Wu L P, Choe K M, Lu Y, Anderson K V
Center for Agricultural Biotechnology, University of Maryland Biotechnology Institute, College Park, Maryland 20742, USA.
Genetics. 2001 Sep;159(1):189-99. doi: 10.1093/genetics/159.1.189.
We have screened the third chromosome of Drosophila melanogaster for mutations that prevent the normal immune response. We identified mutant lines on the basis of their failure to induce transcription of an antibacterial peptide gene in response to infection or their failure to form melanized clots at the site of wounding. These mutations define 14 genes [immune response deficient (ird) genes] that have distinct roles in the immune response. We have identified the molecular basis of several ird phenotypes. Two genes, scribble and kurtz/modulo, affect the cellular organization of the fat body, the tissue responsible for antimicrobial peptide production. Two ird genes encode components of the signaling pathways that mediate responses to bacterial infection, a Drosophila gene encoding a homolog of I kappa B kinase (DmIkk beta) and Relish, a Rel-family transcription factor. These genetic studies should provide a basis for a comprehensive understanding of the genetic control of immune responses in Drosophila.
我们在黑腹果蝇的第三条染色体上筛选了可阻止正常免疫反应的突变。我们根据突变品系在受到感染时无法诱导抗菌肽基因转录,或在伤口部位无法形成黑化凝块来鉴定突变品系。这些突变定义了14个基因[免疫反应缺陷(ird)基因],它们在免疫反应中具有不同作用。我们已经确定了几种ird表型的分子基础。两个基因,scribble和kurtz/modulo,影响脂肪体的细胞组织,脂肪体是负责抗菌肽产生的组织。两个ird基因编码介导对细菌感染反应的信号通路的组成部分,一个果蝇基因编码IκB激酶(DmIkkβ)的同源物,以及Relish,一种Rel家族转录因子。这些遗传学研究应为全面理解果蝇免疫反应的遗传控制提供基础。