This study aimed to investigate the internal relationships between safety investments and construction employees' behavioral performance with safety cognition as the mediating factor. A comprehensive methodology was adopted, including theoretical modeling of safety investments, questionnaire survey, and Structural Equation Modeling (SEM). In the theoretical model, four factors (i.e., personal protection equipment (PPE), safety education, insurance purchased for site employees, and safety incentives) were adopted as safety investment categories. These four categories were studied of their correlation to the overall safety investment, which was tested of its contribution to employees' behavioral safety performance in both direct and indirect ways. Indirectly, safety cognition was introduced as a mediator to bridge safety investments and behavioral performance. A questionnaire consisting of 28 indicators was adopted to describe safety investment, safety cognition, and behavioral performance. A random sampling approach and the top-down method were implemented to recruit construction site employees from the southeastern region of China. The follow-up SEM analysis revealed that all the four investment categories positively contributed to the overall safety investment, which was found significantly correlated to employees' safety cognition and behavioral performance. Safety incentive was identified as the most significant factor contributing to the overall investment. The current study extends

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.

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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 whole genomic sequence demonstrated that the HNU47 belongs to Serratia ureilytica. Through antiSMASH analysis, ten secondary metabolite biosynthesis gene clusters were predicted, but there were only two gene clusters' similarity higher than 95% with the known compounds' gene clusters, the similarities of the other eight gene clusters were lower than 30%, and including three gene clusters with no homology. In addition, biocontrol experiments confirmed that the HNU47 could decrease the incidence of the 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.