The Arabidopsis MAX pathway controls shoot branching by regulating auxin transport.
BACKGROUND
Plants achieve remarkable plasticity in shoot system architecture by regulating the activity of secondary shoot meristems, laid down in the axil of each leaf. Axillary meristem activity, and hence shoot branching, is regulated by a network of interacting hormonal signals that move through the plant. Among these, auxin, moving down the plant in the main stem, indirectly inhibits axillary bud outgrowth, and an as yet undefined hormone, the synthesis of which in Arabidopsis requires MAX1, MAX3, and MAX4, moves up the plant and also inhibits shoot branching. Since the axillary buds of max4 mutants are resistant to the inhibitory effects of apically supplied auxin, auxin and the MAX-dependent hormone must interact to inhibit branching.


RESULTS
Here we show that the resistance of max mutant buds to apically supplied auxin is largely independent of the known, AXR1-mediated, auxin signal transduction pathway. Instead, it is caused by increased capacity for auxin transport in max primary stems, which show increased expression of PIN auxin efflux facilitators. The max phenotype is dependent on PIN1 activity, but it is independent of flavonoids, which are known regulators of PIN-dependent auxin transport.


CONCLUSIONS
The MAX-dependent hormone is a novel regulator of auxin transport. Modulation of auxin transport in the stem is sufficient to regulate bud outgrowth, independent of AXR1-mediated auxin signaling. We therefore propose an additional mechanism for long-range signaling by auxin in which bud growth is regulated by competition between auxin sources for auxin transport capacity in the primary stem.
Department of Biology, University of York, York YO10 5YW, United Kingdom.
Tom
T
Bennett
Tobias
T
Sieberer
Barbara
B
Willett
Jon
J
Booker
Christian
C
Luschnig
Ottoline
O
Leyser
D017360:Arabidopsis / Q000201:enzymology / Q000254:growth & development* / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000378:metabolism / Q000502:physiology*; D001692:Biological Transport; D049308:Dioxygenases; D005419:Flavonoids / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D005838:Genotype; D049452:Green Fluorescent Proteins / Q000032:analysis; D007210:Indoleacetic Acids / Q000378:metabolism* / Q000494:pharmacology; D026901:Membrane Transport Proteins / Q000378:metabolism; D008954:Models, Biological; D009154:Mutation; D010105:Oxygenases / Q000502:physiology*; D010641:Phenotype; D018520:Plant Shoots / Q000033:anatomy & histology / Q000254:growth & development* / Q000378:metabolism; D018547:Plant Stems / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000032:analysis / Q000378:metabolism; D015398:Signal Transduction
C081977:AXR1 protein, Arabidopsis; D029681:Arabidopsis Proteins; D005419:Flavonoids; D007210:Indoleacetic Acids; C470445:MAX1 protein, Arabidopsis; D026901:Membrane Transport Proteins; C116363:PIN1 protein, Arabidopsis; D011993:Recombinant Fusion Proteins; D049452:Green Fluorescent Proteins; C475746:MAX4 protein, Arabidopsis; D010105:Oxygenases; C494441:CCD7 protein, Arabidopsis; D049308:Dioxygenases