RESUMO
The plant shoot body plan is highly variable, depending on the degree of branching. Characterization of the max1-max4 mutants of Arabidopsis demonstrates that branching is regulated by at least one carotenoid-derived hormone. Here we show that all four MAX genes act in a single pathway, with MAX1, MAX3, and MAX4 acting in hormone synthesis, and MAX2 acting in perception. We propose that MAX1 acts on a mobile substrate, downstream of MAX3 and MAX4, which have immobile substrates. These roles for MAX3, MAX4, and MAX2 are consistent with their known molecular identities. We identify MAX1 as a member of the cytochrome P450 family with high similarity to mammalian Thromboxane A2 synthase. This, with its expression pattern, supports its suggested role in the MAX pathway. Moreover, the proposed enzymatic series for MAX hormone synthesis resembles that of two already characterized signal biosynthetic pathways: prostaglandins in animals and oxilipins in plants.
Assuntos
Proteínas de Arabidopsis/metabolismo , Carotenoides/metabolismo , Sistema Enzimático do Citocromo P-450/metabolismo , Oxigenases/metabolismo , Brotos de Planta/metabolismo , Sequência de Aminoácidos , Arabidopsis/citologia , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Sistema Enzimático do Citocromo P-450/genética , Regulação da Expressão Gênica de Plantas/genética , Regulação da Expressão Gênica de Plantas/fisiologia , Hormônios/metabolismo , Dados de Sequência Molecular , Mutação/genética , Oxigenases/genética , Brotos de Planta/citologia , Brotos de Planta/genética , Tromboxano-A Sintase/genéticaRESUMO
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.