Abstract—Copper is an essential micronutrient for all living cells, however, it is extremely toxic at high concentrations and thus copper homeostasis is required to be tightly regulated. copA encodes for a copper-translocating P-type ATPase (CopA) and plays a vital role in copper homeostasis and is involved in copper transport across membranes of many organisms. Little is known about copper homeostasis in Methylococcus capsulatus although copper has a significant physiological role in this methanotroph. In this study we investigated the disruption of a CopA1 homologue (MCA2072; copA1) in M. capsulatus (Bath) by insertional inactivation mutagenesis. The resulting mutant, M. capsulatus ΔcopA1, was copper resistant to elevated copper concentrations (100 μM) than the wild-type strain (80 μM). Furthermore, the intracellular copper measurements revealed that ΔcopA1 accumulated half the amount of copper when compared with the wild-type. No observed phenotypic difference between the mutant strain and wild-type related to growth at different silver concentrations. These observations suggest that M. capsulatus CopA1 has a key role in copper homeostasis.

Index Terms—CopA, copper homeostasis, P-type ATPases, Methylococcus capsulatus

Ashraf Y. Z. Khalifa is with Botany Department, University of Beni-Suef, Beni-Suef, Egypt (e-mail: ashraf_zaky2002@yahoo.com)

Cite:Ashraf Y. Z. Khalifa, "Mutagenesis of a Copper P-Type ATPase Encoding Gene in Methylococcus capsulatus (Bath) Results in Copper-Resistance," International Journal of Bioscience, Biochemistry and Bioinformatics vol. 3, no. 2, pp. 37-42, 2013.