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Wnt-5/尾鳍在脊椎动物轴形成过程中作为Wnt/β-连环蛋白活性的负调节因子发挥作用。

Wnt-5/pipetail functions in vertebrate axis formation as a negative regulator of Wnt/beta-catenin activity.

作者信息

Westfall Trudi A, Brimeyer Ryan, Twedt Jen, Gladon Jean, Olberding Andrea, Furutani-Seiki Makoto, Slusarski Diane C

机构信息

Department of Biological Sciences, University of Iowa, Iowa City, IA 52242, USA.

出版信息

J Cell Biol. 2003 Sep 1;162(5):889-98. doi: 10.1083/jcb.200303107.

DOI:10.1083/jcb.200303107
PMID:12952939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2172822/
Abstract

We provide genetic evidence defining a role for noncanonical Wnt function in vertebrate axis formation. In zebrafish, misexpression of Wnt-4, -5, and -11 stimulates calcium (Ca2+) release, defining the Wnt/Ca2+ class. We describe genetic interaction between two Wnt/Ca2+ members, Wnt-5 (pipetail) and Wnt-11 (silberblick), and a reduction of Ca2+ release in Wnt-5/pipetail. Embryos genetically depleted of both maternal and zygotic Wnt-5 product exhibit cell movement defects as well as hyperdorsalization and axis-duplication phenotypes. The dorsalized phenotypes result from increased beta-catenin accumulation and activation of downstream genes. The Wnt-5 loss-of-function defect is consistent with Ca2+ modulation having an antagonistic interaction with Wnt/beta-catenin signaling.

摘要

我们提供了遗传学证据，确定了非经典Wnt功能在脊椎动物轴形成中的作用。在斑马鱼中，Wnt-4、-5和-11的错误表达会刺激钙（Ca2+）释放，从而定义了Wnt/Ca2+类别。我们描述了两个Wnt/Ca2+成员Wnt-5（pipetail）和Wnt-11（silberblick）之间的遗传相互作用，以及Wnt-5/pipetail中Ca2+释放的减少。在母源和合子Wnt-5产物均被基因敲除的胚胎中，表现出细胞运动缺陷以及过度背化和轴重复表型。背化表型是由β-连环蛋白积累增加和下游基因激活导致的。Wnt-5功能丧失缺陷与Ca2+调节与Wnt/β-连环蛋白信号传导的拮抗相互作用一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5a2353d75470/200303107f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/1e605f554c1c/200303107f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/33637d1298ac/200303107f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/c4a0e0af6533/200303107f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/4a291bceec0f/200303107f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5dd2fe966897/200303107f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5f5ccea66baa/200303107f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5a2353d75470/200303107f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/1e605f554c1c/200303107f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/2ccc9dd1bbc4/200303107f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/33637d1298ac/200303107f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/c4a0e0af6533/200303107f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/4a291bceec0f/200303107f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5dd2fe966897/200303107f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5f5ccea66baa/200303107f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50fd/2172822/5a2353d75470/200303107f8.jpg

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