Mechanism of Action of Auxin-binding Protein I

9808792琼斯博士最近获得的分子遗传学证据表明，生长素结合蛋白I（ABP 1）是一种生长素受体，介导生长素调节的生长和细胞壁的形成。 玉米ABP 1在玉米细胞系中的组成型表达导致细胞大小和壁厚度的增加。 此外，烟草中拟南芥ABP 1的诱导型表达导致叶外植体中测量的生长增加。 与受体功能一致，ABP 1在两个系统中的作用严格依赖于生长素。 ABP 1引起生长增加的分子机制尚不清楚，这是本提案的研究主题。 基于其亚细胞分布，PI假设ABP 1-生长素复合物通过内膜途径触发壁前体和/或生长限制因子的流动速率和/或方向控制的变化，或改变壁前体或其生物合成酶的分选和活性。 为了验证这一假设，PI将研究生长素调节的细胞和组织生长，生长素吸收，并将在拟南芥和烟草植物和外植体中评估生长素极性运输，这些植物和外植体在ABP 1上的水平都增加和减少。 该提案解决了植物细胞生物学、生长和发育中的一个中心问题：生长素如何调节植物生长？ 由生长素和ABP 1描绘的信号转导途径当然只是导致细胞扩增的多种途径的一部分，但迄今为止的所有证据表明它是新颖的。

9808792 Jones Dr. Jones has recently obtained molecular genetic evidence that auxin-binding protein I (ABP1) is an auxin receptor that mediates auxin-regulated growth and cell wall formation. Constitutive expression of maize ABP1 in maize cell lines causes increases in both cell size and wall thickness. Furthermore, inducible expression of arabidopsis ABP1 in tobacco causes increased growth as measured in leaf explants. Consistent with receptor function, the ABP1 effect in both systems is strictly dependent on auxin. The molecular mechanism by which ABP1 causes increase in growth is not known and is the topic of investigation for this proposal. Based on its subcellular distribution, the PI hypothesizes that the ABP1-auxin complex triggers a change in the control of rate and/or direction of flow of wall precursors and/or growth-limiting factors through the endomembrane pathway or alters the sorting and activity of wall precursors or their biosynthetic enzymes. To test this hypothesis, the PI will investigate auxin-regulated cell and tissue growth, auxin uptake, and polar auxin transport will be assessed in arabidopsis and tobacco plants and explants that have both increased and decreased levels on ABP1. This proposal addresses a central question in plant cell biology, growth, and development: How does auxin regulate plant growth? The signal transduction pathway delineated by auxin and ABP1 is certainly only part of multiple pathways that lead to cell expansion but all the evidence so far indicate that it is novel.