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伤口诱导的 Wnt 表达程序控制扁形动物再生的极性。

A wound-induced Wnt expression program controls planarian regeneration polarity.

机构信息

Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.

出版信息

Proc Natl Acad Sci U S A. 2009 Oct 6;106(40):17061-6. doi: 10.1073/pnas.0906823106. Epub 2009 Sep 14.

DOI:10.1073/pnas.0906823106
PMID:19805089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2743725/
Abstract

Regeneration requires specification of the identity of new tissues to be made. Whether this process relies only on intrinsic regulative properties of regenerating tissues or whether wound signaling provides input into tissue repatterning is not known. The head-versus-tail regeneration polarity decision in planarians, which requires Wnt signaling, provides a paradigm to study the process of tissue identity specification during regeneration. The Smed-wntP-1 gene is required for regeneration polarity and is expressed at the posterior pole of intact animals. Surprisingly, wntP-1 was expressed at both anterior- and posterior-facing wounds rapidly after wounding. wntP-1 expression was induced by all types of wounds examined, regardless of whether wounding prompted tail regeneration. Regeneration polarity was found to require new expression of wntP-1. Inhibition of the wntP-2 gene enhanced the polarity phenotype due to wntP-1 inhibition, with new expression of wntP-2 in regeneration occurring subsequent to expression of wntP-1 and localized only to posterior-facing wounds. New expression of wntP-2 required wound-induced wntP-1. Finally, wntP-1 and wntP-2 expression changes occurred even in the absence of neoblast stem cells, which are required for regeneration, suggesting that the role of these genes in polarity is independent of and instructive for tail formation. These data indicate that wound-induced input is involved in resetting the normal polarized features of the body axis during regeneration.

摘要

再生需要指定新组织的身份。这个过程是否只依赖于再生组织的内在调节特性,或者伤口信号是否为组织重编程提供输入尚不清楚。在涡虫中,头部与尾部的再生极性决定需要 Wnt 信号,这为研究再生过程中组织身份指定提供了一个范例。Smed-wntP-1 基因是再生极性所必需的,并且在完整动物的后极表达。令人惊讶的是,wntP-1 在受伤后很快就在前向和后向伤口处表达。wntP-1 的表达被所有类型的伤口诱导,无论伤口是否引发尾部再生。发现再生极性需要 wntP-1 的新表达。抑制 wntP-2 基因增强了由于 wntP-1 抑制引起的极性表型,wntP-2 的新表达发生在 wntP-1 之后,并且仅局限于后向伤口。wntP-2 的新表达需要伤口诱导的 wntP-1。最后,即使在不需要再生的成体干细胞存在的情况下,wntP-1 和 wntP-2 的表达变化也会发生,这表明这些基因在极性中的作用独立于并指导尾部形成。这些数据表明,伤口诱导的输入参与了在再生过程中重置身体轴的正常极化特征。

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A wound-induced Wnt expression program controls planarian regeneration polarity.伤口诱导的 Wnt 表达程序控制扁形动物再生的极性。
Proc Natl Acad Sci U S A. 2009 Oct 6;106(40):17061-6. doi: 10.1073/pnas.0906823106. Epub 2009 Sep 14.
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Smed-betacatenin-1 is required for anteroposterior blastema polarity in planarian regeneration.涡虫再生过程中前后芽基极性的形成需要Smed-β-连环蛋白-1。
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activin-2 is required for regeneration of polarity on the planarian anterior-posterior axis.激活素-2 对于扁形动物前后轴极性的再生是必需的。
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map3k1 suppresses terminal differentiation of migratory eye progenitors in planarian regeneration.Map3k1抑制涡虫再生过程中迁移性眼祖细胞的终末分化。
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本文引用的文献

1
Smed-Evi/Wntless is required for beta-catenin-dependent and -independent processes during planarian regeneration.在涡虫再生过程中,Smed-Evi/Wntless对于β-连环蛋白依赖性和非依赖性过程都是必需的。
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Silencing of Smed-betacatenin1 generates radial-like hypercephalized planarians.沉默Smed-β-连环蛋白1可产生放射状头部过度发育的涡虫。
Development. 2008 Apr;135(7):1215-21. doi: 10.1242/dev.020289. Epub 2008 Feb 20.
7
Beta-catenin defines head versus tail identity during planarian regeneration and homeostasis.β-连环蛋白在涡虫再生和体内平衡过程中决定头部与尾部特征。
Science. 2008 Jan 18;319(5861):323-7. doi: 10.1126/science.1150029. Epub 2007 Dec 6.
8
Smed-betacatenin-1 is required for anteroposterior blastema polarity in planarian regeneration.涡虫再生过程中前后芽基极性的形成需要Smed-β-连环蛋白-1。
Science. 2008 Jan 18;319(5861):327-30. doi: 10.1126/science.1149943. Epub 2007 Dec 6.
9
Molecular basis for the nerve dependence of limb regeneration in an adult vertebrate.成年脊椎动物肢体再生的神经依赖性的分子基础。
Science. 2007 Nov 2;318(5851):772-7. doi: 10.1126/science.1147710.
10
BMP signaling regulates the dorsal planarian midline and is needed for asymmetric regeneration.骨形态发生蛋白信号传导调节涡虫的背侧中线,并且是不对称再生所必需的。
Development. 2007 Nov;134(22):4043-51. doi: 10.1242/dev.007138. Epub 2007 Oct 17.