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Washington State University Molecular Plant Sciences

509-335-3751
chitosan@wsu.edu
Professor of Plant Pathology. Ph.D.1962, Kansas State University.
hadwiger

Research

The research in my lab has centered on a model system for looking at nonhost resistance, in this case the resistance of pea tissue against a challenge by a bean pathogen. Alternately, this process is compared with the same tissue challenged by a related true pathogen of peas.  We developed an assay on pea endocarp tissue that develops total resistance within 6 h to an inappropriate fungus such as the bean pathogen and susceptibility to the pea pathogen within 24 h. The fungal components that elicit the defense response, represented by 6 response genes from peas, have been defined and include the carbohydrate, chitosan, and the enzyme DNase.  We have intensely studied the properties that enable these elicitors to enter the plant cell and activate the response genes, as well as the functions of these genes.  The genes appear to become activated with changes in the plant chromatin adjacent to the defense genes.   The chromatin alterations include DNA damage and removal of nuclear proteins such as histones H2A, H2B via ubiquitination.  We continue to investigate our explanations of these precise gene activation mechanisms. Some of which have not yet been incorporated into the thinking of some mainstream pathologists.

The defense genes of peas and the elicitor DNase from Fusarium solani used were first cloned by us and thus we have engineered them into potatoes, tobacco or canola to demonstrate their individual disease resistance functions.

The precise mechanism by which the fungal DNase activates genes is especially important to us as we now find that all of the fungi sequenced to date possess a mitochondrial DNase gene that codes for a protein with an N-terminal signal peptide that allows it to be released from the fungal cell and enter the plant cell.  This background knowledge has enabled us to develop commercial products that enhance disease resistance.

 

Selected Publications

Hadwiger, L.A., Druffel, K., Humann, J.L., Schroeder, B.K.  Nuclease released by Verticillium dahlia is a signal for non-host resistance.  Plant Science.  2013;201-202(1):98-107.

Hadwiger, L.A., Polashock, J.  Fungal mitochondrial DNases:  Effectors with the potential to activate plant defenses in non-host resistance.  Phytopathology.  2013;103(1):81-90.

Hadwiger, L.A.  Plant science review:  Multiple effects of chitosan on plant systems:  Solid science or hype.  Plant Science.  2013;208:42-49.

Hadwiger, L. A., Druffel, K., Humann, J. L., and Schroeder, B. K. 2013. Nuclease released by Verticillium dahliae is a signal for non-host resistance.  Plant Science 201-202:98-107.    On line (2010), doi10.1016/j.plantsci.2012.11.011.

Hadwiger, L. A.  2009.  Localization predictions for gene products involved in non-host resistance responses in a model plant/fungal pathogen interaction. Plant Sci.177:257–265.

Isaac, J., Hartney, S.L., Druffel, K., and Hadwiger, L. A. 2009.  The non-host disease resistance response in peas; alterations in phosphorylation and ubiquitination of HMG A and histones. H2A/H2B. Plant Science 177:439-449.

Isaac, J., Hartney, S.L., Druffel, K., and Hadwiger, L. A. 2009.  The non-host disease resistance response in peas; alterations in phosphorylation and ubiquitination of HMG A and histones. H2A/H2B. Plant Science 177:439-449.

Hadwiger, L. A. 2008.  Pea-Fusarium solani interactions: contributions of a system toward understanding disease resistance Phytopathology 98:3372-379.

Hartney, S., Carson, J. and Hadwiger, L. A. 2007. The use of chemical genomics to detect functional systems affecting the non-host disease resistance of pea to Fusarium solani f. sp. phaseoli. Plant Science 172:45-56.

Druffel, K., Cason, J. A., Hartney, S., and Hadwiger, L. A. 2006. Inverse PCR to identify DNA sequence upstream of the pea HMG-A open reading frame. Pisum Genetics 37:15-18.

Hadwiger, L. A. and McBride, P. O. 2006. Low-level copper plus chitosan applications provide protection against late blight of potato. Plant Health Progress doi:10.1094/PHP-2006-04XX-01-RS

Hadwiger, L. A., McBride, P. O., Klosterman, S. J. and Choi, J.J. 2004. Chitosan as a component of the plant’s disease resistance response and as a “sticker” for plant protection by antifungal compounds. In: Advances in Chitin Science Vol.VII. Adenda. Eds: Boucher, I., Jamieson, K., and Retnakaran, A. pp. 1-9.

Choi, J.J., Klosterman, S. J. and Hadwiger, L. A. 2004. A promoter from pea gene DRR206 is suitable to regulate an elicitor-coding gene and develop disease resistance Phytopathology 94:651-660.