Elucidating the role of the phenylacetic acid metabolic complex in the pathogenic activity of Rhizoctonia solani anastomosis group 3

Abstract

The soil fungus Rhizoctonia solani produces phytotoxic phenylacetic acid (PAA) and hydroxy (OH-) and methoxy (MeO-) derivatives of PAA. However, limited information is available on the specific role that these compounds play in the development of Rhizoctonia disease symptoms and concentration(s) required to induce a host response. Reports that PAA inhibits the growth of R. solani conflict with the established ability of the fungus to produce and metabolize PAA. Experiments were conducted to clarify the role of the PAA metabolic complex in Rhizoctonia disease. In this study the concentration of PAA and derivatives required to induce tomato root necrosis and stem canker, in the absence of the fungus, and the concentration that inhibits mycelial growth of R. solani were determined. The effect of exogenous PAA and derivatives of PAA on tomato seedling growth also was investigated. Growth of tomato seedlings in medium containing 0.1–7.5 mM PAA and derivatives induced necrosis of up to 85% of root system. Canker development resulted from injection of tomato seedling stems with 7.5 mM PAA, 3-OH-PAA, or 3-MeO-PAA. PAA in the growth medium reduced R. solani biomass, with 50% reduction observed at 7.5 mM. PAA, and derivatives were quantified from the culture medium of 14 isolates of R. solani belonging to three distinct anastomosis groups by GC-MS. The quantities ranged from below the limit of detection to 678 nM, below the concentrations experimentally determined to be phytotoxic. Correlation analyses revealed that isolates of R. solani that produced high PAA and derivatives in vitro also caused high mortality on tomato seedlings. The results of this investigation add to the body of evidence that the PAA metabolic complex is involved in Rhizoctonia disease development but do not indicate that production of these compounds is the primary or the only determinant of pathogenicity.

• aggressiveness
• benzeneacetic acid
• GC-MS
• host response
• Thanatephorus
• virulence factor

Acknowledgments

The authors gratefully acknowledge the contribution of tomato seeds by Dr Mike Klopmeyer from PanAmerican Seed Co., the provision of growth chamber space and assistance by Drs Janet L. Shurtleff and Carole H. Saravitz of the North Carolina State University Phytotron, the assistance of Lucy Liu with inoculation and harvest of the disease assay, the contributions of Nick Taylor toward the development of the root necrosis assay method, the expertise shared by Dr Consuelo Arellano regarding statistical analyses and the guidance provided by Dr Stellos Tavantzis.

This project was supported by Initiative for Future Agriculture and Food Systems Grant No. 2001-52101-11507 from the USDA Cooperative State Research, Education and Extension Service.