Alcaligenes eutrophus hydrogenase genes (Hox)

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Abstract
Mutants of A. eutrophus H16 lacking catalytically active soluble hydrogenase (Hos-) grew very slowly lithoautotrophically with H2. Mutants devoid of particulate hydrogenase activity (Hop-) were not affected in growth with H2. The use of Hos- and Hop- mutants as donors of H2-oxidizing ability in crosses with plasmid-free recipients impaired in both hydrogenases (Hox-) resulted in transconjugants which had inherited the plasmid and the phenotype of the donor. Thus, the structural genes which code for the hydrogenases reside on plasmid pHG1. The Hox function of 1 class of Hox- mutants could not be restored by conjugation. These mutants exhibited a pleiotropic phenotype since they were unable to grow with H2 and also failed to grow heterotrophically with nitrate (Hox- Nit-). Nitrate was scarcely utilized as electron acceptor or as N source. Hox- Nit- mutants did not act as recipients but could act as donors of the Hox character. Transconjugants derived from those crosses were Hox+ Nit+, indicating that the mutation which leads to the Hox- Nit- phenotype maps on the chromosome. Apparently, the product, of a chromosomal gene is involved in the expression of plasmid-encoded Hox genes. The elimination of plasmid pHG1 coincided with the occurrence of multiple resistances to various antibiotics. Since Hox+ transconjugate retained the antibiotic-resistant phenotype, this property is not directly plasmid associated.