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对咽部进行选择性截肢可确定涡虫中一种依赖FoxA的再生程序。

Selective amputation of the pharynx identifies a FoxA-dependent regeneration program in planaria.

作者信息

Adler Carolyn E, Seidel Chris W, McKinney Sean A, Sánchez Alvarado Alejandro

机构信息

Stowers Institute for Medical Research, Kansas City, United States.

出版信息

Elife. 2014 Apr 15;3:e02238. doi: 10.7554/eLife.02238.

DOI:10.7554/eLife.02238
PMID:24737865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3985184/
Abstract

Planarian flatworms regenerate every organ after amputation. Adult pluripotent stem cells drive this ability, but how injury activates and directs stem cells into the appropriate lineages is unclear. Here we describe a single-organ regeneration assay in which ejection of the planarian pharynx is selectively induced by brief exposure of animals to sodium azide. To identify genes required for pharynx regeneration, we performed an RNAi screen of 356 genes upregulated after amputation, using successful feeding as a proxy for regeneration. We found that knockdown of 20 genes caused a wide range of regeneration phenotypes and that RNAi of the forkhead transcription factor FoxA, which is expressed in a subpopulation of stem cells, specifically inhibited regrowth of the pharynx. Selective amputation of the pharynx therefore permits the identification of genes required for organ-specific regeneration and suggests an ancient function for FoxA-dependent transcriptional programs in driving regeneration. DOI: http://dx.doi.org/10.7554/eLife.02238.001.

摘要

涡虫扁形虫在被切断后能再生出每个器官。成体多能干细胞驱动着这种能力，但损伤如何激活干细胞并将其引导至合适的细胞谱系尚不清楚。在此，我们描述了一种单器官再生检测方法，即通过让动物短暂接触叠氮化钠来选择性诱导涡虫咽部排出。为了鉴定咽部再生所需的基因，我们对截肢后上调的356个基因进行了RNA干扰筛选，以成功进食作为再生的替代指标。我们发现，敲低20个基因会导致多种再生表型，并且在干细胞亚群中表达的叉头转录因子FoxA的RNA干扰会特异性抑制咽部的再生。因此，选择性切断咽部能够鉴定出器官特异性再生所需的基因，并提示了FoxA依赖的转录程序在驱动再生方面的古老功能。DOI: http://dx.doi.org/10.7554/eLife.02238.001 。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/932f2c68e3ab/elife02238f007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/fd5910400d88/elife02238f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/603cef468456/elife02238fs001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/61fc52ba29fb/elife02238fs002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/e912d344b0ea/elife02238f002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/87ce2a4427e4/elife02238f003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/e5f537c3f05c/elife02238fs007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8f3/3985184/932f2c68e3ab/elife02238f007.jpg

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The CCR4-NOT complex mediates deadenylation and degradation of stem cell mRNAs and promotes planarian stem cell differentiation.
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