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Flooding of sweetpotatoes in the field leads to development of soft rot on the storage roots while they remain submerged or on subsequent harvest and storage. Incidences of flooding after periods of intense rainy weather are on the rise in the southeastern United States, which is home to the majority of sweetpotato production in the nation. In an effort to characterize the causative agent(s) of this devastating disease, here we describe two distinct bacterial strains isolated from soft-rotted sweetpotato storage roots retrieved from an intentionally flooded field. Both of these anaerobic spore-forming isolates were identified as members of the genus Clostridium based on sequence similarity of multiple housekeeping genes, and both were confirmed to cause soft rot disease on sweetpotato and other vegetable crops. Despite these common features, the isolates were distinguishable by several phenotypic and biochemical properties, and phylogenetic analysis placed them in separate well-supported clades within the genus. Overall, our results demonstrate that multiple plant-pathogenic Clostridium species can cause soft rot disease on sweetpotato and suggest that a variety of other plant hosts may also be susceptible.

Flooding of sweetpotatoes in the field leads to development of soft rot on the storage roots while they remain submerged or on subsequent harvest and storage. Incidences of flooding after periods of intense rainy weather are on the rise in the southeastern United States, which is home to the majority of sweetpotato production in the nation. In an effort to characterize the causative agent(s) of this devastating disease, here we describe two distinct bacterial strains isolated from soft-rotted sweetpotato storage roots retrieved from an intentionally flooded field. Both of these anaerobic spore-forming isolates were identified as members of the genus

Jab1, a co-activator of AP-1 transcription factor and the fifth subunit of the COP9 signalosome, mediates degradation of the tumor suppressor p53 and p27(Kip1) and functions as a tumor promoter in different types of human cancer. In this study, we show that inhibition of Bcr-Abl oncogene by imatinib induces down-regulation of Jab1 in Bcr-Abl-positive K562, Ku812, and MEG01 leukemia cells suggesting Bcr-Abl may regulate Jab1 expression. Promoter deletion and mutation analysis indicate the Tcf-4/β-catenin and STAT1 binding sites located between the -405/-223 region of the human Jab1 promoter are important for the activation of Jab1 by Bcr-Abl. Double mutation of these two sites reverses the inhibitory effect of imatinib. Chromatin immunoprecipitation assay verifies the binding of β-catenin and STAT1 to human Jab1 promoter. Ectopic expression of dominant-negative Tcf-4 mutant significantly attenuates Jab1 expression while over-expression of β-catenin and STAT1 cooperatively up-regulates Jab1 promoter activity and mRNA expression. Our results also demonstrate that the AKT signaling pathway is involved in the regulation of Jab1 by Bcr-Abl because the AKT inhibitor LY294002 but not the ERK inhibitor PD98059 reduces Jab1 promoter activity and mRNA expression. Taken together, our results suggest that Bcr-Abl stimulates Jab1 expression via the cooperative interaction of β-catenin and STAT1 in leukemia cells.