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

SummaryThe 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 (InsP3) and cytosolic Ca2+ levels. Pharmacological and genetic increases in InsP3 or Ca2+ 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 InsP3 levels and Ca2+ signaling antagonized the effects of the supo1 mutation and disrupted preferentially apical PIN localization. InsP3 and Ca2+ 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 Ca2+ signaling-related stimuli could influence auxin-mediated development.

► Suppressor screen highlights role of SAL1 in PIN-dependent auxin transport
► Increasing InsP3 or Ca2+ levels modulates auxin transport and basal PIN polarity
► Decreasing InsP3 or Ca2+ levels preferentially affects apical PIN polarity
► InsP3-mediated Ca2+ signaling influences PIN localization in part via PID kinase