Drosophila UNR is required for translational repression of male-specific lethal 2 mRNA during regulation of X-chromosome dosage compensation
Drosophila UNR is required for translational repression of male-specific lethal 2 mRNA during regulation of X-chromosome dosage compensation
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DOI：
10.1101/gad.371906
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发表时间：
2006-02-01
影响因子：
10.5
通讯作者：
Gebauer, F
中科院分区：
文献类型：
--
作者：
Abaza, I;Coll, O;Gebauer, F
性致死RNA结合蛋白（SXL）抑制雄性特异性致死2（msl-2）mRNA翻译是果蝇X染色体剂量补偿的重要调控步骤。哺乳动物的N-ras上游（UNR）蛋白参与了mRNA稳定性的调节和依赖于内部核糖体进入位点（IRES）的mRNA翻译。在这里，我们已经确定了果蝇同源的哺乳动物UNR作为辅因子所需的SXL介导的抑制ms 1 -2翻译。UNR与SXL相互作用，SXL是一种女性特异性蛋白质。尽管UNR存在于雄性和雌性果蝇中，但SXL与msf-2 mRNA的3'非翻译区（UTR）中富含尿苷的序列的结合将UNR募集到相邻的调节序列，从而赋予UNR性别特异性功能。这些数据确定了一种新的调节剂的剂量补偿果蝇的行为协调与SXL的翻译控制。
The inhibition of male-specific lethal 2 (msl-2) mRNA translation by the RNA-binding protein sex-lethal (SXL) is an essential regulatory step for X-chromosome dosage compensation in Drosophila melanogaster. The mammalian upstream of N-ras (UNR) protein has been implicated in the regulation of mRNA stability and internal ribosome entry site (IRES)-dependent mRNA translation. Here we have identified the Drosophila homolog of mammalian UNR as a cofactor required for SXL-mediated repression of ms1-2 translation. UNR interacts with SXL, a female-specific protein. Although UNR is present in both male and female flies, binding of SXL to uridine-rich sequences in the 3' untranslated region (UTR) of msf-2 mRNA recruits UNR to adjacent regulatory sequences, thereby conferring a sex-specific function to UNR. These data identify a novel regulator of dosage compensation in Drosophila that acts coordinately with SXL in translational control.