The Molecular Mechanism Of CTL1 Controls Seedling Growth And Development In Arabidopsis

Auxin is the most investigated phytohormone that plays a pivotal role in virtually every aspect of plant growth and development and such function is often a result of its differential distribution within plant tissues.It functions in controling organogenesis,apical dominance,lateral root emergence and growth,differential growth during apical hook development and tropism,vascular development and many other developmental processes.Auxin regulates cell elongation,cell division,and cell differentiation at cellular level.Auxin action depends on its differential distribution in plant tissues.Polar auxin transport(PAT)helps to form local auxin maxima or gradients between cells,leading to differential distribution.PAT is mainly mediated by PM-based influx and efflux carriers such as PINs,AUX1,LIKE AUX1(LAX),and ABCB family proteins.The accurate subcellular targeting of these auxin transporters ensure well-organized polar auxin transport in the plant and auxin homeostasis in cells.Endosomal trafficking is one of the effective ways of regulating the dynamic subcellular locations of these auxin transporters.We suggest that Arabidopsis thaliana CTL1 is involved in auxin-regulated development.CTL1 null mutation causes severe growth retardation throughout the whole life cycle,including shorter root,shorter hypocotyl length in dark and dwarf adult plant.The leaves of ctl1 were round and compact.Finally,we provide the evidence that CTL1 is an essential regulator for cell elongation in Arabidopsis.Furthermore,loss-of-function of CTL1 showed defects in apical hook development,abnormal root morphology,reduced hypocotyl phototropic response to unilateral light and less sensitive to high levels of exogenous NAA.These results strongly implicate CTL1 in auxin related physiological process.CTL1 expression is highly correlated with auxin distribution,which is enriched in shoot and root apical meristems,lateral root primordia,vascular system,and the concave side of apical hook.Functional CTL1 is localized to the trans-Golgi network(TGN),pre-vacuolar compartment(PVC),and plasma membrane(PM).We further found that disruption of CTL1 function impaired endomembrane trafficking of several auxin transporters and probably some other unidentified cargo proteins as well.CTL1 protein acts at both secretory vesicles(SVs)and clathrin-coated vesicles(CCVs)of TGN to regulate the trafficking of PIN 1 and PIN3,which explains the phenotypes of ctl1 mutant in seedling growth and apical hook development.We conclude that CTL1 is a previously unrecognized regulator of endomembrane trafficking in plants.Our findings define a critical new regulator of endomembrane trafficking and contribute to the understanding of the complex mechanism that governs auxin signaling regulation through membrane trafficking pathways.This study not only contributes to the understanding of auxin transport but also to the mechanism of vesicular trafficking in plant cells.Further,choline transport has not been previously identified as a required element for secretory trafficking in any organism.This work thus opens a new area of research to address choline metabolism in membrane trafficking processes.