CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
artículos
Título:
Regulation of testosterone degradation in Comamonas testosteroni
Autor/es:
LINARES MAURICIO; PRUNEDA-PAZ JL; REYNA LUCIANA; GENTI-RAIMONDI SUSANA
Revista:
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
Editorial:
Pergamon Press
Referencias:
Lugar: Oxford; Año: 2008 vol. 112 p. 145 - 150
ISSN:
0960-0760
Resumen:
Recently, we have identified a gene encoding a LuxR-type factor, TeiR (Testosterone-inducible Regulator),
which positively regulates steroid degradation in Comamonas testosteroni. Herein, we demonstrate that
TeiR interacts in vivo with steroid catabolic gene promoters. The presence of testosterone induces a significant
TeiR protein increase at the early logarithmic phase of growth. Interestingly, it is not until the
early stationary phase where the activation of a steroid-inducible gene promoter is observed, indicating
that testosterone might not be the true inductor of the steroid degradation pathway. In addition,Testosterone-inducible Regulator),
which positively regulates steroid degradation in Comamonas testosteroni. Herein, we demonstrate that
TeiR interacts in vivo with steroid catabolic gene promoters. The presence of testosterone induces a significant
TeiR protein increase at the early logarithmic phase of growth. Interestingly, it is not until the
early stationary phase where the activation of a steroid-inducible gene promoter is observed, indicating
that testosterone might not be the true inductor of the steroid degradation pathway. In addition,Comamonas testosteroni. Herein, we demonstrate that
TeiR interacts in vivo with steroid catabolic gene promoters. The presence of testosterone induces a significant
TeiR protein increase at the early logarithmic phase of growth. Interestingly, it is not until the
early stationary phase where the activation of a steroid-inducible gene promoter is observed, indicating
that testosterone might not be the true inductor of the steroid degradation pathway. In addition,in vivo with steroid catabolic gene promoters. The presence of testosterone induces a significant
TeiR protein increase at the early logarithmic phase of growth. Interestingly, it is not until the
early stationary phase where the activation of a steroid-inducible gene promoter is observed, indicating
that testosterone might not be the true inductor of the steroid degradation pathway. In addition,
-galactosidase expression driven by a testosterone-inducible promoter is prematurely activated in cells
cultured in medium supplemented with ethyl acetate extracts obtained from the early stationary phase
cell-free supernatants of C. testosteroni grown in presence of testosterone. Complementation experiments
of C. testosteroni wild type performed with teiR deletion constructs indicate that extra-copies of deleted-
TeiR exert a dominant negative effect on the wild-type TeiR protein. While, when C. testosteroni teiR-galactosidase expression driven by a testosterone-inducible promoter is prematurely activated in cells
cultured in medium supplemented with ethyl acetate extracts obtained from the early stationary phase
cell-free supernatants of C. testosteroni grown in presence of testosterone. Complementation experiments
of C. testosteroni wild type performed with teiR deletion constructs indicate that extra-copies of deleted-
TeiR exert a dominant negative effect on the wild-type TeiR protein. While, when C. testosteroni teiRC. testosteroni grown in presence of testosterone. Complementation experiments
of C. testosteroni wild type performed with teiR deletion constructs indicate that extra-copies of deleted-
TeiR exert a dominant negative effect on the wild-type TeiR protein. While, when C. testosteroni teiRC. testosteroni wild type performed with teiR deletion constructs indicate that extra-copies of deleted-
TeiR exert a dominant negative effect on the wild-type TeiR protein. While, when C. testosteroni teiRC. testosteroni teiR
mutants were used to carry out complementation assays only the full length gene can overcome the teiRteiR
mutant phenotype. Altogether these findings indicate that TeiR regulates steroid catabolic genes interacting
with their promoters and suggest that this interaction requires the presence of a testosterone-derived
metabolite to induce the system.