Cheng Jiujun, Sibley Christopher D, Zaheer Rahat, Finan Turlough M
Center for Environmental Genomics, Department of Biology, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
Microbiology (Reading). 2007 Feb;153(Pt 2):375-387. doi: 10.1099/mic.0.2006/001362-0.
Sinorhizobium meliloti differentiates from rod-shaped, free-living cells into pleomorphic, non-dividing, N(2)-fixing bacteroids within alfalfa root nodules. Here, the role of the minCDE genes in bacteroid differentiation and in free-living cell division is examined. Disruption of the minE gene resulted in large, swollen and branched free-living cells, and in symbiosis a minE mutation resulted in a defect in nitrogen fixation with activity reduced by approximately 70 % compared to the wild-type. It has been demonstrated that the minCDE genes form an operon driven by a promoter located 173 bp upstream of minC. The minCDE genes were expressed in free-living cells and in both the infection zone and the symbiotic zone of alfalfa nodules; however, no changes in the free-living cell morphology, growth or symbiotic N(2) fixation were detected as a result of deletion of these genes. Induced production of individual or combinations of Min proteins in S. meliloti altered its rod-shaped cell morphology. Moreover, cell morphologies resulting from the overexpression of the S. meliloti Min proteins in Escherichia coli suggested similar functions for the E. coli and S. meliloti min genes. These data suggest that there is greater redundancy in the roles of cell division genes in S. meliloti compared with E. coli.
苜蓿中华根瘤菌可从杆状的自由生活细胞分化为苜蓿根瘤内多形态、不分裂且固氮的类菌体。本文研究了minCDE基因在类菌体分化和自由生活细胞分裂中的作用。minE基因的破坏导致自由生活细胞变大、肿胀且分支，在共生过程中，minE突变导致固氮缺陷，与野生型相比活性降低约70%。已证明minCDE基因形成一个由位于minC上游173 bp处的启动子驱动的操纵子。minCDE基因在自由生活细胞以及苜蓿根瘤的感染区和共生区均有表达；然而，缺失这些基因后，未检测到自由生活细胞形态、生长或共生固氮的变化。在苜蓿中华根瘤菌中诱导产生单个或组合的Min蛋白会改变其杆状细胞形态。此外，苜蓿中华根瘤菌Min蛋白在大肠杆菌中过表达所产生的细胞形态表明大肠杆菌和苜蓿中华根瘤菌的min基因具有相似功能。这些数据表明，与大肠杆菌相比，苜蓿中华根瘤菌中细胞分裂基因的作用存在更大的冗余。
