Disruption of sscR encoding a gamma-butyrolactone autoregulator receptor in Streptomyces scabies NBRC 12914 affects production of secondary metabolites
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- bakteriální proteiny chemie genetika metabolismus MeSH
- gama-butyrolakton metabolismus MeSH
- klonování DNA MeSH
- molekulární sekvence - údaje MeSH
- receptory GABA-A chemie genetika metabolismus MeSH
- regulace genové exprese u bakterií MeSH
- regulační geny * MeSH
- sekvence aminokyselin MeSH
- sekvenční seřazení MeSH
- Streptomyces chemie genetika metabolismus MeSH
- umlčování genů * MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 4-butyrolactone receptor MeSH Prohlížeč
- bakteriální proteiny MeSH
- gama-butyrolakton MeSH
- receptory GABA-A MeSH
We report the cloning and sequence analysis of a gamma-butyrolactone autoregulator regulatory island that includes an sscR gene encoding the gamma-butyrolactone autoregulator receptor from Streptomyces scabies NBRC 12914, a plant pathogenic strain. gamma-Butyrolactone autoregulators trigger secondary metabolism, and sometimes morphological differentiation in the Gram-positive genus Streptomyces through binding to a specific autoregulator receptor. This gene cluster showed close similarity to other regulatory islands of Streptomyces origin that are responsible for the control of secondary metabolism. The recombinant SscR protein expressed in Escherichia coli prefers a gamma-butyrolactone autoregulator containing a long C-2 side chain and beta-hydroxyl group at the C-6 position. An inactivation experiment confirmed that this gamma-butyrolactone autoregulator receptor was involved in secondary metabolism but had no effects on the morphological differentiation. In the sscR-deleted mutant, the binding activity of the gamma-butyrolactone autoregulator was completely abolished, suggesting that its primary role is to detect the presence of an autoregulator in the environment. HPLC analysis of the culture broth showed that some peaks disappeared and new peaks that were not present in the broth of the wild-type strain appeared.
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J Bacteriol. 1997 Nov;179(22):6986-93 PubMed
J Bacteriol. 1999 Jan;181(1):204-11 PubMed
Biosci Biotechnol Biochem. 2005 Mar;69(3):431-9 PubMed
J Bacteriol. 2002 Apr;184(7):2019-29 PubMed
FEMS Microbiol Lett. 1999 May 15;174(2):251-3 PubMed
Mol Microbiol. 1991 Dec;5(12):2861-7 PubMed
J Bacteriol. 1999 Aug;181(16):5081-4 PubMed
Gene. 1992 Jul 1;116(1):43-9 PubMed
Biosci Biotechnol Biochem. 2007 Feb;71(2):283-99 PubMed
Mol Microbiol. 2000 Apr;36(2):302-13 PubMed
Curr Opin Microbiol. 2006 Jun;9(3):287-94 PubMed
J Bacteriol. 2001 Jul;183(14):4357-63 PubMed
Mol Microbiol. 2003 Jun;48(6):1501-10 PubMed
J Bacteriol. 2005 Apr;187(7):2491-500 PubMed
Mol Microbiol. 2000 Nov;38(4):794-804 PubMed
Biosci Biotechnol Biochem. 1993 Dec;57(12):2020-5 PubMed
Nature. 2004 May 6;429(6987):79-82 PubMed
Proc Natl Acad Sci U S A. 2003 Nov 25;100 Suppl 2:14555-61 PubMed
Mol Microbiol. 2007 Feb;63(3):838-47 PubMed
J Bacteriol. 1997 Aug;179(16):5131-7 PubMed
J Mol Biol. 2004 Feb 13;336(2):409-19 PubMed
J Biol Chem. 2001 Nov 23;276(47):44297-306 PubMed
J Bacteriol. 2004 Jun;186(11):3423-30 PubMed
J Antibiot (Tokyo). 1989 May;42(5):769-78 PubMed
Dokl Akad Nauk SSSR. 1967 Nov-Dec;177(1):232-5 PubMed
J Bacteriol. 1998 Jul;180(13):3317-22 PubMed
J Bacteriol. 2002 Sep;184(18):5151-7 PubMed
FEMS Microbiol Rev. 2006 Sep;30(5):651-72 PubMed
Arch Microbiol. 2005 Dec;184(4):249-57 PubMed
Z Allg Mikrobiol. 1973;13(8):647-55 PubMed
Arch Microbiol. 2004 Jan;181(1):52-9 PubMed
J Biol Chem. 1995 May 19;270(20):12319-26 PubMed
Proc Natl Acad Sci U S A. 2007 Feb 13;104(7):2378-83 PubMed
Chem Biol. 1999 Sep;6(9):617-24 PubMed
Mol Microbiol. 2001 Sep;41(5):1015-28 PubMed
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