Molecular Genetic Analysis of Shoot Apical Meristem Development in Arabidopsis Thaliana

芽顶分生组织（shoot apical merisystem， SAM）在被子植物芽的发育中起着核心作用，它决定了植物几乎所有地上部结构的形成。SAM同时有两个作用：它既是模式形成的地点，也是多能干细胞或初始细胞的来源。因此，SAM以重复和可预测的模式，利用来自SAM中心的新细胞产生芽、叶和茎的基本亚单位。该项目的长期目标是了解SAM如何形成植物的分子基础。通过分离完全缺乏SAM或在SAM发育的某些方面有缺陷的突变体，有可能确定在SAM功能中唯一重要的基因。其中之一是SHOOTMERISTEMLESS （STM）基因，这是一个含有同源结构域的基因，是模式植物拟南芥SAM形成和功能所必需的。STM似乎在SAM的外围起作用，形成器官之间的分离，这样做可能在植物体的形成中起重要作用。我们将通过在SAM外围特异性表达STM基因产物来验证这一观点，并询问这是否可以挽救STM突变体子叶分离的缺陷。这个实验也将使我们能够衡量STM在SAM内细胞自主作用的程度。其他在SAM发育中有缺陷的突变体也将被研究。外围区特异性报告基因构建体将被用来确定一些被认为在中心区有缺陷的突变体是否错误表达了该构建体。PINHEAD基因是SAM中位置信息正确发挥作用所必需的基因，它将被克隆出来，以找出SAM中位置信息是如何起作用的——这一过程几乎是未知的。最后，Adnormal突变体表明叶片正面侧与SAM形成之间存在正相互作用。我们将通过分离不产生正面叶结构域的突变体来验证这一假设，并询问它们是否可以形成腋生和初级sam。我们还将研究“过度”优化突变体抑制SAM形成缺陷突变体表型的能力。

Barton 9724163 The shoot apical meristem (SAM) plays a central role in angiosperm shoot development giving rise to nearly all of the above-ground structures of the plant. The SAM simultaneously serves two purposes: it acts both as a site of pattern formation and as a source of pluripotent stem cells or initial cells. Thus, the SAM produces the basic subunits of the shoot, leaves and stem, in repeated and predictable patterns, using new cells derived from the center of the SAM. The long term goal of this project is to understand the molecular basis for how a SAM makes a plant. By isolating mutants that either entirely lack a SAM or are defective in some aspect of SAM development, it is possible to identify genes that are uniquely important in SAM function. One of these is the SHOOTMERISTEMLESS (STM) gene, a homeodomain-containing gene that is required for SAM formation and function in the model plant Arabidopsis. The STM appears to act in the periphery of the SAM to form the separations between organs, and in doing so, may play an important role in the shaping of the plant body. We will test this notion by specifically expressing the STM gene product in the periphery of the SAM and asking whether this can rescue the defect in cotyledon separation in stm mutants. This experiment will also allow us to gauge the degree to which STM acts cell autonomously within the SAM. Other mutants defective in SAM development will be studied as well. A Peripheral Zone specific reporter construct will be used to determine if several mutants suggested to have defects in the Central Zone misexpress this construct. The PINHEAD gene, a gene required for the correct functioning of positional information in the SAM, will be cloned to find out how positional information works in the SAM - a process about which almost nothing is known. Finally, the Adnormal mutant has suggested the existence of a positive interaction between the adaxial side of the leaf and SAM formation. We will test this hypothesis by i solating mutants that do not make an adaxial leaf domain and asking whether they can form axillary and primary SAMs. We will also investigate the ability of an "overly" adaxialized mutant to suppress the phenotypes of mutants defective in SAM formation.