Mycobacterium tuberculosis gene expression profiling within the context of protein networks.
As one of the world's most successful intracellular pathogens, Mycobacterium tuberculosis, the causative agent of human tuberculosis, is responsible for two to three million deaths annually. The pathogenicity of M. tuberculosis relies on its ability to survive and persist within host macrophage cells during infection. It is of central importance, therefore, to identify genes and pathways that are involved in the survival and persistence of M. tuberculosis within these cells. Utilizing genome-wide DNA arrays we have identified M. tuberculosis genes that are specifically induced during macrophage infection. To better understand the cellular context of these differentially expressed genes, we have also combined our array analyses with computational methods of protein network identification. Our combined approach reveals certain signatures of M. tuberculosis residing within macrophage cells, including the induction of genes involved in DNA damage repair, fatty acid degradation, iron metabolism, and cell wall metabolism.
Rachman
Helmy
H
Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 21-22, 10117 Berlin, Germany.
Strong
Michael
M
Schaible
Ulrich
U
Schuchhardt
Johannes
J
Hagens
Kristine
K
Mollenkopf
Hans
H
Eisenberg
David
D
Kaufmann
Stefan H E
SH
D000596:Amino Acids / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism*; D001692:Biological Transport / Q000235:genetics; D002462:Cell Membrane / Q000378:metabolism; D002473:Cell Wall / Q000378:metabolism; D016000:Cluster Analysis; D004260:DNA Repair / Q000235:genetics / Q000502:physiology; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D007501:Iron / Q000378:metabolism; D050356:Lipid Metabolism; D009169:Mycobacterium tuberculosis / Q000235:genetics* / Q000378:metabolism*; D015854:Up-Regulation
D000596:Amino Acids; D001426:Bacterial Proteins; D007501:Iron