INVESTIGADORES
BIGI Fabiana
artículos
Título:
Mce2R from Mycobacterium tuberculosis represses the expression of the mce2 operon.
Autor/es:
M. SANTANGELO; F. BLANCO; E. CAMPOS; M. SORIA; M. BIANCO; L. KLEPP; A. ALITO; O. ZABAL; A. CATALDI; F. BIGI
Revista:
Tuberculosis (Edinb)
Editorial:
Elsevier
Referencias:
Lugar: Edimburgo; Año: 2009 vol. 89 p. 22 - 28
ISSN:
1472-9792
Resumen:
The mce2 operon is one of the four mce operons present in Mycobacterium tuberculosis that encode exported proteins with a probable role in the virulence mechanisms of this bacterium. In the present study we demonstrated that Rv0586, which encodes a putative GntR-like regulator, is part of the mce2 operon. By using a promoter-lacZ fusion approach and bioinformatics tools, we found that Rv0586 represses the expression of Mce2 proteins and of a putative endonuclease IV, encoded by end (Rv0670) gene. For this reason, we have re-named the repressor protein Mce2R. By gel-shift experiments Mce2R binding was determined to be located within the mce2 promoter region. In addition, two FadR-like operator motifs were identified within the promoter regions of both the mce2 operon and the end gene. These motifs overlap putative -10 and -35 promoter boxes. M. tuberculosis carrying mce2 and end promoter-lacZ fusions were used to infect J774 macrophage-like cells. Expression of beta-galactosidase was induced after phagocytocis, suggesting that some cellular factor could be a key component of the molecular switch regulation expression of the mce2 operon. In conclusion, these results add novel evidence of the complex regulation of mce operon expression.