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lpcC基因的失活改变了日本慢生根瘤菌的表面相关特性和共生能力。

Inactivation of the lpcC gene alters surface-related properties and symbiotic capability of Bradyrhizobium japonicum.

作者信息

Lee H-I, In Y-H, Jeong S-Y, Jeon J-M, Noh J G, So J-S, Chang W-S

机构信息

Department of Biology, University of Texas, Arlington, TX, USA.

出版信息

Lett Appl Microbiol. 2014 Jul;59(1):9-16. doi: 10.1111/lam.12232. Epub 2014 Mar 6.

Abstract

UNLABELLED

We investigated the role of the Bradyrhizobium japonicum lpcC gene, encoding a mannosyl transferase, involved in the lipopolysaccharide (LPS) biosynthesis. The inactivation of the lpcC gene considerably altered the LPS structure and the cell surface properties. LPS analysis showed that the lpcC mutant JS715 had an abnormal LPS structure deficient in O-antigen. The cell surface hydrophobicity increased approximately threefold in JS715 compared to the wild type. The increased cell surface hydrophobicity is likely to be related with cell aggregation in the mutant culture. For the growth comparison, JS715 showed slower growth rate than the wild type. The motility of JS715 decreased in soft agar plates, but it showed enhanced biofilm-forming ability. Interestingly, JS715 was not able to nodulate the host legume soybean (Glycine max). This study shows not only that lpcC is involved in the biosynthesis of O-antigen in the B. japonicum LPS, but also that inactivation of the lpcC gene affects symbiotic capability of B. japonicum and surface-related properties such as cell hydrophobicity, biofilm formation and motility.

SIGNIFICANCE AND IMPACT OF THE STUDY

This study demonstrates the role of the B. japonicum lpcC in nodulation with soybean and importance of cell surface hydrophobicity. The results also highlight that intact LPS is required for successful symbiosis between B. japonicum and soybeans. Our findings not only support previous studies emphasizing the necessity of LPS on the interaction between the two symbiotic partners, but also contribute to a better understanding of the symbiotic mechanisms.

摘要

未标记

我们研究了慢生根瘤菌中编码甘露糖基转移酶的lpcC基因在脂多糖(LPS)生物合成中的作用。lpcC基因的失活极大地改变了LPS结构和细胞表面特性。LPS分析表明,lpcC突变体JS715具有异常的LPS结构,缺乏O抗原。与野生型相比,JS715的细胞表面疏水性增加了约三倍。细胞表面疏水性的增加可能与突变体培养物中的细胞聚集有关。为了比较生长情况,JS715的生长速度比野生型慢。JS715在软琼脂平板上的运动性下降,但它表现出增强的生物膜形成能力。有趣的是,JS715无法使宿主豆科植物大豆(Glycine max)结瘤。这项研究不仅表明lpcC参与了慢生根瘤菌LPS中O抗原的生物合成,还表明lpcC基因的失活会影响慢生根瘤菌的共生能力以及与表面相关的特性,如细胞疏水性、生物膜形成和运动性。

研究的意义和影响

本研究证明了慢生根瘤菌lpcC在与大豆结瘤中的作用以及细胞表面疏水性的重要性。结果还突出了完整的LPS对于慢生根瘤菌与大豆成功共生的必要性。我们的发现不仅支持了先前强调LPS在两个共生伙伴相互作用中必要性的研究,还有助于更好地理解共生机制。

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