1887

Abstract

Several features distinguish laboratory and undomesticated strains of . For example, unlike the laboratory strain 168, the undomesticated strain ATCC 6051 is deficient in sporulation in a rich sporulation medium, 2× SG. ATCC 6051 cannot induce transcription of the operon, suggesting that this strain has a defect in initiation of sporulation. To determine the genetic difference between 168 and ATCC 6051, the DNA region responsible for the Spo phenotype was transferred to strain 168. Genetic mapping and DNA sequencing analysis revealed that a stop codon (TAA) for in 168 is replaced with Lys (TAT) in ATCC 6051, making the open reading frame 201 bp longer in the undomesticated strain ATCC 6051. Introduction of from strain 168 restored sporulation in ATCC 6051, indicating that the difference in is responsible for the Spo phenotype of ATCC 6051. A potential -independent terminator is located upstream of a stop codon for the extended open reading frame in ATCC 6051. Northern blot analysis showed that transcription of terminated at this terminator, and mRNA is missing a stop codon in ATCC 6051. Moreover, deletion of tmRNA suppresses the sporulation defect in ATCC 6051. These observations indicate that in ATCC 6051 the absence of a stop codon in mRNA affects sporulation, probably by leading to rapid degradation of KinA via the -translation process. In ATCC 6051, the mutation affects sporulation but not other Spo0A-dependent phenomena such as biofilm formation, which can be activated by a low level of Spo0A∼P. This is due to the fact that KinA activity is kept low during the exponential phase via transcriptional and post-translational regulation. Thus, the stop-codon-less probably affects only sporulation. DNA sequencing of 30 strains revealed that another strain also produces stop-codon-less mRNA. This observation suggests that the lack of a stop codon for mRNA may give rise to a selective advantage under certain conditions.

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2008-01-01
2024-04-25
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