Hanna-Rose W, Han M
Howard Hughes Medical Institute and Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.
Development. 1999 Jan;126(1):169-79. doi: 10.1242/dev.126.1.169.
In screens for mutants defective in vulval morphogenesis, multiple mutants were isolated in which the uterus and the vulva fail to make a proper connection. We describe five alleles that define the gene cog-2, for connection of gonad defective. To form a functional connection between the vulva and the uterus, the anchor cell must fuse with the multinucleate uterine seam cell, derived from uterine cells that adopt a (pi) lineage. In cog-2 mutants, the anchor cell does not fuse to the uterine seam cell and, instead, remains at the apex of the vulva, blocking the connection between the vulval and uterine lumens, resulting in an egg-laying defective phenotype. According to lineage analysis and expression assays for two (pi)-cell-specific markers, induction of the (pi) fate occurs normally in cog-2 mutants. We have cloned cog-2 and shown that it encodes a Sox family transcription factor that is expressed in the (pi) lineage. Thus, it appears that COG-2 is a transcription factor that regulates a late-stage aspect of uterine seam cell differentiation that specifically affects anchor cell-uterine seam cell fusion.
在筛选外阴形态发生缺陷的突变体时，分离出了多个突变体，其中子宫和外阴未能建立正常连接。我们描述了五个等位基因，它们定义了基因cog-2，即性腺连接缺陷基因。为了在外阴和子宫之间形成功能性连接，锚定细胞必须与多核子宫缝细胞融合，该细胞源自采用(pi)谱系的子宫细胞。在cog-2突变体中，锚定细胞不与子宫缝细胞融合，而是停留在外阴顶端，阻断外阴和子宫腔之间的连接，导致产卵缺陷表型。根据对两种(pi)细胞特异性标记物的谱系分析和表达检测，(pi)命运的诱导在cog-2突变体中正常发生。我们已经克隆了cog-2，并表明它编码一种在(pi)谱系中表达的Sox家族转录因子。因此，COG-2似乎是一种转录因子，它调节子宫缝细胞分化的晚期阶段，特别影响锚定细胞与子宫缝细胞的融合。
