bioRxivPlant BiologyPreprint
Lotus japonicus CLV1-Like Receptor HAR1 Promotes Nitrogen Utilization and Growth Under Non-Symbiotic Conditions.
Nao OkumaiD, Daisuke SugiuraiD, Ichiro TerashimaiD, Masayoshi KawaguchiiD
Abstract
Legumes establish mutualistic symbiosis with nitrogen (N)-fixing bacteria, which allows them to utilize atmospheric N2. Because the maintenance of symbiosis requires abundant carbon (C) sources, legumes regulate the balance between carbon consumption and nitrogen acquisition by systemically controlling the nodule number through CLAVATA1 (CLV1)-like receptors. In Lotus japonicus, the CLV1-like receptor HYPERNODULATION ABERRANT ROOT FORMATION1 (HAR1) acts in shoots to regulate root nodulation and contributes to symbiotic C/N coordination. This raises the possibility that HAR1 may also influence plant growth and nitrogen utilization beyond symbiotic nodulation. In this study, we showed that HAR1 plays a critical role in regulating nitrogen use to enhance growth under conditions of high nitrate availability, even in non-symbiotic environments. Unlike the wild-type, the har1 mutant failed to increase its growth in response to higher nitrate availability. This lack of growth response was associated with a lower rate of net biomass production per unit leaf area and a reduced capacity for biomass production per unit plant nitrogen. We further found that nitrate-responsive TCA cycle-related organic acids were higher in har1 leaves than in wild-type leaves even under low nitrate conditions. Because the HAR1 mutation did not affect photosynthetic traits, we propose that HAR1 promotes growth under non-symbiotic conditions by coordinating nitrogen utilization with primary metabolism. One-sentence summaryLotus japonicus CLV1-like receptor HAR1 improves nitrogen utilization and growth at high nitrate conditions by regulating organic acid metabolism, independent of root nodule symbiosis.
- organism: plant (other)
- assay: metabolomics
- research focus: metabolism & bioenergetics
- approach: genetic perturbation / CRISPR
- Citations
- 0
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