真核生物GTP酶对原核生物孢子形成和运动缺陷的互补作用。
Complementation of sporulation and motility defects in a prokaryote by a eukaryotic GTPase.
作者信息
Hartzell P L
机构信息
Department of Microbiology, Molecular Biology, and Biochemistry, University of Idaho, Moscow, ID 83844-3052, USA.
出版信息
Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9881-6. doi: 10.1073/pnas.94.18.9881.
The complex prokaryote, Myxococcus xanthus, undergoes a program of multicellular development when starved for nutrients, culminating in sporulation. M. xanthus makes MglA, a 22-kDa, soluble protein that is required for both multicellular development and gliding motility. MglA is similar in sequence to the Saccharomyces cerevisiae SAR1 protein, a member of the Ras/Rab/Rho superfamily of small eukaryotic GTPases. The SAR1 gene, when integrated into the M. xanthus genome, complements the sporulation defect of a DeltamglA strain. A forward, second-site mutation on the M. xanthus chromosome, rpm, in combination with SAR1, restores fruiting body morphogenesis and gliding motility to a DeltamglA strain. The result that the rpm mutation suppresses the substitution of SAR1 for mglA suggests that Sar1p interacts with other M. xanthus proteins to control the motility-dependent aggregation of cells during development.
复杂的原核生物黄色粘球菌（Myxococcus xanthus）在缺乏营养时会经历一个多细胞发育过程，最终形成孢子。黄色粘球菌产生MglA，这是一种22 kDa的可溶性蛋白质，多细胞发育和滑行运动都需要它。MglA在序列上与酿酒酵母（Saccharomyces cerevisiae）的SAR1蛋白相似，后者是小真核GTP酶的Ras/Rab/Rho超家族成员。当SAR1基因整合到黄色粘球菌基因组中时，可弥补ΔmglA菌株的孢子形成缺陷。黄色粘球菌染色体上的一个正向第二位点突变rpm与SAR1共同作用，可恢复ΔmglA菌株的子实体形态发生和滑行运动。rpm突变抑制了用SAR1替代mglA的结果，这表明Sar1p与黄色粘球菌的其他蛋白质相互作用，以控制发育过程中细胞的运动依赖性聚集。
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