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母源 Cdx2 对于小鼠发育并非必需。

Maternal Cdx2 is dispensable for mouse development.

机构信息

Department of Molecular, Cell, and Developmental Biology, University of California Santa Cruz, Santa Cruz, CA 95064, USA.

出版信息

Development. 2012 Nov;139(21):3969-72. doi: 10.1242/dev.086025. Epub 2012 Sep 19.

DOI:10.1242/dev.086025
PMID:22992952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3472595/
Abstract

In many invertebrate and vertebrate species, cell fates are assigned through the cellular inheritance of differentially localized maternal determinants. Whether mammalian embryogenesis is also regulated by deterministic mechanisms is highly controversial. The caudal domain transcription factor CDX2 has been reported to act as a maternal determinant regulating cell fate decisions in mouse development. However, this finding is contentious because of reports that maternal Cdx2 is not essential for development. Notably, all of the previously published studies of maternal Cdx2 relied on injected RNA interference constructs, which could introduce experimental variation. Only deletion of the maternal gene can unambiguously resolve its requirement in mouse development. Here, we genetically ablated maternal Cdx2 using a Cre/lox strategy, and we definitively establish that maternal Cdx2 is not essential for mouse development.

摘要

在许多无脊椎动物和脊椎动物物种中,细胞命运是通过差异定位的母体决定因素的细胞遗传来分配的。哺乳动物胚胎发生是否也受确定性机制调节是一个高度争议的问题。尾部域转录因子 CDX2 已被报道作为一种母体决定因素,调节小鼠发育中的细胞命运决定。然而,由于有报道称母体 Cdx2 对发育不是必需的,这一发现存在争议。值得注意的是,以前所有关于母体 Cdx2 的研究都依赖于注射 RNA 干扰构建体,这可能会引入实验变异。只有删除母体基因才能明确确定其在小鼠发育中的需求。在这里,我们使用 Cre/lox 策略从遗传上剔除了母体 Cdx2,并且明确确定母体 Cdx2 对小鼠发育不是必需的。

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本文引用的文献

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Decisions, decisions: how are they made in the early embryo--and does it matter?决策,决策:早期胚胎中的决策是如何做出的——这重要吗?
Reprod Biomed Online. 2011 Jun;22(6):509-11. doi: 10.1016/j.rbmo.2011.03.001. Epub 2011 Mar 5.
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5
Initiation of trophectoderm lineage specification in mouse embryos is independent of Cdx2.在小鼠胚胎中滋养外胚层谱系特化的起始不依赖于 Cdx2。
Development. 2010 Dec;137(24):4159-69. doi: 10.1242/dev.056630.
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Development. 2010 Mar;137(6):859-70. doi: 10.1242/dev.039487.
10
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