SUPPRESSORS OF A SPO0A MISSENSE MUTATION AND THEIR EFFECTS ON SPORULATION IN BACILLUS-SUBTILIS
SUPPRESSORS OF A SPO0A MISSENSE MUTATION AND THEIR EFFECTS ON SPORULATION IN BACILLUS-SUBTILIS
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DOI：
10.1016/0300-9084(92)90140-a
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发表时间：
1992-07-01
期刊：
影响因子：
3.9
通讯作者：
DEVIVO, R
中科院分区：
文献类型：
--
作者：
GROSSMAN, AD;LEWIS, T;DEVIVO, R
枯草芽孢杆菌的spo0A基因产物是孢子形成起始所需的转录调节因子。尚不可能分离抑制由spo0A无效突变引起的孢子形成缺陷的突变。我们描述的突变，抑制严重的孢子形成缺陷引起的spo0A错义突变（spo0A9V）的分离和表征。两个抑制基因突变，spa2和spa4，其特征在于与spo0A9V突变的组合，并从spo0A9V突变分离。两者都位于Spo0A的羧基一半，在推定的DNA结合，转录激活区。spa2位于密码子174，导致亮氨酸变为精氨酸（spo0A174LR），spa4位于密码子162（共267个），导致组氨酸变为精氨酸（spo0A162HR）。spa2和spa4显著恢复spo0A9V突变体的孢子形成，然而，耐热孢子的出现相对于野生型延迟。当与spo0A9V分离时，即作为spo0A中的单突变，spa4引起孢子形成延迟，而spa2允许明显正常的孢子形成。当与其他早期孢子形成突变相结合时，spa突变引起了有趣的表型。spa2抑制spo0E11引起的孢子形成缺陷。这在spo0E11 abrB双突变体中最容易看到，其具有比spo0E11单突变体严重得多的孢子形成缺陷。也就是说，spo0E11和abrB突变导致合成（协同）孢子形成表型。spa2 spo0A9V和spa4 spo0A9V等位基因都大大增强了spoIIJ、spo0J和spo0K突变引起的孢子形成缺陷。这些合成孢子形成缺陷的意义进行了讨论。
The spo0A gene product of Bacillus subtilis is a transcriptional regulator that is required for the initiation of sporulation. It has not been possible to isolate mutations that suppress the sporulation defect caused by spo0A null mutations. We describe the isolation and characterization of mutations that suppress the severe sporulation defect caused by a spo0A missense mutation (spo0A9V). Two suppressor mutations, spa2 and spa4, have been characterized in combination with, and separated from, the spo0A9V mutation. Both were located in the carboxyl half of Spo0A, in the putative DNA binding, transcriptional activation region. spa2 was in codon 174, causing a leucine to arginine change (spo0A174LR), and spa4 was in codon 162 (of 267), causing a histidine to arginine change (spo0A162HR). spa2 and spa4 significantly restored sporulation to the spo0A9V mutant, however, the appearance of heat resistant spores was delayed relative to wild-type. When separated from spo0A9V, that is, as single mutations in spo0A, spa4 caused a delay in sporulation, while spa2 allowed apparently normal sporulation. The spa mutations caused interesting phenotypes when combined with other early sporulation mutations. spa2 suppressed the sporulation defect caused by spo0E11. This was most easily seen in spo0E11 abrB double mutants, which had a much more severe sporulation defect than the spo0E11 single mutant. That is, spo0E11 and abrB mutations caused a synthetic (synergistic) sporulation phenotype. Both the spa2 spo0A9V and the spa4 spo0A9V alleles greatly enhanced the sporulation defect caused by mutations in spoIIJ, spo0J and spo0K. The significance of these synthetic sporulation defects is discussed.