Twisted gastrulation is a conserved extracellular BMP antagonist

被引:231
作者
Ross, JJ
Shimmi, O
Vilmos, P
Petryk, A
Kim, H
Gaudenz, K
Hermanson, S
Ekker, SC
O'Connor, MB [1 ]
Marsh, JL
机构
[1] Univ Minnesota, Dept Genet, Minneapolis, MN 55455 USA
[2] Univ Minnesota, Dept Dev & Cell Biol, Minneapolis, MN 55455 USA
[3] Univ Minnesota, Howard Hughes Med Inst, Minneapolis, MN 55455 USA
[4] Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA
[5] Univ Minnesota, Arnold & Mabel Beckman Ctr Transposon Res, Minneapolis, MN 55455 USA
[6] Univ Calif Irvine, Dept Dev & Cell Biol, Irvine, CA 92697 USA
关键词
D O I
10.1038/35068578
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Bone morphogenetic protein (BMP) signalling regulates embryonic dorsal-ventral cell fate decisions in flies, frogs and fish(1). BMP activity is controlled by several secreted factors including the antagonists chordin and short gastrulation (SOG)(2,3). Here we show that a second secreted protein, Twisted gastrulation (Tsg)(4), enhances the antagonistic activity of Sog/chordin. In Drosophila, visualization of BMP signalling using anti-phospho-Smad staining(5) shows that the tsg and sog loss-of-function phenotypes are very similar. In S2 cells and imaginal discs, TSG and SOG together make a more effective inhibitor of BMP signalling than either of them alone. Blocking Tsg function in zebrafish with morpholino oligonucleotides causes ventralization similar to that produced by chordin mutants. Co-injection of sub-inhibitory levels of morpholines directed against both Tsg and chordin synergistically enhances the penetrance of the ventralized phenotype. We show that Tsgs from different species are functionally equivalent, and conclude that Tsg is a conserved protein that functions with SOG/chordin to antagonize BMP signalling.
引用
收藏
页码:479 / 483
页数:5
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