Louvet-Vallée Sophie, Kolotuev Irina, Podbilewicz Benjamin, Félix Marie-Anne
Institut Jacques Monod, CNRS-Universités Paris 6 et 7, 75251 Paris Cedex 05, France.
Genetics. 2003 Jan;163(1):133-46. doi: 10.1093/genetics/163.1.133.
To compare vulva development mechanisms in the nematode Oscheius sp. 1 to those known in Caenorhabditis elegans, we performed a genetic screen for vulva mutants in Oscheius sp. 1 CEW1. Here we present one large category of mutations that we call cov, which affect the specification of the Pn.p ventral epidermal cells along the antero-posterior axis. The Pn.p cells are numbered from 1 to 12 from anterior to posterior. In wild-type Oscheius sp. 1 CEW1, the P(4-8).p cells are competent to form the vulva and the progeny of P(5-7).p actually form the vulva, with the descendants of P6.p adopting a central vulval fate. Among the 17 mutations (defining 13 genes) that we characterize here, group 1 mutations completely or partially abolish P(4-8).p competence, and this correlates with early fusion of the Pn.p cells to the epidermal syncytium. In this group, we found a putative null mutation in the lin-39 HOM-C homolog, the associated phenotype of which could be weakly mimicked by injection of a morpholino against Osp1-lin-39 in the mother's germ line. Using cell ablation in a partially penetrant competence mutant, we show that vulval competence is partially controlled by a gonadal signal. Most other mutants found in the screen display phenotypes unknown in C. elegans. Group 2 mutants show a partial penetrance of Pn.p competence loss and an abnormal centering of the vulva on P5.p, suggesting that these two processes are coregulated by the same pathway in Oscheius sp. 1. Group 3 mutants display an enlarged competence group that includes P3.p, thus demonstrating the existence of a specific mechanism inhibiting P3.p competence. Group 4 mutants display an abnormal centering of the vulval pattern on P7.p and suggest that a specific mechanism centers the vulval pattern on a single Pn.p cell.
为了比较线虫Oscheius sp. 1与秀丽隐杆线虫已知的外阴发育机制,我们对Oscheius sp. 1 CEW1中的外阴突变体进行了遗传筛选。在此,我们展示了一大类我们称为cov的突变,这些突变影响沿前后轴的Pn.p腹侧表皮细胞的特化。Pn.p细胞从前到后编号为1至12。在野生型Oscheius sp. 1 CEW1中,P(4 - 8).p细胞有能力形成外阴,P(5 - 7).p的后代实际上形成外阴,其中P6.p的后代采用中央外阴命运。在我们在此表征的17个突变(定义13个基因)中,第1组突变完全或部分消除了P(4 - 8).p的能力,这与Pn.p细胞与表皮合胞体的早期融合相关。在这一组中,我们在lin - 39 HOM - C同源物中发现了一个推定的无效突变,其相关表型可通过在母体生殖系中注射针对Osp1 - lin - 39的吗啉代寡核苷酸而被微弱模拟。在一个部分显性的能力突变体中使用细胞消融,我们表明外阴能力部分受性腺信号控制。筛选中发现的大多数其他突变体表现出秀丽隐杆线虫中未知的表型。第2组突变体显示Pn.p能力丧失的部分显性以及外阴在P5.p上的异常居中,表明这两个过程在Oscheius sp. 1中由同一途径共同调节。第3组突变体显示能力组扩大,包括P3.p,从而证明存在抑制P3.p能力的特定机制。第4组突变体显示外阴模式在P7.p上的异常居中,并表明存在一种特定机制使外阴模式以单个Pn.p细胞为中心。