Interactions and biocontrol of pathogenic Streptomyces strains co-occurring in potato scab lesions.

AIMS: To test interactions between pathogenic strains of Streptomyces turgidiscabies, S. scabies and S. aureofaciens. To study biological control of S. turgidiscabies and S. scabies using the nonpathogenic Streptomyces strain (346) isolated from a scab lesion and a commercially available biocontrol agent (S. griseoviridis strain K61; 'Mycostop'). METHODS AND RESULTS: Pathogenic strains of S. turgidiscabies and S. aureofaciens inhibited growth of S. scabies in vitro, whereas strain 346 and S. griseoviridis inhibited the pathogenic strains and were subsequently tested for control of scab in the greenhouse and field. Strains 346 and K61 suppressed development of common scab disease caused by S. turgidiscabies in the greenhouse. Strain 346 reduced incidence of S. turgidiscabies in scab lesions on potato tubers in the field. CONCLUSIONS: Streptomyces turgidiscabies shows antagonism against S. scabies that occurs in the same scab lesions and shares the ecological niche in the field. Biocontrol of S. turgidiscabies is possible with nonpathogenic Streptomyces strains but interactions may be complicated. SIGNIFICANCE AND IMPACT OF THE STUDY: Streptomyces turgidiscabies may have potential to displace S. scabies under the Scandinavian potato growing conditions. Biological control of the severe potato scab pathogen, S. turgidiscabies, is demonstrated for the first time. The results can be applied to enhance control of common scab.

Infection with Rhizoctonia solani induces defense genes and systemic resistance in potato sprouts grown without light.

Rhizoctonia solani is an important soilborne and seedborne fungal pathogen of potato (Solanum tuberosum). The initial infection of sprouts prior to emergence causes lesions and may be lethal to the sprout or sprout tip, which results in initiation and compensatory growth of new sprouts. They emerge successfully and do not suffer significant damage. The mechanism behind this recovery phenomenon is not known. It was hypothesized that infection may induce pathogen defense in sprouts, which was investigated in the present study. Tubers were sprouted in cool and moist conditions in darkness to mimic conditions beneath soil. The basal portion of the sprout was isolated from the apical portion with a soft plastic collar and inoculated with highly virulent R. solani. Induction of defense-related responses was monitored in the apical portion using microarray and quantitative polymerase chain reaction techniques at 48 and 120 h postinoculation (hpi) and by challenge-inoculation with R. solani in two experiments. Differential expression of 122 and 779 genes, including many well-characterized defense-related genes, was detected at 48 and 120 hpi, respectively. The apical portion of the sprout also expressed resistance which inhibited secondary infection of the sprouts. The observed systemic induction of resistance in sprouts upon infection with virulent R. solani provides novel information about pathogen defense in potato before the plant emerges and becomes photosynthetically active. These results advance our understanding of the little studied subject of pathogen defense in subterranean parts of plants.