Disease relevance of furA

• Regulation of catalase-peroxidase (KatG) expression, isoniazid sensitivity and virulence by furA of Mycobacterium tuberculosis [1].

High impact information on furA

• Interestingly, a furA-lacking strain induced the complex at lower concentrations of INH compared with the control strain, whereas higher INH concentrations were necessary to induce the complex in a strain that lacks katG, suggesting that INH needs to be activated by KatG to induce the KasA-containing complex [2].
• No promoter activity was demonstrated downstream of the furA start codon, using different gene reporter systems, indicating that furA and katG are co-transcribed from a common regulatory region [1].
• In this work we analyzed the M. tuberculosis furA promoter region [3].
• The Mycobacterium tuberculosis genome encodes two ferric uptake regulator homologues, furA and furB, the function of which is under investigation [4].

Biological context of furA

• Transcriptional regulation of furA and katG upon oxidative stress in Mycobacterium smegmatis [5].

Associations of furA with chemical compounds

• In the absence of furA, katG was upregulated, cells became hypersensitive to isoniazid, and full virulence was restored, indicating that furA regulates the transcription of both genes [1].

Regulatory relationships of furA

• This association suggested that furA might regulate katG and other genes involved in pathogenesis [1].

Other interactions of furA

• Transcript mapping showed katG to be expressed from a strong promoter, with consensus -10 and -35 elements, preceding furA [1].

Analytical, diagnostic and therapeutic context of furA

• The transcription pattern of furA and katG in M. smegmatis upon oxidative stress was analyzed by Northern blotting and primer extension [5].
• M. tuberculosis FurA was purified and found to bind upstream of furA by gel shift analysis [3].
• Although transcription of both furA and katG was induced upon oxidative stress, transcripts covering both genes could not be identified either by Northern blotting or by reverse transcriptase PCR [5].

References