Auxin Biosynthesis and Signaling Mechanisms

描述（由申请人提供）：生长素是植物生长和发育的几乎每个方面的基本调节剂。该建议的总体目标是阐明生长素调节植物器官发生和其他发育过程的分子机制。在上一个资助期间，我们证明了YUCCA（YUC）黄素单加氧酶在生长素生物合成和各种发育过程中起着重要作用，包括胚胎发生，幼苗生长，维管图案和花发育。以往关于生长素信号转导的遗传学研究主要集中在对外源生长素抗性突变体的分析上。我们对生长素生物合成的理解使我们能够从一个完全不同的角度阐明生长素在植物发育中作用的分子机制。我们从部分生长素缺乏的yuc 1和yuc 4双突变体的增强子遗传筛选中鉴定出npy 1（yuc突变体中的裸钉）。npy 1 yuc 1 yuc 4三重突变体形成了针状花序，但不能形成任何花，这是生长素途径缺陷引起的标志性表型。NPY 1属于一个大家族，与非向光性下胚轴3（NPH 3）同源，NPH 3是一种与AGC激酶PHOT 1一起沿着调节向光性的BTB蛋白。NPY 1与PHOT 1同源物PID一起工作，使用与NPH 3/PHOT 1在向光性中使用的机制类似的机制来调节生长素介导的器官发生。这一发现将yuc、npy 1和已知的生长素突变体pin 1、pid和mp放在一个遗传框架中，以进一步了解生长素调控植物发育的机制。这些发现也揭示了植物中AGC激酶介导的信号转导的新机制。这些研究的主要目的是：（1）分析YUC基因在生长素生物合成和植物发育中的作用机制;（2）阐明NPY 1在生长素调控器官发生中的生化机制;（3）确定NPY 1家族基因在生长素调控植物发育中的独特和重叠功能;（4）从遗传学角度剖析生长素调控植物发育的机制。该实验将为植物生长素在植物发育，特别是器官发生中的分子作用机制提供新的见解。清楚地了解生长素调节复杂发育过程的机制对植物生物学具有根本的重要性，并将对农业产生重大影响。拟议的研究还将扩展我们对控制其他真核生物复杂发育过程的信号机制的理解，特别是AGC激酶的机制，这些机制与包括人类在内的其他生物的多种发育程序有关。公共卫生相关性：拟议的研究旨在阐明生长素控制植物器官形成的分子机制。拟议的研究将增加我们对包括人类在内的真核生物中控制器官发生和其他发育过程的复杂信号转导机制的理解。

DESCRIPTION (provided by applicant): Auxin is an essential regulator for almost every aspect of plant growth and development. The general goal of this proposal is to elucidate the molecular mechanisms by which auxin regulates plant organogenesis and other developmental processes. During the last grant period, we demonstrated that the YUCCA (YUC) flavin monooxygenases play an essential role in auxin biosynthesis and various developmental processes including embryogenesis, seedling growth, vascular patterning, and floral development. Previous genetic studies on auxin signaling were centered on analysis of mutants resistant to exogenous auxin. Our understanding of auxin biosynthesis allowed us to elucidate the molecular mechanisms of auxin action in plant development from a completely different perspective. We identified npy1 (naked pins in yuc mutants) from a genetic screen for enhancers of the yuc1 yuc4 double mutants that are partially auxin deficient. The npy1 yuc1 yuc4 triple mutants developed pin-like inflorescences and failed to form any flowers, a hallmark phenotype caused by defects in auxin pathways. NPY1 belongs to a large family and is homologous to non-phototropic hypocotyl 3 (NPH3), a BTB protein regulating phototropism along with the AGC kinase PHOT1. NPY1 works with PID, a PHOT1 homolog, to regulate auxin-mediated organogenesis using a mechanism analogous to that used by NPH3/PHOT1 in phototropism. The findings put yuc, npy1, and known auxin mutants pin1, pid, and mp in a genetic framework for further understanding of the mechanisms governing auxin-regulated plant development. The findings also reveal a novel mechanism for AGC kinase-mediated signal transduction in plants. The primary aims of the proposed studies are (1) Analysis of the mechanisms of YUC genes in auxin biosynthesis and plant development; (2) Elucidation of the biochemical mechanisms of NPY1 in auxin-regulated organogenesis; (3) Determination of the unique and overlapping functions of the NPY1 family genes in auxin-regulated plant development; (4) Genetic dissection of the mechanisms by which auxin regulates plant development. The proposed experiments will provide significant new insight into the molecular mechanisms of auxin action in plant development, particularly in organogenesis. A clear understanding of the mechanisms by which auxin regulates complex developmental processes is of fundamental importance to plant biology and will have a significant agricultural impact. The proposed study will also extend our understanding of signaling mechanisms controlling complex developmental processes in other eukaryotes, particularly the mechanisms of AGC kinases, which have been implicated in diverse developmental programs in other organisms including humans. PUBLIC HEALTH RELEVANCE: The proposed research is aimed to elucidate the molecular mechanisms by which auxin controls the formation of plant organs. The proposed research will augment our understanding of complex signal transduction mechanisms governing organogenesis and other developmental processes in eukaryotes including humans.