Heat shock transcription factor σ32 defective in membrane transport can be suppressed by transposon insertion into genes encoding a restriction enzyme subunit or a putative autotransporter in Escherichia coli

• Published in: Genes & Genetic Systems Vol. 93; no. 6; pp. 229 - 235
• Main Authors: Yura, Takashi, Miyazaki, Ryoji, Fujiwara, Keigo, Ito, Koreaki, Chiba, Shinobu, Mori, Hiroyuki, Akiyama, Yoshinori
• Format: Journal Article
• Language: English
• Published: The Genetics Society of Japan 01.12.2018
• Subjects: feedback control; heat shock response; membrane transport; protein homeostasis; σ32
• ISSN: 1341-7568; 1880-5779
• DOI: 10.1266/ggs.18-00040

Heat shock transcription factor σ32 of Escherichia coli plays a major role in protein homeostasis and requires membrane localization for regulation. We here report that a strongly deregulated I54N-σ32 mutant defective in association with the membrane can be phenotypically suppressed by Tn5 insertion into the mcrC or ydbA2 gene, encoding a restriction enzyme subunit or part of a putative autotransporter, respectively. The suppression is specific for mutant I54N-σ32 and reduces its activity but not its abundance or stability. Moreover, the deregulated phenotype of I54N-σ32 is effectively suppressed by a plasmid carrying the same mcrC::Tn5 mutation. In contrast, deletion of the mcrC or ydbA2 gene hardly affects I54N-σ32 activity. These results, taken together, suggest that the truncated form of McrC (and presumably also of YdbA2) protein produced by the Tn5 insertion interacts specifically with I54N-σ32 to reduce its activity without substantially affecting its amount or stability.