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与蒺藜苜蓿根瘤侵染相关的宿主特异性结瘤因子差异诱导根毛中的钙内流和钙峰。

Host-specific Nod-factors associated with Medicago truncatula nodule infection differentially induce calcium influx and calcium spiking in root hairs.

机构信息

John Innes Centre, Norwich Research Park, Colney, Norwich, NR4 7UH, UK.

Centre de Recherches sur les Macromolécules Végétales, CNRS, B.P. 53, F-38041, Grenoble CEDEX 9, France.

出版信息

New Phytol. 2013 Nov;200(3):656-662. doi: 10.1111/nph.12475. Epub 2013 Sep 10.

Abstract

Rhizobial nodulation (Nod) factors activate both nodule morphogenesis and infection thread development during legume nodulation. Nod factors induce two different calcium responses: intra-nuclear calcium oscillations and a calcium influx at the root hair tip. Calcium oscillations activate nodule development; we wanted to test if the calcium influx is associated with infection. Sinorhizobium meliloti nodL and nodF mutations additively reduce infection of Medicago truncatula. Nod-factors made by the nodL mutant lack an acetyl group; mutation of nodF causes the nitrogen (N)-linked C16:2 acyl chain to be replaced by C18:1. We tested whether these Nod-factors differentially induced calcium influx and calcium spiking. The absence of the NodL-determined acetyl group greatly reduced the induction of calcium influx without affecting calcium spiking. The calcium influx was even further reduced if the N-linked C16:2 acyl group was replaced by C18:1. These additive effects on calcium influx correlate with the additive effects of mutations in nodF and nodL on legume infection. Infection thread development is inhibited by ethylene, which also inhibited Nod-factor-induced calcium influx. We conclude that Nod-factor perception differentially activates the two developmental pathways required for nodulation and that activation of the pathway involving the calcium influx is important for efficient infection.

摘要

根瘤菌的结瘤因子(Nod)在豆科植物结瘤过程中,既能激活根瘤的形态发生,又能诱导侵染线的发育。结瘤因子诱导两种不同的钙离子响应:细胞核内钙离子振荡和根毛尖端的钙离子内流。钙离子振荡激活根瘤发育;我们想测试钙离子内流是否与侵染有关。Sinorhizobium meliloti 的 nodL 和 nodF 突变会累加减少 Medicago truncatula 的侵染。nodL 突变体产生的结瘤因子缺乏乙酰基;nodF 突变导致氮(N)连接的 C16:2 酰链被 C18:1 取代。我们测试了这些结瘤因子是否能诱导钙离子内流和钙离子峰的形成。nodL 决定的乙酰基的缺失极大地降低了钙离子内流的诱导,而不影响钙离子峰的形成。如果将 N 连接的 C16:2 酰基替换为 C18:1,则钙离子内流甚至进一步降低。这种钙离子内流的累加效应与 nodF 和 nodL 突变对豆科植物侵染的累加效应相关。侵染线的发育受到乙烯的抑制,乙烯也抑制了结瘤因子诱导的钙离子内流。我们得出结论,结瘤因子感知通过不同的机制激活了两个对结瘤至关重要的发育途径,而涉及钙离子内流的途径的激活对高效侵染是重要的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b68/3908372/a378e47d265f/nph0200-0656-f1.jpg

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