Molecular Mechanism Of Phytohormone ABA In Regulation Of Arabidopsis Growth And Development Via Modulation Of Auxin Transport

The phytohormone abscisic acid(ABA)is not only known as "stress hormone" responding to both biotic and abiotic stress,but also associated with a range of essential plant traits that include seed maturation and dormancy,stomatal movement,leaf abscission,etc.Given the universal role of this phytohormone in regulating plant development,it is not surprising that numerous connections between ABA and other key plant growth-regulating phytohormones such as auxin.Despite the molecular knowledge on the ABA signaling,it remains still largely obscure,by which mechanism ABA induces the cellular changes that define their auxin-related developmental output.In this study,it was found that ABA interferes with several basic developmental aspects,such as lateral root organogenesis and leaf patterning,as well as root gravitropic response after gravi-stimulation.The impairment of ABA perception mediated by key members of the PYR/PYLs family(PYR1,PYL1,PYL2 and PYL4;abbreviated as 1124)results in the dramatic ABA-insensitive phenotypes.However,other established ABA-insensitive mutants such as PP2C dominant-negative mutant abil-1(Col-0)and SnRK2s-defictive mutant snrk2.2/2.3 still actively respond to ABA.All these observations suggest that ABA receptors PYR/PYLs but not their downstream components of classic ABA signalling pathway are necessarily required for these ABA-mediated developmental contexts.The PIN proteins play the essential role in mediating auxin flow and thus diverse plant development.The reversible PIN phosphorylation,mediated by the antagonistic action of PID kinase and PP2A phosphatase regulatory subunits,determines PIN activity.Here,we found that the phosphorylated PIN proteins over-accumulate in the 1124 quadruple mutants,and quintuple mutants pyr1 pyl1 pyl4 pyl5 pyl8(abbreviated as 11458)display the fused cotyledon formation and defective root development,as previously observed in the pp2aas multiple mutants or PID gain-of-function lines.The partial loss of phosphatase activity in pp2ac3 or pp2ac4 single mutants leads to ABA insensitive phenotypes overlapped with those of PYR/PYLs-defective mutant 1124.Both in vitro and in vivo assays of phosphatase activity showed that ABA signaling negatively regulates PP2A activity through the action of PYR/PYLs.PP2AC3 or PP2AC4 phosphatase could interact with and also dephosphorylate the PID kinase as well as its established substrates,the PIN proteins to directly control reversible PIN phosphorylation.These collected lines of evidences put forward a proposed mechanism:the increase of ABA levels suppresses the phosphatase activity of PP2ACs via PYR/PYLs receptors;PP2ACs act antagonistically to PID in mediating PIN phosphorylation and in turn PIN polar targeting;effect of ABA on PINs relocation through this PYR/PYLs-PP2ACs combinable module eventually allows the regulation of auxin transport and auxin-mediated plant development,such as root gravitropism,lateral root organogenesis,and leaf patterning.This study highlights a novel ABA regulatory mechanism for at least part of ABA signaling-mediated processes.