The fly trachea is the equivalent of the mammalian lung and is a useful model for human respiratory diseases. However, little is known about the molecular mechanisms underlying tracheal air filling during larval development. In this study, we discover that PTPMT1 has a function in tracheal air filling. PTPMT1 is a widely conserved, ubiquitously expressed mitochondrial phosphatase. To reveal PTPMT1's functions in genetically tractable invertebrates and whether those functions are tissue specific, we generate a Drosophila model of PTPMT1 depletion. We find that fly PTPMT1 mutants show impairments in tracheal air filling and subsequent activation of innate immune responses. On a cellular level, these defects are preceded by aggregation of mitochondria within the tracheal epithelial cells. Our work demonstrates a cell-type-specific role for PTPMT1 in fly tracheal epithelial cells to support air filling and to prevent immune activation. The establishment of this model will facilitate exploration of PTPMT1's physiological functions in vivo.

苍蝇的气管相当于哺乳动物的肺，是人类呼吸系统疾病的有用模型。然而，关于幼虫发育期间气管充气的分子机制知之甚少。在这项研究中，我们发现PTPMT1在气管充气中具有功能。PTPMT1是一种广泛保存的，普遍表达的线粒体磷酸酶。为了揭示PTPMT1在可遗传遗传的无脊椎动物中的功能以及这些功能是否是组织特异性的，我们生成了PTPMT1耗竭的果蝇模型。我们发现苍蝇PTPMT1突变体显示气管空气充盈受损，并随后激活先天免疫反应。在细胞水平上，这些缺陷先于气管上皮细胞内线粒体的聚集。我们的工作证明了PTPMT1在气管上皮细胞中的细胞类型特异性作用，以支持空气充填并防止免疫激活。该模型的建立将有助于探索PTPMT1的体内生理功能。