Yamashita S, Yoshikawa H, Kawamura F, Takahashi H, Yamamoto T, Kobayashi Y, Saito H
Mol Gen Genet. 1986 Oct;205(1):28-33. doi: 10.1007/BF02428029.
We have constructed spo0A-lacZ and spo0F-lacZ fusions with a temperate phage vector and have investigated how spo0 gene products are involved in the expression of each of these genes. The expression of spo0A-lacZ and spo0F-lacZ was stimulated at about the time of cessation of vegetative growth in Spo+ cells. This stimulation of spo0A-lacZ was impaired by mutations in the spo0B, D, E, F or H genes but was not affected by mutations in the spo0J or K genes. Similar results were obtained with the spo0F-lacZ fusion. The effect of the spo0A mutation on spo0A-lacZ expression was characteristic: the spo0A-directed beta-galactosidase activity found during vegetative growth was significantly enhanced in the spo0A mutant. This result suggests that spo0A gene expression is auto-regulated being repressed by its own gene product. Another remarkable observation was the effect of the sof-1 mutation, which is known to be a spo0A allele; it suppressed the sporulation deficiency of spo0B, spo0D and spo0F mutants. The spo0A-lacZ stimulation, which is impaired by any one of these spo0 mutations, was restored by the additional sof-1 mutation.
我们用一种温和噬菌体载体构建了spo0A - lacZ和spo0F - lacZ融合体，并研究了spo0基因产物如何参与这些基因中每一个的表达。spo0A - lacZ和spo0F - lacZ的表达在Spo + 细胞营养生长停止时受到刺激。spo0A - lacZ的这种刺激因spo0B、D、E、F或H基因的突变而受损，但不受spo0J或K基因的突变影响。spo0F - lacZ融合体也得到了类似的结果。spo0A突变对spo0A - lacZ表达的影响具有特征性：在营养生长期间发现的spo0A指导的β - 半乳糖苷酶活性在spo0A突变体中显著增强。这一结果表明spo0A基因表达受到自身基因产物的抑制而进行自我调节。另一个显著的观察结果是sof - 1突变的影响，已知它是一个spo0A等位基因；它抑制了spo0B、spo0D和spo0F突变体的孢子形成缺陷。这些spo0突变中的任何一个都会损害的spo0A - lacZ刺激，通过额外的sof - 1突变得以恢复。
