TRANSCRIPTIONAL REGULATION OF A PAIR-RULE STRIPE IN DROSOPHILA
TRANSCRIPTIONAL REGULATION OF A PAIR-RULE STRIPE IN DROSOPHILA
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DOI：
10.1101/gad.5.5.827
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发表时间：
1991-05-01
影响因子：
10.5
通讯作者：
LEVINE, M
中科院分区：
文献类型：
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作者：
SMALL, S;KRAUT, R;LEVINE, M
初级配对规则基因even skipped（eve）的周期性七条纹模式是由早期果蝇胚胎中母体和gap基因蛋白质的粗糙重叠梯度启动的。 先前的遗传学研究表明，条纹之一，条纹2，是由母体形态原bicoid（bcd）和差距蛋白hunchback（hb）发起的，而条纹的边界是由选择性抑制形成的，涉及差距蛋白巨人（gt）在前部区域和Kruppel（Kr）蛋白在后部区域。 在这里，我们提出了几条线的证据，这是与该模型相一致的条纹2的表达，包括在体外DNA结合实验和瞬时共转染测定培养细胞。 这些实验表明，阻遏涉及竞争或短程淬灭机制，由此gt和Kr的结合干扰bcd和hb激活剂在eve stripe 2启动子元件内重叠或相邻位点的结合或活性。 这种短程抑制可能反映了由多个但自主的调节元件组成的启动子的一般性质。
The periodic, seven-stripe pattern of the primary pair-rule gene even-skipped (eve) is initiated by crude, overlapping gradients of maternal and gap gene proteins in the early Drosophila embryo. Previous genetic studies suggest that one of the stripes, stripe 2, is initiated by the maternal morphogen bicoid (bcd) and the gap protein hunchback (hb), while the borders of the stripe are formed by selective repression, involving the gap protein giant (gt) in anterior regions and the Kruppel (Kr) protein in posterior regions. Here, we present several lines of evidence that are consistent with this model for stripe 2 expression, including in vitro DNA-binding experiments and transient cotransfection assays in cultured cells. These experiments suggest that repression involves a competition or short-range quenching mechanism, whereby the binding of gt and Kr interferes with the binding or activity of bcd and hb activators at overlapping or neighboring sites within the eve stripe 2 promoter element. Such short-range repression could reflect a general property of promoters composed of multiple, but autonomous regulatory elements.