Pearce S M
Can J Microbiol. 1976 Jul;22(7):1007-12. doi: 10.1139/m76-147.
Previous studies on this cortexless mutant of Bacillus cereus var. alesti indicated that the forespore membrane was the site of the biochemical lesion. This hypothesis is supported by the results presented here: fatty acid composition of sporulating cells of themutant is altered, while in vegetative cells it is comparable to the parent; soluble precursors of peptidoglycan synthesis are accumulated in the mutant, at the time of cortex formation; homogenates of the mutant prepared at the time of cortex formation are unable to incorporate tritiated diaminopimelic acid into peptidoglycan, while homogenates of cells forming germ cell wall do so to an extent comparable to that of the parent; lipid-linked intermediates are formed by the mutant as in the parent. Apparently the mutant is unable either to transfer disaccharide penta-peptide units from the carrier lipid to the growing peptidoglycan acceptor, or to transport lipid-linked intermediates across the forespore membrane.
先前对蜡样芽孢杆菌变种阿莱斯特无皮层突变体的研究表明,前芽孢膜是生化损伤的部位。本文给出的结果支持了这一假说:突变体芽孢形成细胞的脂肪酸组成发生了改变,而营养细胞中的脂肪酸组成与亲本相当;在皮层形成时,突变体中积累了肽聚糖合成的可溶性前体;在皮层形成时制备的突变体匀浆无法将氚标记的二氨基庚二酸掺入肽聚糖中,而形成生殖细胞壁的细胞匀浆掺入的程度与亲本相当;突变体与亲本一样形成脂质连接中间体。显然,突变体要么无法将二糖五肽单元从载体脂质转移到正在生长的肽聚糖受体上,要么无法将脂质连接中间体转运过前芽孢膜。