摘要

The distribution and survival of Listeria monocytogenes (L. monocytogenes) in food processing environment is linked to its ability to form biofilms, however the genetic mechanisms remain unclear. In our previous study, a Himar1 mariner-based transposon muta genesis was performed and 42 mutants were confirmed to have reduced biofilm formation. Among the 42 biofilm deficient mutants, two isolates (s25-10C and s55-1D) harbored single insertion in lmo 1386, a gene encoding a putative DNA translocase. The lmo 1386 mutants had impaired biofilm formation in both static and flow conditions. The mutant strain s55-1D was complemented by cloning the entire lmo 1386 gene into pPL2-gtcAP, a derivative of the integration vector pPL2 with the L. monocyto genes gtcA promoter. The genetically complemented mutant restored its biofilm phenotype, demonstrating the role of lmo1386 in the biofilm formation of L. monocytogenes. The lmo 1386 Mutant had reduced initial adhesion ability, which could at least partially contribute to the impaired biofilm phenotype. Additionally, the lmo 1386 mutant formed elongated cell chains when grown in a nutrient TSBYE media, while no obvious cell morphology changes were observed when grown in the minimal MWB media. Overall, our findings suggest that the disruption of lmo 1386, a putative DNA translocase gene affects the biofilm formation of L. monocytogenes on abiotic surfaces, which may further advance the understanding of the complicated process of biofilm formation.

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