HigA is the antitoxin of the translation-dependent mRNA interferase toxin HigB .
Ectopic expression of higB causes inhibition of cell growth which is alleviated by co-expression of higA .
The promoter upstream of higB appears to be autorepressed by HigA; Lon protease is required for activation of transcription. Transcription is induced by chloramphenicol treatment as well as amino acid starvation induced by serine hydroxamate .
Two HigA monomers dimerize at their N-terminal domain, and α1 is essential for this dimerization which generates the arrangement of the HigB-(HigA)2-HigB complex. The HigA C-terminal domain with a helix-turn-helix (HTH) fold is essential for DNA binding and for expression of the higBA operon 
HigA has the highest affinity at the -27 site overlapping with the promoter -35 region 
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|Connectivity class:||Local Regulator|
|Length:||417 bp / 138 aa|
|TU(s) encoding the TF:||
|Regulated gene(s)||higA, higB|
|Multifun term(s) of regulated gene(s)||
MultiFun Term (List of genes associated to the multifun term)
transcriptional level (1)
translation attenuation and efficiency (1)
|First gene in the operon(s)||higB|
|Simple and complex regulons|
|Simple and complex regulatory phrases||
Regulatory phrase (List of promoters regulated by the phrase)
|Functional conformation||Function||Promoter||Sigma factor||Central Rel-Pos||Distance to first Gene||Genes||Sequence||LeftPos||RightPos||Evidence (Confirmed, Strong, Weak)||References|
|Evolutionary conservation of regulatory elements|
 Christensen-Dalsgaard M., Jorgensen MG., Gerdes K., 2010, Three new RelE-homologous mRNA interferases of Escherichia coli differentially induced by environmental stresses., Mol Microbiol. 75(2):333-48