Sulphate repression of ssuD -dependent alkanesulphonate-sulphur assimilation in Escherichia coli

cells utilize alkanesulphonates including taurine as the sulphur source. We previously reported that when cells carrying a double deletion in and were inoculated into a taurine-containing minimal medium, they started to grow only after long-term incubation (Nishikawa . 2018, 164: 1446-1456). We show...

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Veröffentlicht in:Microbiology (Society for General Microbiology) 2022-06, Vol.168 (6)
Hauptverfasser: Nishikawa, Masanobu, Noda, Soichiro, Henmi, Kenji, Ogawa, Ken'ichi
Format: Artikel
Sprache:eng
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Zusammenfassung:cells utilize alkanesulphonates including taurine as the sulphur source. We previously reported that when cells carrying a double deletion in and were inoculated into a taurine-containing minimal medium, they started to grow only after long-term incubation (Nishikawa . 2018, 164: 1446-1456). We show here that cells that can induce -dependent alkanesulphonate-sulphur assimilation (SASSA) are essentially rare, but suppressors that can induce SASSA appear during long-term incubation. Mutant cells carrying and or generated suppressor cells that can induce SASSA at a frequency of about 10 in a population. Whereas cells without prior SASSA did not express even when necessary, the cells with prior SASSA properly expressed . Whole-genome DNA sequencing of a clone isolated from cells with prior SASSA revealed that the influx of sulphate or thiosulphate may be related to the regulation of SASSA. To clarify whether sulphate or thiosulphate affects the induction of SASSA, the effect of mutations in and , which are responsible for sulphate and thiosulphate uptake with different preferences for substrates, was examined. Only the mutant did not show repression of SASSA when no sulphate was added to the medium. When the concentration of the sulphate added was over 10 μM, the mutant showed repression of SASSA. Therefore, it was considered that the influx of extracellular sulphate resulted in repression of SASSA.
ISSN:1350-0872
1465-2080
DOI:10.1099/mic.0.001190