A G protein coupled receptor like protein systematically modulates nutrient-growth by Ca2+ mediated phosphatidylcholine perception during evolutionary adaptation
Huang, Z.; Tong, Y.; He, X.; Teng, W.; Hu, M.; Li, H.; Zhang, Y.; Li, J.; Zhao, X.
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Nutrients are important for growth in both plants and animals, uncovering of signaling pathway in nutrients determined growth is essential. Here we cloned TaPCGR1-3B (Phospholipid Coordinated Growth and nutrients Response 1), controlled by SNPs on alternative splicing and transcription factors binding, conferring nitrogen deficiency response. TaPCGR1-3B was localized in plasma membrane and endoplasmic reticulum of meristem cell. Nitrogen deprivation stimulated interaction of TaPCGR1-3B with G protein alpha subunit and phospholipase C 9, which was inhibited by phosphatidylcholine, to trigger Ca2+ signaling and inhibit normal growth. Knockdown of TaPCGR1 rescued the growth inhibition caused by nutrient deficient conditions by modulation of phosphatidylcholine induced growth gene expression through Ca2+ signaling disruption. Modulating of phosphatidylcholine mediated TaPCGR1 activity thus tightly regulated growth through Ca2+ signaling.
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