日本黄色小说视频,日韩在线一区二区三区免费视频,亚洲电影在线,精品欧美日韩一区二区三区,久久香蕉国产线看观看亚洲卡,美女浴室,美女脱衣诱惑

    每時每刻，人體內(nèi)成千上萬的細胞在不停的移動，尤其是免疫反應(yīng)、創(chuàng)傷修復(fù)等過程中。細胞遷移過程發(fā)生錯誤可造成腫瘤的形成和癌細胞的擴散。最近加州理工學(xué)院的研究人員利用線蟲對細胞遷移的過程進行了深入研究，相關(guān)論文發(fā)表在PNAS上。

    文章的通訊作者Paul Sternberg教授說，我們知道如何找到原發(fā)腫瘤，知道癌細胞何時擴散，但卻對細胞何時遷移不清楚。Sternberg已對秀麗隱桿線蟲（Caenorhabditis elegans）進行過多年的研究，盡管秀麗隱桿線蟲的體型很小，卻與人類有著很多相同的基因。

    共同作者Mihoko Kato說，細胞遷移是一個非常保守的過程，因此無論發(fā)生在線蟲或哺乳動物還是人中，我們都認為參與此過程的是一群相同的基因。

    人或線蟲的細胞中都有成千上萬個基因，每個基因都有特定的功能，它們中約1/3比較活躍。為找到在細胞遷移過程中表達的基因，研究者以線蟲體內(nèi)一種名叫l(wèi)inker cell （LC）的細胞為研究對象，因為在線蟲發(fā)育過程中，LC細胞的遷移基本跨越了整個線蟲的長度。

    利用高性能的顯微鏡，在相隔12小時的兩個時間點，研究者觀察并分離了幼蟲的LC細胞，而后根據(jù)測序結(jié)果和計算分析找出在這兩個遷移時間點高表達的基因。這種方法叫做transc**tional profiling，優(yōu)點是可以使用任何細胞。

    研究人員選擇線蟲和人共有的基因，如果發(fā)現(xiàn)某個基因在線蟲細胞遷移中發(fā)揮作用，那么可以認為它在人體中也有助細胞遷移。

    對細胞遷移進行深入研究有助于開發(fā)阻止這一過程的特定基因靶向的藥物。進一步的研究中，研究人員希望找到遷移細胞的分子標記，進而為診斷提供便利。這項工作為找到癌細胞擴散的分子機制奠定了基礎(chǔ)。

    編譯自：New insight into complexities of cell migration

    Functional transc**tomics of a migrating cell in Caenorhabditis elegans

    Erich M. Schwarza,b,1, Mihoko Katoa,b,1, and Paul W. Sternberg

    In both metazoan development and metastatic cancer, migrating cells must carry out a detailed, complex program of sensing cues, binding substrates, and moving their cytoskeletons. The linker cell in Caenorhabditis elegans males undergoes a stereotyped migration that guides gonad organogenesis, occurs with precise timing, and requires the nuclear hormone receptor NHR-67. To better understand how this occurs, we performed RNA-seq of individually staged and dissected linker cells, comparing transc**tomes from linker cells of third-stage （L3） larvae, fourth-stage （L4） larvae, and nhr-67-RNAi–treated L4 larvae. We observed expression of 8,000–10,000 genes in the linker cell, 22–25% of which were up- or down-regulated 20-fold during development by NHR-67. Of genes that we tested by RNAi, 22% （45 of 204） were required for normal shape and migration, suggesting that many NHR-67–dependent, linker cell-enriched genes play roles in this migration. One unexpected class of genes up-regulated by NHR-67 was tandem pore potassium channels, which are required for normal linker-cell migration. We also found phenotypes for genes with human orthologs but no previously described migratory function. Our results provide an extensive catalog of genes that act in a migrating cell, identify unique molecular functions involved in nematode cell migration, and suggest similar functions in humans.