关键词: Medicago truncatula NCR peptides bacteroid early senescence nodule cell terminal differentiation

Mesh : Medicago truncatula / genetics metabolism Peptides / metabolism Rhizobium Cell Differentiation Symbiosis / physiology Nitrogen / metabolism Nitrogen Fixation / physiology Root Nodules, Plant / metabolism

来  源:   DOI:10.1111/nph.19180

Abstract:
Bacteroid (name for rhizobia inside nodule cells) differentiation is a prerequisite for successful nitrogen-fixing symbiosis. In certain legumes, under the regulation of host proteins, for example, a large group of NCR (nodule cysteine rich) peptides, bacteroids undergo irreversible terminal differentiation. This process causes them to lose the ability to propagate inside nodule cells while boosting their competency for nitrogen fixation. How host cells maintain the viability of differentiated bacteroids while maximizing their nitrogen-reducing activities remains elusive. Here, through mutant screen, map-based cloning, and genetic complementation, we find that NCR343 is required for the viability of differentiated bacteroids. In Medicago truncatula debino1 mutant, differentiated bacteroids decay prematurely, and NCR343 is proved to be the casual gene for debino1. NCR343 is mainly expressed in the nodule fixation zone, where bacteroids are differentiated. In nodule cells, mature NCR343 peptide is secreted into the symbiosomes. RNA-Seq assay shows that many stress-responsive genes are significantly induced in debino1 bacteroids. Additionally, a group of stress response-related rhizobium proteins are identified as putative interacting partners of NCR343. In summary, our findings demonstrate that beyond promoting bacteroid differentiation, NCR peptides are also required in maintaining the viability of differentiated bacteroids.
摘要:
细菌(根瘤细胞内根瘤菌的名称)分化是成功固氮共生的先决条件。在某些豆类中,在宿主蛋白的调节下,例如,一大组NCR(富含结节半胱氨酸)肽,类细菌经历不可逆的终末分化。此过程导致它们失去在结节细胞内繁殖的能力,同时增强其固氮能力。宿主细胞如何维持分化的类细菌的生存力,同时最大限度地发挥其减氮活性仍然难以捉摸。这里,通过突变筛选,基于地图的克隆,和遗传互补,我们发现NCR343是分化的类细菌的生存力所必需的。在Medicagotruncatuladebino1突变体中,分化的类细菌过早腐烂,NCR343被证明是debino1的偶然基因。NCR343主要表达于结节固定区,细菌是有区别的。在结节细胞中,成熟的NCR343肽被分泌到共生体中。RNA-Seq分析表明,许多应激反应基因在debino1类细菌中被显着诱导。此外,一组与应激反应相关的根瘤菌蛋白被鉴定为NCR343的推定相互作用伴侣。总之,我们的发现表明,除了促进类细菌分化,NCR肽也是维持分化的类细菌的活力所必需的。
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