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Mechanisms of iron regulation in mycobacteria: role in physiology and virulence
Author(s) -
Rodriguez G. Marcela,
Smith Issar
Publication year - 2003
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2003.03384.x
Subject(s) - biology , repressor , oxidative stress , virulence , microbiology and biotechnology , mycobacterium tuberculosis , bacteria , siderophore , transcription factor , oxidative phosphorylation , regulator , gene , tuberculosis , biochemistry , genetics , medicine , pathology
Summary The role of iron in mycobacteria as in other bacteria goes beyond the need for this essential cofactor. Limitation of this metal triggers an extensive response aimed at increasing iron acquisition while coping with iron deficiency. In contrast, iron‐rich environments prompt these prokaryotes to induce synthesis of iron storage molecules and to increase mechanisms of protection against iron‐mediated oxidative damage. The response to changes in iron availability is strictly regulated in order to maintain sufficient but not excessive and potentially toxic levels of iron in the cell. This response is also linked to other important processes such as protection against oxidative stress and virulence. In bacteria, iron metabolism is regulated by controlling transcription of genes involved in iron uptake, transport and storage. In mycobacteria, this role is fulfilled by the i ron‐ d ependent r egulator IdeR. IdeR is an essential protein in Mycobacterium tuberculosis , the causative agent of human tuberculosis. It functions as a repressor of iron acquisition genes, but is also an activator of iron storage genes and a positive regulator of oxidative stress responses.