Prinz S, Klein F, Auer H, Schweizer D, Primig M
Institut für Botanik, Abteilung für Cytologie und Cytogenetik, Vienna, Austria.
Nucleic Acids Res. 1995 Sep 11;23(17):3449-56. doi: 10.1093/nar/23.17.3449.
We have studied the bipartite regulatory element UASH/URS1 in the promoter of HOP1, whose product is required for synapsis and correct pairing of homologous chromosomes during the first meiotic division. HOP1 is transcriptionally repressed by the URS1 motif during vegetative growth and induced during meiotic prophase by the UASH motif in cooperation with the bifunctional URS1 site, which is required for full induction of HOP1. While URS1 is bound in vitro by the Buf and Ume6 repressor proteins, we demonstrate for the first time by electrophoretic mobility shift assays and interference footprinting that the UASH site interacts in vitro with a novel factor called UBF (UASH binding factor) which is present in haploid and diploid cycling, as well as sporulating cells. Point mutations in the HOP1 UASH motif abolish UBF-dependent DNA binding activity in vitro and meiotic HOP1 gene expression in vivo. Furthermore, we show that UBF binds in vitro to UASH-like sequences in the promoter regions of several meiosis-specific and non-specific genes and propose that UBF mediates gene expression through its interaction with the UASH motif in both cycling and sporulating cells.
我们研究了HOP1启动子中的二分调控元件UASH/URS1,其产物是第一次减数分裂期间同源染色体联会和正确配对所必需的。在营养生长期间,HOP1被URS1基序转录抑制,而在减数分裂前期,UASH基序与双功能URS1位点协同作用诱导HOP1表达,URS1位点是HOP1完全诱导所必需的。虽然URS1在体外与Buf和Ume6阻遏蛋白结合,但我们首次通过电泳迁移率变动分析和干涉足迹法证明,UASH位点在体外与一种名为UBF(UASH结合因子)的新因子相互作用,该因子存在于单倍体和二倍体循环细胞以及孢子形成细胞中。HOP1 UASH基序中的点突变消除了体外UBF依赖性DNA结合活性和体内减数分裂HOP1基因表达。此外,我们表明UBF在体外与几个减数分裂特异性和非特异性基因启动子区域中的UASH样序列结合,并提出UBF通过其在循环细胞和孢子形成细胞中与UASH基序的相互作用介导基因表达。