INITITATION OF SPORULATION IN BACILLUS SUBTILIS

枯草芽孢杆菌中的孢子形成是一个相对复杂的过程。 这是一个简单的差异化例子，涉及到许多变化， 细胞生理学、基因表达和形态学。 产孢 是在营养缺乏的情况下， 信息素类因子 这项研究的目的是 了解控制启动的机制 孢子形成 这涉及到定义所需的外部刺激 开始孢子的形成， 参与信号传导， 在孢子形成条件下被激活的基因。 我们的工作将集中在两个调控基因，spoOA和spoOH， 是孢子形成的起始条件。 spooa基因 产物与其他原核调节蛋白同源， 参与了信号转导。 spoOH基因产物是一种 控制基因表达的RNA聚合酶的σ因子 需要启动孢子形成 具体而言，我们将确定和 表征由这两种调节基因控制的基因， 基因. 我们使用了一种融合转座子来鉴定 其表达依赖于spoOH的基因，并将采用 类似的策略来鉴定由spoOA控制的基因。 我们将确定这些基因在生长过程中是如何表达的， 孢子形成和它们的表达取决于 spoo调控基因，我们将表征调控区域 这些基因的上游。 此外，我们会研究 spoOA在孢子形成起始中的作用， 分离和表征spoOA错义假回复突变体 突变 基因外抑制因子可能会识别调节基因， 涉及SpoOA或与SpoOA相互作用的蛋白质的途径。 基因内抑制基因是指引起基因改变的突变， SpoOA的功能，而不是功能的丧失。 最后我们 建议确定参与细胞外控制的基因， 通过分离突变， 产生胞外孢子形成因子。 表征 这种突变体的生物化学鉴定可能有助于 这些因素将有助于确定细胞如何感知和 屏蔽外部信号。 我们对这一分化的研究 实验上可获得微生物应该提供重要的 深入了解信号转导的一般机制，基因 表达以及正常和异常分化。

Spore formation in the bacterium Bacillus subtilis is a relatively simple example of differentiation and involves numerous changes in cellular physiology, gene expression, and morphology. Sporulation is initiated in response to nutrient deprivation in the presence of pheromone-like factors. The goal of this research is to understand the mechanisms that control the initiation of sporulation. This involves defining the external stimuli needed to initiate spore formation, identifying the cellular components involved in signal transduction, and identifying and characterizing genes that are activated in response to sporulation conditions. Our work will focus on two regulatory genes, spoOA and spoOH, that are required for the initiation of sporulation. The spoOA gene product is homologous to other prokaryotic regulatory proteins that are involved in signal transduction. The spoOH gene product is a sigma factor of RNA polymerase that controls expression of genes needed to initiate sporulation. Specifically, we will identify and characterize genes that are controlled by these two regulatory genes. We have used a fusion-generating transposon to identify genes whose expression is dependent on spoOH, and will employ a similar strategy to identify genes that are controlled by spoOA. We will determine how these genes are expressed during growth and sporulation and the extent to which their expression depends on the spoO regulatory genes and we will characterize regulatory regions upstream of some of these genes. In addition, we will study the role of spoOA in the initiation of sporulation by continuing to isolate and characterize pseudorevertants of a spoOA missense mutation. Extragenic suppressors might identify regulatory pathways involving spoOA or proteins with which SpoOA interacts. Intragenic suppressors will be mutations that cause altered function of SpoOA, rather than loss of function. Finally, we propose to identify genes involved in the extracellular control of sporulation by isolating mutations that cause defects in the production of extracellular sporulation factors. Characterization of such mutants might facilitate the biochemical identification of these factors and will help to determine how cells sense and transduce external signals. Our studies on differentiation of this experimentally accessible microbe should provide significant insights into general mechanisms of signal transduction, gene expression, and normal and abnormal differentiation.