Baba K, Takeshita A, Majima K, Ueda R, Kondo S, Juni N, Yamamoto D
Developmental Genetics Group, Mitsubishi Kasei Institute of Life Sciences, Machida, Tokyo 194-8511, Japan.
Mol Cell Biol. 1999 Jun;19(6):4405-13. doi: 10.1128/MCB.19.6.4405.
We isolated a Drosophila fickleP (ficP) mutant with a shortened copulatory duration and reduced adult-stage life span. The reduced copulatory duration is ascribable to incomplete fusion of the left and right halves of the apodeme that holds the penis during copulation. ficP is an intronic mutation occurring in the Btk gene, a gene which encodes two forms (type 1 and type 2) of a Bruton's tyrosine kinase (Btk) family cytoplasmic tyrosine kinase as a result of alternative exon usage. The ficP mutation prevents the formation of the type 2 isoform but leaves expression of the type 1 transcript intact. Ubiquitous overexpression of the wild-type cDNA by using a heat shock 70 promoter during the late larval or pupal stages rescued the life span and genital defects in the mutant, respectively, establishing the causal relationship between the ficP phenotypes and the Btk gene mutation. The stage specificity of the rescuing ability suggests that the Btk gene is required for the development of male genitalia and substrates required for adult survival.
我们分离出了一种果蝇 fickleP（ficP）突变体，其交配持续时间缩短，成虫期寿命缩短。交配持续时间缩短归因于交配时固定阴茎的表皮左右两半未完全融合。ficP 是发生在 Btk 基因内含子中的突变，该基因由于外显子的选择性使用，编码布鲁顿酪氨酸激酶（Btk）家族细胞质酪氨酸激酶的两种形式（1 型和 2 型）。ficP 突变阻止了 2 型异构体的形成，但 1 型转录本的表达保持完整。在幼虫后期或蛹期使用热休克 70 启动子对野生型 cDNA 进行全身性过表达，分别挽救了突变体的寿命和生殖缺陷，从而确立了 ficP 表型与 Btk 基因突变之间的因果关系。挽救能力的阶段特异性表明，Btk 基因是雄性生殖器发育和成虫存活所需底物所必需的。
