J. Bacteriol., Jan 1998, 195-200, Vol 180, No. 2
X Zhang and R Schleif
We have studied catabolite gene activator protein (CAP) activation at the
araBAD promoter, pBAD, in the absence of DNA looping. We ruled out the two
most plausible indirect activation mechanisms: CAP-induced folding of
upstream DNA back upon RNA polymerase, and CAP-induced stabilization of
AraC binding to DNA. Therefore, a direct CAP-RNA polymerase interaction
seemed likely. We sought and found CAP mutants defective in transcription
activation at pBAD that retained normal DNA binding affinity. Some
mutations altered residues in the interval from positions 150 to 164 that
includes CAP activating region 1 (AR1), which has been shown to contact RNA
polymerase at a number of promoters. Unexpectedly, additional mutations
were found that altered residues in the region between positions 46 and 68
and at position 133. This includes the region known as activating region 3
(AR3). Mutations from both groups also affect the araFGH and rhaBAD
promoters.
Copyright © 1998, American Society for Microbiology
Catabolite gene activator protein mutations affecting activity of the araBAD promoter [In Process Citation]
Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, USA.
This article has been cited by other articles:
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
| ALL ASM JOURNALS |