Genome Sequence Resource of Serratia ureilytica HNU47: A Strain with Biocontrol Potential Against Bacterial Wilt Pathogen Ralstonia solanacearum.

Serratia ureilytica HNU47 was originally isolated from rhizosphere soil of stock in a continuous cropping tomato-planting field, which has excellent antagonistic ability against Ralstonia solanacearum. Here, we sequenced the genome of HNU47 to gain insights into the underlying basis of its antagonistic activity. Results of phylogenetic analysis of the whole genomic sequence demonstrated that HNU47 belongs to S. ureilytica. Through antiSMASH analysis, 10 secondary metabolite biosynthesis gene clusters were predicted. There were only two gene clusters with similarity higher than 95% with known compounds' gene clusters and the similarities of the other eight gene clusters were lower than 30%, including three gene clusters with no homology. In addition, biocontrol experiments confirmed that HNU47 could decrease the incidence of bacterial wilt caused by R. solanacearum on tomato. These findings support the potential of developing S. ureilytica HNU47 as a biocontrol agent against R. solanacearum by producing some unknown active compounds. The genome sequence reported here is also useful for revealing the modulation mechanisms underlying biosynthesis of active compounds.

Bioactive secondary metabolites from tomato-derived bacterium Bacillus velezensis Hnu24.

A series of secondary metabolites have been isolated from the genus of Bacillus velezensis, most of which show antibacterial and insecticidal activities. In order to find more bioactive secondary metabolites from B. velezensis, one new natural component aminoindole dimer baciindole A (1), together with seven known compounds (2-8) were isolated from the tomato-derived bacterium Bacillus velezensis Hnu24. The structure of compound 1 was elucidated by its HR-ESI-MS spectral data and 1 D/2D NMR spectroscopic analysis. Compound 3 showed antibacterial activity against Staphylococcus aureus, S. epidermidis and Ralstonia solanacearum with the MIC values of 3.125, 12.5 and 50 µg/mL, respectively. Compound 4 showed antibacterial activity against S. aureus with the MIC value of 12.5 µg/mL. Compound 3 showed cytotoxic activity for human colon cancer HTC116 cancer cells with the IC50 value of 8.42 ± 0.48 µM. Five compounds (1-4 and 8) were obtained from the strain of B. velezensis for the first time. These results indicated that 3 will be useful in developing antimicrobial and treatment of colon cancer agents.

PhcA and PhcR Regulate Ralsolamycin Biosynthesis Oppositely in Ralstonia solanacearum.

Ralsolamycin, one of secondary metabolites in Ralstonia solanacearum, is known to be involved in crosstalk between R. solanacearum and fungi. Ralsolamycin formation is catalyzed by two-hybrid synthetases of RmyA (non-ribosomal peptide synthetase) and RmyB (polyketide synthase). A methyltransferase PhcB catalyzes formation of 3-OH MAME or 3-OH PAME, signals for the quorum sensing (QS) in R. solanacearum, while PhcB positively modulates ralsolamycin biosynthesis. A two-component system of PhcS and PhcR can response these QS signals and activate phcA expression. Here, we experimentally demonstrated that deletion of phcA (ΔphcA) substantially impaired the ralsolamycin production and expression of rmyA and rmyB in R. solanacearum strain EP1, and failed to induce chlamydospore formation of plant fungal pathogen Fusarium oxysporum f. cubense (stran FOC4). However, deletion of phcR significantly increased ralsolamycin production and expression of rmyA and rmyB, and phcR mutants exhibited enhanced ability to induce chlamydospore formation of FOC4. Results of the electrophoretic mobility shift assay suggested that both PhcA and PhcR bind to promoter of rmy operon. Taken together, these results demonstrated that both PhcA and PhcR bind to promoter of rmy operon, but regulate ralsolamycin biosynthesis in an opposite way. It could extend our knowledge on the sophisticated regulatory networks of ralsolamycin biosynthesis in R. solanacearum.