Silakowski B, Pospiech A, Neumann B, Schairer H U
Zentrum für Molekulare Biologie der Universität Heidelberg, Germany.
J Bacteriol. 1996 Dec;178(23):6706-13. doi: 10.1128/jb.178.23.6706-6713.1996.
Stigmatella aurantiaca is a prokaryotic organism that undergoes a multicellular cycle of development resulting in the formation of a fruiting body. For analyzing this process, mutants defective in fruiting body formation have been induced by transposon mutagenesis using a Tn5-derived transposon. About 800 bp upstream of the transposon insertion of mutant AP182 which inactivates a gene (fbfB) involved in fruiting, a further gene (fbfA) needed for fruiting body formation was detected. Inactivation of fbfA leads to mutants which form only non-structured clumps instead of the wild-type fruiting body. The mutant phenotype of fbfA mutants can be partially suppressed by mixing the mutant cells with cells of some independent mutants defective in fruiting body formation. The fbfA gene is transcribed after 8 h of development as determined by measuring the induction of beta-galactosidase activity of a fbfA-delta(trp)-lacZ fusion gene and by Northern (RNA) analysis using an insertion encoding a stable mRNA. The predicted polypeptide FbfA shows a homology of about 30% to NodC of rhizobia, an N-acetylglucosamine-transferase which is involved in the synthesis of the sugar backbone of lipo-oligosaccharides. These induce the formation of the root nodules in the Papilionaceae. Besides the predicted molecular mass of 45.5 kDa, the hydropathy profile reveals a structural relationship to the NodC polypeptide.
橙色粘球菌是一种原核生物,经历多细胞发育周期,最终形成子实体。为了分析这一过程,利用源自Tn5的转座子通过转座子诱变诱导了子实体形成缺陷的突变体。在使参与子实体形成的基因(fbfB)失活的突变体AP182的转座子插入位点上游约800 bp处,检测到另一个子实体形成所需的基因(fbfA)。fbfA失活导致突变体仅形成无结构的团块,而非野生型子实体。将fbfA突变体的细胞与一些子实体形成缺陷的独立突变体的细胞混合,可以部分抑制fbfA突变体的突变表型。通过测量fbfA-δ(trp)-lacZ融合基因的β-半乳糖苷酶活性的诱导情况以及使用编码稳定mRNA的插入片段进行Northern(RNA)分析确定,fbfA基因在发育8小时后转录。预测的多肽FbfA与根瘤菌的NodC具有约30%的同源性,NodC是一种参与脂寡糖糖骨架合成的N-乙酰葡糖胺转移酶。这些物质在豆科植物中诱导根瘤的形成。除了预测的45.5 kDa分子量外,亲水性图谱揭示了与NodC多肽的结构关系。