EXPRESSION OF NODULE-SPECIFIC GENES IN ALFALFA ROOT-NODULES BLOCKED AT AN EARLY STAGE OF DEVELOPMENT

EXPRESSION OF NODULE-SPECIFIC GENES IN ALFALFA ROOT-NODULES BLOCKED AT AN EARLY STAGE OF DEVELOPMENT
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DOI:
10.1101/gad.2.6.677
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发表时间:
1988-06-01
影响因子:
10.5
通讯作者:
AUSUBEL, FM
AUSUBEL, FM
中科院分区:
生物学1区
文献类型:
--
作者:
DICKSTEIN, R;BISSELING, T;AUSUBEL, FM

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为了帮助剖析根瘤菌-豆科植物共生的分子基础,我们利用根瘤RNA的体外翻译和Northern印迹分析,检测了紫花苜蓿根瘤菌诱导的两种发育缺陷根瘤中表达的紫花苜蓿特异基因(根瘤蛋白)。紫花苜蓿nif突变体诱导的FIX结瘤受到根瘤菌的侵染,含有分化的类杆菌。‘空’根瘤由紫花苜蓿外显子突变体、NDV突变体和携带紫花苜蓿结瘤基因的根癌农杆菌菌株诱导,这些根瘤含有根瘤分生组织,但缺乏侵染线、胞内细菌和类杆菌。固定结节含有类似于野生型结节的结节素谱。相反,在空瘤中只检测到NMS-30和一种与大豆ENOD2同源的根瘤蛋白。虽然neliliti ndv和exo突变体诱导的根瘤具有相同的缺陷表型,但ndv和exo突变体(exoC突变体除外)具有不同的生化表型。紫花苜蓿突变株ndvA和ndvB缺乏环状葡聚糖的产生,而酸性胞外多糖的合成不足;exoA、exoB和exoF突变株的情况正好相反。ExoC突变株在胞外多糖和环状葡聚糖的生物合成方面均存在缺陷。我们的结果支持这样的模型,即草地早熟禾节点基因产生的信号导致了根瘤分生组织的诱导。然而,胞外多糖和环状葡聚糖似乎都在发育过程的下一步发挥作用,并参与产生允许侵染线形成和侵袭根瘤的信号(或结构)。
To help dissect the molecular basis of the Rhizobium-legume symbiosis, we used in vitro translation and Northern blot analysis of nodule RNA to examine alfalfa-specific genes (nodulins) expressed in two types of developmentally defective root nodules elicited by Rhizobium meliloti. Fix- nodules were elicited by R. meliloti nif mutants; these nodules were invaded by rhizobia and contained differentiated bacteroids. ''Empty'' nodules were elicited by R. meliloti exo and ndv mutants and by Agrobacterium tumefaciens strains carrying the R. meliloti nod genes; these nodules contained a nodule meristem but lacked infection threads, intracellular bacteria, and bacteroids. Fix- nodules contained a spectrum of nodulins similar to wild-type nodules. In contrast, only two nodulins, Nms-30 and a nodulin homologous to ENOD2 of soybean, were detected in empty nodules. Although R. neliliti ndv and exo mutants elicited nodules with the same defective phenotype, ndv and exo mutants (except for exoC mutants) had distinct biochemical phenotypes. R. meliloti ndvA and ndvB mutants were deficient in cyclic glucan production but not the acidic exopolysaccharide; the converse wase true for exoA, and exoB, and exoF mutants. exoC mutants were defective in both exopolysaccharide and cyclic glucan biosynthesis. Our results support the model that the R. meliloti nod genes produce a signal that results in nodule meristem induction. Both the exopolysaccharide and cyclic glucan, however, appear to act at the next step in the developmental process and are involved in the production of a signal (or structure) that allows infection thread formation and invasion of the nodule.