A Sinorhizobium meliloti minE mutant has an altered morphology and exhibits defects in legume symbiosis

Abstract

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.

Polar growth in the Alphaproteobacterial order Rhizobiales

“…1A) suggests an ancestral origin of budding, indicating that members of the Rhizobiaceae and Brucellaceae families may also grow by polar extension rather than their usually assumed dispersed mode of growth. Further support for this hypothesis is provided by the observation that mutations or treatments that impair cell division in Brucella abortus (10,11), Sinorhizobium meliloti (12,13), and Agrobacterium tumefaciens (14-18) cause branching morphologies to arise, rather than filamentation. Finally, the genomes of bacteria belonging to the Rhizobiaceae and Brucellaceae families lack known modulators of cell elongation, including a single gene cluster encoding the elongase proteins MreBCD, RodA, and PBP2, suggesting that cell growth may proceed via an alternative mechanism (19,20).…”

Molecular Determinants of a Symbiotic Chronic Infection

“…Several S. meliloti genes involved in cell division have been characterized, for instance ftsZ1 and ftsZ2 (108,110,111), as well as minCDE (28). Blocking the process of cell division via overexpression of ftsZ1 or minCD causes altered cell morphology during free-living growth that is reminiscent of the branched and filamentous bacteroid (28,95). Treatment of S. meliloti with DNA-damaging agents, which impinge on DNA replication and cell division in other bacteria, also inhibits cell division and results in branched cell morphology (95).…”

Global analysis of cell cycle gene expression of the legume symbiontSinorhizobium meliloti

“…For example, it has been shown that altering the expression of genes central to S. meliloti cell cycle processes (i.e., ftsZ, dnaA, minE, and ccrM) produces bacteroid-like polyploid cells (10)(11)(12)(13) and that mutation of conserved cell cycle regulators (cbrA, cpdR1, and divJ) blocks bacteroid formation and symbiosis (14)(15)(16). Furthermore, in the α-proteobacterium Caulobacter crescentus, the cellular differentiation program governing morphological and replicative asymmetry in progeny cells is genetically integrated with the cell cycle (17).…”