Autosomal dominant polycystic kidney disease (ADPKD) is a renal disorder caused by mutations in the PKD2 gene, which encodes polycystin-2/Pkd2, a transient receptor potential channel. The precise role of Pkd2 in cyst formation remains unclear. The fission yeast Schizosaccharomyces pombe has a putative transient receptor potential channel, Pkd2, which shares similarities with human Pkd2. In this study, truncation analyses of fission yeast Pkd2 were conducted to investigate its localization and function. The results revealed that Pkd2 localizes not only to the plasma membrane but also to the endoplasmic reticulum (ER) in fission yeast. Furthermore, Pkd2 regulates calcium signaling in fission yeast, with the transmembrane domains of Pkd2 being sufficient for these processes. Specifically, the C-terminal region of Pkd2 plays a crucial role in the regulation of calcium signaling. Interestingly, human Pkd2 also localized to the ER and had some impact on calcium signaling in fission yeast. However, human Pkd2 failed to suppress the loss of fission yeast Pkd2. These findings indicate that hPkd2 may not completely substitute for cellular physiology of fission yeast Pkd2. This study provides insights into the localization and functional characteristics of Pkd2 in fission yeast, contributing to our understanding of the pathogenesis of ADPKD.

中文翻译：

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Pkd2 是与常染色体显性多囊肾病相关的突变，定位于内质网并调节裂殖酵母中的钙信号传导

常染色体显性多囊肾病 (ADPKD) 是一种由PKD2基因突变引起的肾脏疾病，该基因编码多囊蛋白-2/Pkd2（一种瞬时受体电位通道）。Pkd2 在囊肿形成中的确切作用仍不清楚。裂殖酵母裂殖酵母具有假定的瞬时受体电位通道 Pkd2，它与人类 Pkd2 具有相似之处。在本研究中，对裂殖酵母 Pkd2 进行截短分析以研究其定位和功能。结果表明，在裂殖酵母中，Pkd2 不仅定位于质膜，还定位于内质网 (ER)。此外，Pkd2 调节裂殖酵母中的钙信号传导，Pkd2 的跨膜结构域足以完成这些过程。具体来说，Pkd2 的 C 末端区域在钙信号传导的调节中起着至关重要的作用。有趣的是，人类 Pkd2 也定位于 ER，并对裂殖酵母中的钙信号传导产生一些影响。然而，人Pkd2未能抑制裂殖酵母Pkd2的损失。这些发现表明 hPkd2 可能无法完全替代裂殖酵母 Pkd2 的细胞生理学。这项研究深入了解了裂殖酵母中 Pkd2 的定位和功能特征，有助于我们了解 ADPKD 的发病机制。