Lints Robyn, Emmons Scott W
Department of Molecular Genetics, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Genes Dev. 2002 Sep 15;16(18):2390-402. doi: 10.1101/gad.1012602.
Mutations in Caenorhabditis elegans gene mab-23 cause abnormal male tail morphology and abolish male fecundity but have no obvious effect in the hermaphrodite. Here we show that mab-23 encodes a DM (Doublesex/MAB-3) domain transcription factor necessary for specific aspects of differentiation in sex-specific tissues of the male. mab-23 is required for the patterning of posterior sensory neurons in the male nervous system, sex muscle differentiation, and morphogenesis of the posterior hypodermis, spicules, and proctodeum. Failure of mab-23 mutant males to sire progeny is due primarily to defective sex muscle-mediated turning during copulatory behavior and likely compounded by impairment of sperm passage through the proctodeum. In the male nervous system, mab-23 refines ray neuron subtype distribution by restricting expression of dopaminergic neurotransmitter identity through interactions with the Hox gene egl-5 and a TGF-beta-related signaling pathway. mab-23 has distinct roles and functions independent of mab-3, indicating different aspects of C. elegans male sexual differentiation are coordinated among DM domain family members. Our results support the hypothesis that DM domain genes derive from an ancestral male sexual regulator and suggest how regulation of sexual development has evolved in distinct ways in different phyla.
秀丽隐杆线虫基因mab - 23的突变会导致雄性尾部形态异常并使雄性生育力丧失,但对雌雄同体却没有明显影响。我们在此表明,mab - 23编码一种DM(双性/MAB - 3)结构域转录因子,该因子对于雄性性别特异性组织分化的特定方面是必需的。mab - 23对于雄性神经系统中后部感觉神经元的模式形成、性肌肉分化以及后部皮下组织、交合刺和直肠的形态发生是必需的。mab - 23突变雄性无法产生后代主要是由于交配行为中性肌肉介导的转向缺陷,并且可能因精子通过直肠的受损而加剧。在雄性神经系统中,mab - 23通过与Hox基因egl - 5和一条TGF - β相关信号通路相互作用,限制多巴胺能神经递质特性的表达,从而优化射线神经元亚型分布。mab - 23具有独立于mab - 3的不同作用和功能,这表明秀丽隐杆线虫雄性性别分化的不同方面在DM结构域家族成员之间是协调的。我们的结果支持了DM结构域基因源自一个祖先雄性性别调节因子的假说,并揭示了性别发育调控在不同门中是如何以不同方式进化的。