BMCB-Faculty Research, Hans D. VanEtten

Professor of Plant Pathology and Molecular & Cellular Biology
Ph.D., Cornell University

Molecular mechanisms of plant pathogenesis, habitat specific genes on dispensable chromosomes, and synthesis of plant antibiotics.

Research Interests

My main research interests are in elucidating the molecular and genetic properties that allow pathogenic fungi to overcome natural resistance mechanisms in plants. Many plants synthesize antibiotics (phytoalexins) in response to infection by microorganisms, and these compounds can serve as a natural barrier to potential pathogens. We have been investigating the possibility that some successful pathogens are able to overcome this resistance mechanism by evolving specific enzymes to detoxify the phytoalexin(s) produced by their host plants. Our main model pathogen- plant interaction is the disease on pea caused by the fungus Nectria haematococca. Our results indicate that maximum pathogenicity requires pisatin demethylase (pda), a substrate-inducible cytochrome P-450 that detoxifies the pea phytoalexin pisatin. The sequence of the PDA genes are highly divergent from all other members of the cytochrome P-450 superfamily of genes consistent with the adaptation of PDA for a specific function in pathogenesis. PDA activity is present in most pathogens of pea, and we are characterizing these other cytochrome P-450 genes and their products to determine if specific cytochrome P-450s have evolved in fungi for plant pathogenesis by horizontal gene transfer or convergent evolution. PDA genes are on dispensable (DS) chromosomes in N. haematococca and recent results indicate that other genes for pea pathogenesis (PEP genes) as well as genes allowing for saprophytic growth on root surfaces (the rhizosphere) are contained on these DS chromosomes. N. haematococca occupies many diverse biological habitats. This includes comensal relationship as well as pathogenic relationship with many plants in addition to pea. Our hypothesis is that the DS chromosomes in this organism serve as a reservoir for unique genes that allow an individual isolate to inhabit a specific habitat. We are testing this hypothesis by 1) determining the effect of loss of DS chromosomes on habit association, 2) identifying the PEP genes and rhizosphere conditioning genes on the DS chromosomes, and 3) determining the extent of recombination among different DS chromosomes and non-dispensable chromosomes and its effect on habitat association. A portion of our research effort is also devoted to identifying the plant genes involved in phytoalexin biosynthesis. The ultimate objective is to produce transgenic plants that either lack the ability to produce phytoalexins or have the ability to produce new types of chemicals as phytoalexins. Such transgenic plants can be used to determine the precise role of these plant antibiotics in the resistance of plants to disease.

Select Publications

Any link on the below references will take you off of the BMCB site and to an abstract of that particular paper.

DiCenzo, G.L., and H.D. VanEtten. 2006. Studies on the late steps of (+) pisatin biosynthesis: evidence for (-) enantiomeric intermediates. Phytochemistry 67: 675-683.

Gunawardena, U., M. Rodriguez, D. Straney, J.T. Romeo, H.D. VanEtten, and M.C. Hawes. 2005. Tissue-specific localization of pea root infection by Nectria haematococca. Mechanisms and consequences. Plant Physiology 137: 1363-1374.

Wu, Q., and H.D. VanEtten. 2004. Introduction of plant and fungal genes into pea (Pisum sativum L.) hairy roots reduces their ability to produce pisatin and affects their response to a fungal pathogen. Molecular Plant- Microbe Interactions 17: 798-804.

Temporini, E.D., and H.D. VanEtten. 2004. An analysis of the phylogenetic distribution of the pea pathogenicity genes of Nectria haematococca MPVI supports the hypothesis of their origin by horizontal transfer and uncovers a potentially new pathogen of garden pea: Neocosmospora boniensis. Current Genetics 46: 29-36.

Liu, X., M. Inlow, and H.D. VanEtten. 2003. Expression profiles of pea pathogenicity ( PEP) genes in vivo and in vitro, characterization of the flanking regions of the PEP cluster and evidence that the PEP cluster region resulted from horizontal gene transfer in the fungal pathogen Nectria haematococca. Current Genetics 44: 95-103.

Funnell, D.L., P.S. Matthews, and H.D. VanEtten. 2002. Identification of new pisatin demethylase genes (PDA5 and PDA7) in Nectria haematococca and non-Mendelian segregation of pisatin demethylating ability and virulence on pea due to loss of chromosomal elements. Fungal Genetics and Biology 37: 121-133.

Funnell, D.L., and H.D. VanEtten. 2002. Pisatin demethylase genes are on dispensable chromosomes while genes for pathogenicity on carrot and ripe tomato are on other chromosomes in Nectria haematococca. Molecular Plant-Microbe Interactions 15: 840-846.

Temporini, E.D., and H.D. VanEtten. 2002. Distribution of the pea pathogenicity ( PEP) genes in the fungus Nectria haematococca mating population VI. Current Genetics 41: 107-114.

VanEtten, H.D., E. Temporini, and C. Wasmann. 2001. Phytoalexin (and phytoanticipin) tolerance as a virulence trait: why is it not required by all pathogens? Physiological and Molecular Plant Pathology 59: 83-93.

George, H.L., and H.D. VanEtten. 2001. Characterization of pisatin-inducible cytochrome p450s in fungal pathogens of pea that detoxify the pea phytoalexin pisatin. Fungal Genetics and Biology 33: 37-48.

Han, Y., X. Liu, U. Benny, H.C. Kistler, and H.D. VanEtten. 2001. Genes determining pathogenicity to pea are clustered on a supernumerary chromosome in the fungal plant pathogen Nectria haematococca. Plant Journal 25: 305-314.

Contact Information

Mailing:
Hans D. Van Etten, Professor
Division of Plant Pathology & Microbiology
University of Arizona
Marley 341A
P.O. Box 210036
Tucson AZ 85721-0036

Web Site: Home Page

Telephone:
520-621-9355 (Office)
520-621-9390 (Lab)

Fax:
520-621-9290

Email:
vanetten@ag.arizona.edu

Please e-mail any comments to:
bmcb@email.arizona.edu