Søgaard-Andersen L, Slack F J, Kimsey H, Kaiser D
Department of Biochemistry, Stanford University School of Medicine, California, 94305, USA.
Genes Dev. 1996 Mar 15;10(6):740-54. doi: 10.1101/gad.10.6.740.
C-factor, the product of the csgA gene, is a cell-surface associated short-range intercellular signaling protein in Myxococcus xanthus. C-factor is required for at least four responses during starvation-induced fruiting body morphogenesis: rippling, aggregation, sporulation, and full expression of the csgA gene, all of which fail in a csgA mutant. To analyze the C-factor signaling pathway, eight Tn5 lac insertion mutants that began but failed to complete fruiting body aggregation were characterized. Seven of the insertions identified genes whose products function in the csgA signaling pathway. The seven mutants were differentially deficient in the C-factor responses, and could be divided into two classes on the basis of those differences. On one hand, the four mutants in class I were deficient in rippling and aggregation, but sporulated and produced C-factor at wild-type levels. The Tn5 lac insertions in the class I mutants mapped to the frz locus, which encodes a signal transduction system that controls the frequency of single cell reversals. On the other hand, mutants carrying any of the three closely linked class II Tn5 lac insertions had deficiencies in all four C-factor responses. Because the sporulation defect in the class 11 mutants is cell autonomous, the data suggest that the primary defect in these mutants is an inability to respond to the C-factor signal. All the data can be explained by a model in which the first part of the C-factor signaling pathway is common to all four C-factor-dependent responses. The genes identified by the class 11 insertions would function in the common part. Downstream of class II, the pathway branches. One branch includes the frz genes and leads to aggregation and rippling; the second branch leads to sporulation and controls the level of csgA gene expression. This model was confirmed in epistasis tests with characterized frz mutations, a csgA null mutation, and a class II mutation.
C因子是csgA基因的产物,是黄色粘球菌中一种与细胞表面相关的短程细胞间信号蛋白。在饥饿诱导的子实体形态发生过程中,C因子至少参与四种反应:波动、聚集、孢子形成以及csgA基因的完全表达,而在csgA突变体中,所有这些反应均无法进行。为了分析C因子信号通路,对八个开始但未能完成子实体聚集的Tn5 lac插入突变体进行了表征。其中七个插入突变体鉴定出了其产物在csgA信号通路中起作用的基因。这七个突变体在C因子反应中存在不同程度的缺陷,可根据这些差异分为两类。一方面,I类中的四个突变体在波动和聚集方面存在缺陷,但能形成孢子并产生野生型水平的C因子。I类突变体中的Tn5 lac插入位点定位于frz基因座,该基因座编码一个控制单细胞反转频率的信号转导系统。另一方面,携带三个紧密连锁的II类Tn5 lac插入突变体中的任何一个在所有四种C因子反应中均存在缺陷。由于II类突变体中的孢子形成缺陷是细胞自主的,数据表明这些突变体中的主要缺陷是无法对C因子信号作出反应。所有数据都可以用一个模型来解释,即C因子信号通路的第一部分对于所有四种依赖C因子的反应是共同的。II类插入突变体鉴定出的基因将在共同部分起作用。在II类下游,通路发生分支。一个分支包括frz基因,导致聚集和波动;第二个分支导致孢子形成并控制csgA基因的表达水平。在与特征性frz突变、csgA无效突变和II类突变进行的上位性测试中,该模型得到了证实。