Tsai C, Gergen P
Department of Biochemistry and Cell Biology, State University of New York at Stony Brook 11794-5215, USA.
Development. 1995 Feb;121(2):453-62. doi: 10.1242/dev.121.2.453.
The segmentation genes runt and hairy are required for the proper transcriptional regulation of the pair-rule gene fushi tarazu during the blastoderm stage of Drosophila embryogenesis. The expression of different fushi tarazu reporter genes was examined in runt and hairy mutant embryos, as well as in runt over-expressing embryos in order to identify DNA elements responsible for mediating these regulatory effects. The results indicated that runt and hairy act through a common 32 base-pair element. This element, designated as fDE1, contains a binding site for a small family of orphan nuclear receptor proteins that are uniformly expressed in blastoderm embryos. The pair-rule expression of reporter gene constructs containing multimerized fDE1 elements depends on activation by runt and repression by hairy. Examination of reporter genes with mutated fDE1 elements provided further evidence that this element mediates both transcriptional activation and repression. Genetic experiments indicated that the opposing effects of runt and hairy were not due solely to cross-regulatory interactions between these two genes and that fDE1-dependent expression is regulated by factors in addition to runt and hairy.
在果蝇胚胎发育的胚盘阶段,分节基因runt和hairy对于体节极性基因ftz(fushi tarazu)的正确转录调控是必需的。为了鉴定负责介导这些调控作用的DNA元件,我们检测了不同ftz报告基因在runt和hairy突变胚胎以及runt过表达胚胎中的表达情况。结果表明,runt和hairy通过一个共同的32个碱基对的元件发挥作用。这个元件被命名为fDE1,它包含一个孤儿核受体蛋白小家族的结合位点,这些蛋白在胚盘胚胎中均匀表达。含有多聚化fDE1元件的报告基因构建体的体节极性表达取决于runt的激活和hairy的抑制。对含有突变fDE1元件的报告基因的检测提供了进一步的证据,证明该元件介导转录激活和抑制。遗传实验表明,runt和hairy的相反作用并非仅仅由于这两个基因之间的交叉调控相互作用,并且fDE1依赖的表达除了受runt和hairy调控外,还受其他因子的调控。