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The mycobacterial iron‐dependent regulator IdeR induces ferritin ( bfrB ) by alleviating L sr2 repression
Author(s) -
Kurthkoti Krishna,
Tare Priyanka,
Paitchowdhury Rakhi,
Gowthami Vykuntham Naga,
Garcia Maria J.,
Colangeli Roberto,
Chatterji Dipankar,
Nagaraja Valakunja,
Rodriguez G. Marcela
Publication year - 2015
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 - 10.1111/mmi.13166
Subject(s) - repressor , biology , psychological repression , transcription (linguistics) , microbiology and biotechnology , transcription factor , regulator , transcriptional regulation , regulation of gene expression , gene , gene expression , biochemistry , linguistics , philosophy
Summary Emerging evidence indicates that precise regulation of iron ( F e) metabolism and maintenance of F e homeostasis in M ycobacterium tuberculosis ( Mtb ) are essential for its survival and proliferation in the host. IdeR is a central transcriptional regulator of Mtb genes involved in F e metabolism. While it is well understood how IdeR functions as a repressor, how it induces transcription of a subset of its targets is still unclear. We investigated the molecular mechanism of IdeR ‐mediated positive regulation of bfrB , the gene encoding the major F e‐storage protein of Mtb . We found that bfr B induction by F e required direct interaction of IdeR with a DNA sequence containing four tandem IdeR ‐binding boxes located upstream of the bfr B promoter. Results of in vivo and in vitro transcription assays identified a direct repressor of bfr B , the histone‐like protein L sr2. IdeR counteracted L sr2‐mediated repression in vitro , suggesting that IdeR induces bfrB transcription by antagonizing the repressor activity of Lsr 2. Together, these results elucidate the main mechanism of bfrB positive regulation by IdeR and identify Lsr 2 as a new factor contributing to F e homeostasis in mycobacteria.