and pelB. These data support a model where P. carotovorum uses the T3SS early in leaf infection to initiate pathogenesis through elicitation of DspE-mediated host cell death.