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

Abstract

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.