The RadB protein from Pyrococcus does not complement E. coli recA mutations in vivo

Abstract

A previous publication claimed that the radB gene called Pk-REC from Pyrococcus furiosus complemented an E. coli recA mutation. We found that a sequencing error had led to the test of a mutant form of Pk-REC. The wild-type radB gene from P. furiosus cloned in a similar expression vector to the mutant Pk-REC also appeared to complement an E. coli recA mutation. However, the cloned P. furiosus gdh (glutamate dehydrogenase) gene showed the same activity. We therefore concluded that overexpression of any protein can produce an artificial growth inhibition or stationary phase in recA mutant cells, which allows cells to recover from UV damage due to the action of repair systems that do not require RecA-like activity.