Transcription Of The Brucella abortus VirB Operon Is Metabolically Linked To Histidine Catabolism

SIEIRA, R.; DIEGO JOSE COMERCI; UGALDE, R. A.

Mar del Plata

Congreso; XLIII Reunion Anual Sociedad Argentina de Investigacion en Bioquimica y Biologia Molecular; 2007

The virB operon codes for a type-IV secretion system that is essential for the pathogenesis of bacteria belonging to the genus Brucella. During the first hours of intracellular infection of macrophages the VirB expression is tightly regulated invirB operon codes for a type-IV secretion system that is essential for the pathogenesis of bacteria belonging to the genus Brucella. During the first hours of intracellular infection of macrophages the VirB expression is tightly regulated inBrucella. During the first hours of intracellular infection of macrophages the VirB expression is tightly regulated in Brucella abortus. Recently, as a part of a virB-transcription factor identification project, we identified a protein that binds specifically the virB promoter. This protein (HutC) is a transcriptional regulator involved in control of the hut (for histidine-utlilization) operon and it also participates in transcriptional regulation of the virB operon. Here we show that DNA-binding activity of HutC is negatively regulated by urocanate (an intermediate of histidine catabolism) in both hut and virB promoters. Apparent dissociation constants for HutC binding to both promoters were analyzed. In order to study the possible regulatory link between hut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered by. Recently, as a part of a virB-transcription factor identification project, we identified a protein that binds specifically the virB promoter. This protein (HutC) is a transcriptional regulator involved in control of the hut (for histidine-utlilization) operon and it also participates in transcriptional regulation of the virB operon. Here we show that DNA-binding activity of HutC is negatively regulated by urocanate (an intermediate of histidine catabolism) in both hut and virB promoters. Apparent dissociation constants for HutC binding to both promoters were analyzed. In order to study the possible regulatory link between hut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byvirB promoter. This protein (HutC) is a transcriptional regulator involved in control of the hut (for histidine-utlilization) operon and it also participates in transcriptional regulation of the virB operon. Here we show that DNA-binding activity of HutC is negatively regulated by urocanate (an intermediate of histidine catabolism) in both hut and virB promoters. Apparent dissociation constants for HutC binding to both promoters were analyzed. In order to study the possible regulatory link between hut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byhut (for histidine-utlilization) operon and it also participates in transcriptional regulation of the virB operon. Here we show that DNA-binding activity of HutC is negatively regulated by urocanate (an intermediate of histidine catabolism) in both hut and virB promoters. Apparent dissociation constants for HutC binding to both promoters were analyzed. In order to study the possible regulatory link between hut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byvirB operon. Here we show that DNA-binding activity of HutC is negatively regulated by urocanate (an intermediate of histidine catabolism) in both hut and virB promoters. Apparent dissociation constants for HutC binding to both promoters were analyzed. In order to study the possible regulatory link between hut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byhut and virB promoters. Apparent dissociation constants for HutC binding to both promoters were analyzed. In order to study the possible regulatory link between hut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byhut and virB systems, we constructed B. abortus deletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered bydeletion mutants for different hut genes that participate in urocanate metabolism. These mutants have a defective intracellular virB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byvirB-expression, indicating that its regulation is connected to histidine catabolism. Using different culture media we observed that HutC participates in transcriptional regulation of the virB operon under a very definite culture condition that resembles the harsh environment encountered byvirB operon under a very definite culture condition that resembles the harsh environment encountered by Brucella during its intracellular transit.during its intracellular transit.