Ozga D A, Lara J C, Leig J A
Department of Microbiology, University of Washington, Seattle 98195.
Mol Plant Microbe Interact. 1994 Nov-Dec;7(6):758-65. doi: 10.1094/mpmi-7-0758.
We show that two exopolysaccharide overproducing Tn5 mutants of Rhizobium meliloti, exoR and exoS, have distinct symbiotic defects. While the exoR mutant is unable to colonize nodules, the exoS mutant retains that ability but varies in its ability to produce nitrogen-fixing nodules. We correlate these defects with different degrees of exopolysaccharide overproduction and growth impairment. We further show that the exoR mutant is able to enter developing infection threads but is unable to invade nodule cells. The exoR mutant gives rise to spontaneous pseudorevertants containing second-site suppressor mutations that decrease exopolysaccharide synthesis. These pseudorevertants form nitrogen-fixing nodules. Although the suppressor mutations have the opposite effect on exopolysaccharide production compared to the exoS::Tn5 mutation, they consistently map to the exoS::Tn5 region and belong to the same genetic complementation group as defined by transposon insertion mutations. The effect of the suppressor mutations on exopolysaccharide production is correlated with effects on the expression of exo genes involved in exopolysaccharide synthesis. Finally, we provide evidence that the exoR gene is not required for the regulation of exopolysaccharide synthesis by ammonia.
我们发现，苜蓿根瘤菌的两个胞外多糖高产Tn5突变体exoR和exoS具有不同的共生缺陷。exoR突变体无法在根瘤中定殖，而exoS突变体保留了这种能力，但在产生固氮根瘤的能力上有所不同。我们将这些缺陷与不同程度的胞外多糖过量产生和生长受损联系起来。我们进一步表明，exoR突变体能够进入正在发育的感染丝，但无法侵入根瘤细胞。exoR突变体会产生含有第二位点抑制突变的自发假回复体，这些突变会减少胞外多糖的合成。这些假回复体形成固氮根瘤。尽管与exoS::Tn5突变相比，抑制突变对胞外多糖产生的影响相反，但它们始终定位在exoS::Tn5区域，并且属于由转座子插入突变定义的同一遗传互补群。抑制突变对胞外多糖产生的影响与对参与胞外多糖合成的exo基因表达的影响相关。最后，我们提供证据表明，氨对胞外多糖合成的调控不需要exoR基因。
