El gen narG y el operón moa (ABCDE) como posibles reguladores de la respiración anaeróbica del nitrato, en Escherichia coli K1

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In E. coli K12, both narC-8 y narC-78 mutations of the narC(narGHJI) operon confer the Nit- phenotype and block the expression of the F(moa::lac)25 transcriptional fusion. In the present work, both mutations were comparatively studied and identifyed as narG-. Trans-dominance analysis showed that Nit+ restauration levels were influenced by growing with molybdenum, particular mutation and bacterianne genotype. Immunoelectrophoresis assay indicated differences in the NRA asubunit recognition. Mapped-linking reveled the sequential order ... narG-78... narG-8 ... trp. Genetic analysis evidenced in isogenic strains that, the narG+ substitutive recombination by narG-, restored the fusion expression and viceverse. Surprisingly, trans-dominance analysis showed in isogenic strains that Nit+ restoration was (i) moa(ABCDE)+ operon mediated and (ii) F(moa::lac)25 narG-78 double mutation conditioned. The results obtained confirmed the narG+ regulatory role over the moa operon transcriptional expression and suggested a regulatory role of both (narG+,moa) in the nitrate respiration.

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