Inositol Trisphosphate-Induced Ca2+ Signaling Modulates Auxin Transport and PIN Polarity

Abstract

The phytohormone auxin is an important determinant of plant development. Directional auxin flow within tissues depends on polar localization of PIN auxin transporters. To explore regulation of PIN-mediated auxin transport, we screened for suppressors of PIN1 overexpression (supo) and identified an inositol polyphosphate 1-phosphatase mutant (supo1), with elevated inositol trisphosphate (InsP(3)) and cytosolic Ca(2+) levels. Pharmacological and genetic increases in InsP(3) or Ca(2+) levels also suppressed the PIN1 gain-of-function phenotypes and caused defects in basal PIN localization, auxin transport and auxin-mediated development. In contrast, the reductions in InsP(3) levels and Ca(2+) signaling antagonized the effects of the supo1 mutation and disrupted preferentially apical PIN localization. InsP(3) and Ca(2+) are evolutionarily conserved second messengers involved in various cellular functions, particularly stress responses. Our findings implicate them as modifiers of cell polarity and polar auxin transport, and highlight a potential integration point through which Ca(2+) signaling-related stimuli could influence auxin-mediated development.

Master and servant: Regulation of auxin transporters by FKBPs and cyclophilins

“…However, it is not clear whether documented calmodulin or HPS90 interactions with FKBPs (such as TWD1) or cyclophilins (such as SQN/Cyp40) are involved in regulation of auxin transport or rather represent unrelated functional relationships. While an involvement of calcium in the regulation of auxin transport has been documented [125], the role of heat-shock proteins is entirely unclear.…”

Inactivation of Plasma Membrane–Localized CDPK-RELATED KINASE5 Decelerates PIN2 Exocytosis and Root Gravitropic Response inArabidopsis

“…Mutations impairing starch biosynthesis, biogenesis, and sedimentation of starch-containing plastids (i.e., statoliths) and their interactions with actin filaments, endoplasmic reticulum, and plasma membrane highlight the importance of mechanosensitive ion channels and components of calcium/calmodulin and inositol-phosphate signaling pathways that connect gravisensing with the regulation of polar localization of PINs and PGPs (Baldwin et al, 2013;Blancaflor, 2013;Kurusu et al, 2013). Emerging data indicate that cortical actin accumulation regulates clathrin-dependent endocytosis Nagawa et al, 2012), whereas enhanced inositol triphosphate and Ca 2+ levels decelerate exocytosis of PIN1 and PIN2 similarly to mutations of inositol polyphosphate 1-phosphatase and phosphatidylinositol monophosphate 5-kinase genes (Zhang et al, 2011;Mei et al, 2012). Furthermore, signaling through the 3-phosphoinositidedependent kinase1 and interactions with Ca 2+ binding or calmodulinlike proteins appear to regulate the activity of AGC kinases that phosphorylate central hydrophilic loops of PINs, as well as ABCB/ PGPs (Benjamins et al, 2003;Zegzouti et al, 2006;Henrichs et al, 2012;Rademacher and Offringa, 2012).…”

Arabidopsis phosphatidylinositol monophosphate 5-kinase 2 is involved in root gravitropism through regulation of polar auxin transport by affecting the cycling of PIN proteins

“…Root gravitropism is also regulated by auxin, especially polar auxin transport, which is mediated by membranelocalized auxin-influx and -efflux carriers, including AUX1/LAX proteins, the PIN-FORMED (PIN) efflux carriers and the MULTIDRUG RESISTANCE/P-GLY-COPROTEIN (PGP) class of ATP-binding cassette auxin transporters [32][33][34][35]. Genetic analyses have revealed the critical roles of the influx carrier AUX1 and efflux carrier PIN proteins in gravity response.…”