Small S, Kraut R, Hoey T, Warrior R, Levine M
Department of Biological Sciences, Fairchild Center, Columbia University, New York, New York 10027.
Genes Dev. 1991 May;5(5):827-39. doi: 10.1101/gad.5.5.827.
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 Krüppel (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.
果蝇早期胚胎中，初级成对规则基因even-skipped（eve）的周期性七条纹模式，是由母体和间隙基因蛋白的粗略重叠梯度启动的。先前的遗传学研究表明，其中一条条纹，即条纹2，是由母体形态发生素双胸蛋白（bcd）和间隙蛋白驼背蛋白（hb）启动的，而条纹的边界则是由选择性抑制形成的，在前部区域涉及间隙蛋白巨人蛋白（gt），在后部区域涉及克虏伯蛋白（Kr）。在这里，我们提供了几条与条纹2表达的这一模型一致的证据，包括体外DNA结合实验和培养细胞中的瞬时共转染试验。这些实验表明，抑制涉及竞争或短程淬灭机制，即gt和Kr的结合会干扰bcd和hb激活剂在eve条纹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调节元件组成的启动子的一般特性。
