GENETICS OF USTILAGO HORDEI

大麦黑粉病是一种引起大麦黑穗病的担子菌。 无性生长以非致病、单倍体、萌芽的形式发生。 酵母状的孢子虫。孢子虫的融合，由一个单一的 具有两个等位基因的交配型基因座，导致致病的菌丝体 双核细胞。我们已经证明交配涉及细胞之间的交流。 交配类型相反的，导致接合的形成 管子。一个非常令人兴奋的发现是小分子化合物， 或信息素，起到信号的作用。我们已经从人类基因组中分离出大量突变体 这两种交配类型都不能交配。其中一些突变体 不能产生活性信息素，其他人不能制造 共轭管。这项研究的长期目标是 纯化信息素的生化特性及相关基因的克隆 在这种信息素介导的细胞间相互作用中，为了更好地 了解涉及到的非 病原体对病原体的作用。参与此项目的MBRS学生将 继续根据前一笔赠款开始的工作。形成稳定的 通过营养缺陷型突变体的互补获得二倍体。 演示了。这打开了利用性别性遗传学来 分析这种宿主-病原体的相互作用。之前的遗传分析已经 表明这种相互作用是由基因对基因的关系控制的。 从事这一项目的MBRS学生将分离出美国人的ade突变体。 霍尔代伊，表现为红色。因为这个突变是 隐性的二倍体将是透明的。然而，重新单倍化将 在二倍体细胞集落中产生红色扇区。这些红色单倍体将 被分离和分析以确定营养缺乏性标记的分离， 交配型和一种毒力基因。这将是迈向 克隆与该病原菌毒力直接相关的基因 以及它的真核宿主。

Ustilago hordei is a basidiomycetes which causes covered smut of barley. Asexual growth occurs in the form of non-pathogenic, haploid, budding yeast-like sporidia. Fusion of sporidia, which is controlled by a single mating-type locus with two alleles, results in a pathogenic, mycelial dikaryon. We have shown that mating involves communication between cells of the opposite mating type, resulting in the formation of conjugation tubes. A very exciting finding is that small molecular weight compounds, or pheromones, act as signals. We have isolated numerous mutants from both mating types which are incapable of mating. Some of these mutants are unable to produce active pheromone and others are incapable of making conjugation tubes. The long range goal of this research effort is to biochemically characterize purified pheromones and clone genes involved in this pheromone mediated cell-cell interaction in order to better understand the basic mechanisms involved in the conversion of a non- pathogen to a pathogen. The MBRS student involved in this project will continue work started under the previous grant. The formation of stable U. hordei diploids by complementation of auxotrophic mutants was demonstrated. This opens the door to using parasexual genetics to analyze this host-pathogen interaction. Previous genetic analyses have shown this interaction to be governed by a gene-for-gene relationship. The MBRS student working on this project will isolate ade mutants of U. hordei which display a red color phenotype. Since this mutation is recessive, diploids will be hyaline. However, rehaploidization will yield red sectors in colonies of diploid cells. These red haploids will be isolated and analyzed to determine segregation of auxotrophic markers, mating-type and a virulence genes. This will be the first step toward cloning genes directly involved in virulence of this pathogenic fungus and its eukaryotic host.