Team:Shanghai YGQ/Basic Part

Shanghai_YGQ

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Basic Part

    In contrast the ginI promoter was inactive in the ginI mutant (Fig. 5A, lane 2); however, transcription from the ginI promoter was detected . The endogenous ginR proin a ginI mutant harboring pGinIA (Fig. 5A, lane 3) at a level greater than that observed in the wild-type strain (Fig. 5A, lane 1). This enhanced transcription was probably caused by the increased copy number of the ginI promoter because we failed to distinguish between the signals from the endogenous ginI promoter and those from the exogenous ginI promoter on pGinIA. These results suggest that GinI is also required for nated ginA, is present just downstream of ginI. Because there ginI transcription. This is probably because GinR activates the ginI promoter in the presence of AHLs, as has been suggested for most LuxR homologues in quorum-sensing systems.