德國伯恩大學(xué)的科學(xué)家發(fā)現(xiàn)了一種先前未知的果蠅基因，該基因能夠調(diào)控脂肪代謝,。如果果蠅幼蟲中缺乏這種基因，則幼蟲會丟失了它們?nèi)康闹敬鎯?。因此,，研究人員叫這種基因為'schlank'。在哺乳動物中也存在一組基因,，其在結(jié)構(gòu)上與'schlank'非常相似,，這些基因可能在能量代謝方面與'schlank'有著相似的功能。
如果科學(xué)家破譯了一個基因的功能,，那么他們就可以去命名該基因,。但是果蠅基因的命名并不是按照傳統(tǒng)方式的,，基因的名字通常暗示著果蠅變成的樣子在單獨缺失某種基因的情況下。Schlank基因的命名也是這樣的,。如果該基因是完整的,，那么果蠅幼蟲能夠建立脂肪存儲，它將變肥,，而基因schlank變異的幼蟲,，會變得“苗條”。Michael Hoch教授解釋說,，在極端的例子中,，該基因的缺失甚至能夠致死。
研究人員對'schlank'做了進一步檢測,。根據(jù)他們的結(jié)果,，該基因包含一種結(jié)構(gòu)已知的神經(jīng)酰胺合酶（ceramide synthase）的功能。該酶是作為一種薄膜的原材料能夠?qū)C體的細胞圍住,。此外schlank也有一個調(diào)控功能,，能夠在促進脂質(zhì)合成的同時抑制存儲在體內(nèi)的脂肪代謝。
這不僅僅在果蠅中發(fā)生,，人類同樣可以產(chǎn)生神經(jīng)酰胺合酶,。人類中存在一組相關(guān)的基因稱之為Lass基因。神經(jīng)酰胺合酶對動物來說是很重要的,，相關(guān)基因的變異將導(dǎo)致嚴(yán)重的代謝紊亂和身體機能故障,。研究表明，老鼠的Lass基因能夠部分補償變異果蠅的schlank缺失,。
研究人員表示,，現(xiàn)在還沒有找到哺乳動物的Lass基因與類脂代謝調(diào)控的關(guān)聯(lián)。但是根據(jù)與schlank基因的比較,，他們認為兩者的功能應(yīng)該是非常相似的,。如果被證實將有助于開發(fā)新的減肥療法。（生物谷Bioon.com）
生物谷推薦原始出處：
The EMBO Journal 15 October 2009; doi:10.1038/emboj.2009.305
schlank, a member of the ceramide synthase family controls growth and body fat in Drosophila
Reinhard Bauer1, André Voelzmann1, Bernadette Breiden2, Ute Schepers2, Hany Farwanah2, Ines Hahn1, Franka Eckardt1, Konrad Sandhoff2 and Michael Hoch1
1 LIMES-Institute, Program Unit Development, Genetics & Molecular Physiology, Laboratory for Molecular Developmental Biology, University of Bonn, Bonn, Germany
2 LIMES-Institute, Program Unit Membrane Biology & Lipid Biochemistry, c/o Kekulé Institute of Organic Chemistry and Biochemistry, University of Bonn, Bonn, Germany
Ceramide synthases are highly conserved transmembrane proteins involved in the biosynthesis of sphingolipids, which are essential structural components of eukaryotic membranes and can act as second messengers regulating tissue homeostasis. However, the role of these enzymes in development is poorly understood due to the lack of animal models. We identified schlank as a new Drosophila member of the ceramide synthase family. We demonstrate that schlank is involved in the de novo synthesis of a broad range of ceramides, the key metabolites of sphingolipid biosynthesis. Unexpectedly, schlank mutants also show reduction of storage fat, which is deposited as triacylglyerols in the fat body. We found that schlank can positively regulate fatty acid synthesis by promoting the expression of sterol-responsive element-binding protein (SREBP) and SREBP-target genes. It further prevents lipolysis by downregulating the expression of triacylglycerol lipase. Our results identify schlank as a new regulator of the balance between lipogenesis and lipolysis in Drosophila. Furthermore, our studies of schlank and the mammalian Lass2 family member suggest a novel role for ceramide synthases in regulating body fat metabolism.
