A G protein coupled receptor like protein systematically modulates nutrient-growth by Ca2+mediated phosphatidylcholine perception during evolutionary adaptation

Abstract

AbstractNutrients are important for growth in both plants and animals, uncovering of signaling pathway in nutrients determined growth is essential. Here we clonedTaPCGR1-3B(Phospholipid Coordinated Growth and nutrients Response1), 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 ofTaPCGR1rescued the growth inhibition caused by nutrient deficient conditions by modulation of phosphatidylcholine induced growth gene expression through Ca2+signaling disruption. Modulating of phosphatidylcholine mediatedTaPCGR1activity thus tightly regulated growth through Ca2+signaling.