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