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Texas Has a New Pathotype of Peronosclerospora sorghi, the Cause of Sorghum Downy Mildew

May 2005 , Volume 89 , Number  5
Pages  529.1 - 529.1

T. Isakeit , Department of Plant Pathology and Microbiology, Texas A&M University, College Station 77843 ; and J. Jaster , Pioneer Hi-Bred International, Taft, TX 78390



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Accepted for publication 11 February 2005.

Three pathotypes of Peronosclerospora sorghi were known to occur in Texas as of 1980, with pathotype 3 (P3) predominant on sorghum (Sorghum bicolor) grown in the Upper Coast area. Following the use of hybrids resistant to P3, combined with metalaxyl or mefenoxam seed treatment, sorghum downy mildew (SDM) became a minor disease in Texas until the occurrence of a widespread outbreak caused by a P3 strain resistant to metalaxyl and mefenoxam in Wharton County in 2001 (2). During July 2004, <1% of plants in a commercial field in Wharton County planted to two Pioneer Brand P3-resistant hybrids had white stripes on the leaves and leaf shredding typical of systemic SDM. To obtain inoculum for pathogenicity studies, several infected plants were removed from the field and transplanted to pots for growth in a greenhouse. Systemically infected leaves suitable for inoculum production subsequently developed from tillers. Conidia were collected from leaves using a tiered temperature system (1). One-week-old seedlings of 10 sorghum lines used as pathotype differentials for Texas were sprayed until runoff with a conidial suspension (8 × 104 per ml) and incubated for 24 h at 20°C and 100% relative humidity. Seedlings were grown for 6 days in the greenhouse and then incubated overnight at 20°C and 100% relative humidity to promote sporulation of lesions, while systemic symptoms were evaluated after an additional 2 weeks in the greenhouse. There were 10 seeds planted per replicate and four replicates per line. The experiment was repeated once. Sporulation occurred on 54 and 64% of plants, and systemic symptoms on 53 and 82% of plants of P3-resistant line SC155 in two experiments, respectively. There were no local lesions or systemic symptoms on SC155 plants inoculated with several P3 isolates. Lines SC414-12E, QL3-India, 82BDM499, and 85EON495, which are resistant to P3, were also resistant to this isolate (i.e., no local lesions or systemic symptoms). Lines RTx2536, RTx430, CS3541, RTx7078, and SC170-6-17, which are susceptible to P3, were also susceptible to this isolate (54 to 100% incidence of systemic symptoms). An experiment (repeated once) that compared the reaction of this new pathotype on metalaxyl-treated and nontreated seed of a P3-resistant hybrid and a P3-susceptible hybrid, with reactions of metalaxyl-resistant P3 isolate and a metalaxyl-sensitive P3 isolate, showed that this pathotype, in addition to overcoming the genetic resistance, was also fungicide resistant. The pathogenicity of this new pathotype to other commercial P3-resistant hybrids is not yet known. There was no yield loss associated with this outbreak. However, the presence of a new pathotype, in combination with fungicide resistance, could lead to further outbreaks of SDM in the Upper Coast of Texas with the potential for yield loss.

References: (1) J. Craig. Plant Dis. 71:356, 1987. (2) T. Isakeit et al. (Abstr.) Phytopathology 93:S39, 2003.



© 2005 The American Phytopathological Society