Tel: (05)2720411 ext. Office 66502 Lab 61515
Fax: (05)2722871
Email: biomlh@ccu.edu.tw
Associate Professor, Department of Biomedical Sciences, National Chung Cheng University
The human transmembrane protein TMEM258 is a component of the evolutionarily conserved oligosaccharyltransferase (OST) complexes, which are essential for N-linked protein glycosylation. Aberrant TMEM258 expression is associated with spinocerebellar ataxia type 20 and inflammatory bowel diseases. We previously identified the Drosophila ortholog Kuduk (Kud) and found that Kud modulates the nuclear envelope architecture and autophagy. Interestingly, we found that Kud can localize not only at endoplasmic reticulum where OST-mediated glycosylation occurs, but also at the nuclear envelope and unidentified cytoplasmic puncta. The observation suggests that Kud exhibits OST-independent functions. Our study will provide the knowledge not only for the molecular functions of Kud, but also for the pathogenesis of the diseases associated with TMEM258.
人類跨膜蛋白TMEM258是演化上具有高度保留性之寡醣轉移酶（OST）複合體的次單元，OST複合體負責調控蛋白質的N-醣基化，TMEM258的表現異常與脊髓小腦失調症和炎症性腸病的發生有關，但其病理機制尚待釐清。我們先前的研究找到TMEM258在果蠅的同源蛋白Kuduk(Kud)，並證實Kud能夠調控細胞核的形態(圖A-B)及細胞自噬作用(圖C-E)。我們發現Kud除了座落在OST複合體作用的內質網，亦會座落於核膜和一些未知的細胞質囊泡上，這表示Kud可能具有獨立於OST複合體以外的功能。我們將深入探討Kud的分子功能，進而釐清TMEM258相關疾病之病理機轉。
Dendrites are cell-specific characteristics of neurons, and are critical to receive stimulations from upstream neurons or the environment. Aberrant dendritic morphologies impair neuronal circuits and are correlated with neurological and neurodevelopmental disorders. The knowledge of mechanisms for controlling the dendrite pattering remains largely unclear. The Drosophila nervous system is well characterized in the cellular number and morphology. We aim to use Drosophila as a platform to carry out genetic screenings to study the cellular machineries for dendrite morphogenesis.
樹突是神經元特有的構造，負責接收來自上游神經元或外在環境的刺激。樹突形態異常會損害神經元迴路並可能導致神經發育相關之疾病。目前對於調控樹突形態發育之機制仍有許多尚未明瞭之處。果蠅是一個歷史悠久的模式生物，具有完備的遺傳資料，其神經系統的細胞數目及形態已被研究得很清楚。本實驗室利用果蠅進行遺傳篩選，尋找與探討調控神經樹突形態形成之細胞分子機制。
