LEF-1, a nuclear factor coordinating signaling inputs from wingless and decapentaplegic

被引:381
作者
Riese, J
Yu, XN
Munnerlyn, A
Eresh, S
Hsu, SC
Grosschedl, R
Bienz, M
机构
[1] UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT MICROBIOL,SAN FRANCISCO,CA 94143
[2] UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT BIOCHEM,SAN FRANCISCO,CA 94143
关键词
SEGMENT POLARITY GENE; HOMEOTIC DROSOPHILA GENE; ALPHA-ENHANCER; HMG DOMAIN; NUCLEOPROTEIN STRUCTURES; ACTIVATION DOMAIN; DORSAL MESODERM; CELL-ADHESION; BETA-CATENIN; PROTEIN;
D O I
10.1016/S0092-8674(00)81924-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
wingless and decapentaplegic signal during endoderm induction in Drosophila to regulate expression of the homeotic gene Ultrabithorax. Here, we define a minimal wingless response sequence in the midgut enhancer of Ultrabithorax. We show that this sequence is recognized by the murine transcription factor LEF-1 (lymphocyte enhancer binding factor 1) in a ternary complex with armadillo protein, the cytoplasmic target of the wingless signaling pathway. In stable transformants, transcriptional stimulation of the Ultrabithorax enhancer by LEF-1 depends on armadillo. Furthermore, overexpression of LEF-1 bypasses the need for wingless signaling and causes phenotypes in the midgut, notum, and wing that mimic wingless hyperstimulation. Finally, efficient transcriptional stimulation by LEF-1 in the midgut depends also on the decapentaplegic response sequence and is limited spatially by decapentaplegic signaling. Thus, LEF-1 coordinates inputs from multiple positional signals, consistent with its architectural role in regulating the assembly of multiprotein enhancer complexes.
引用
收藏
页码:777 / 787
页数:11
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