4.8 Article

Rhizobial and Mycorrhizal Symbioses in Lotus japonicus Require Lectin Nucleotide Phosphohydrolase, Which Acts Upstream of Calcium Signaling

Journal

PLANT PHYSIOLOGY
Volume 161, Issue 1, Pages 556-567

Publisher

AMER SOC PLANT BIOLOGISTS
DOI: 10.1104/pp.112.206110

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Funding

  1. National Institute of General Medical Sciences-National Institutes of Health [GM21882]
  2. U.S. Department of Agriculture [97-35305-4630]
  3. Ceres, Inc.
  4. Australian Research Council Centre of Excellence Fund and the Queensland Smart State Fund
  5. European Research Council
  6. European Research Council [MRTN-CT-2006-035546]
  7. Biotechnology and Biological Sciences Research Council [BBS/E/J/00000603] Funding Source: researchfish
  8. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM021882] Funding Source: NIH RePORTER

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Nodulation in legumes requires the recognition of rhizobially made Nod factors. Genetic studies have revealed that the perception of Nod factors involves LysM domain receptor-like kinases, while biochemical approaches have identified LECTIN NUCLEOTIDE PHOSPHOHYDROLASE (LNP) as a Nod factor-binding protein. Here, we show that antisense inhibition of LNP blocks nodulation in Lotus japonicus. This absence of nodulation was due to a defect in Nod factor signaling based on the observations that the early nodulation gene NODULE INCEPTION was not induced and that both Nod factor-induced perinuclear calcium spiking and calcium influx at the root hair tip were blocked. However, Nod factor did induce root hair deformation in the LNP antisense lines. LNP is also required for infection by the mycorrhizal fungus Glomus intraradices, suggesting that LNP plays a role in the common signaling pathway shared by the rhizobial and mycorrhizal symbioses. Taken together, these observations indicate that LNP acts at a novel position in the early stages of symbiosis signaling. We propose that LNP functions at the earliest stage of the common nodulation and mycorrhization symbiosis signaling pathway downstream of the Nod factor receptors; it may act either by influencing signaling via changes in external nucleotides or in conjunction with the LysM receptor-like kinases for recognition of Nod factor.

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