E7F5和Ets2以剂量依赖性协同方式维持小鼠胚胎外胚层。

Elf5 and Ets2 maintain the mouse extraembryonic ectoderm in a dosage dependent synergistic manner.

作者信息

Donnison Martyn, Broadhurst Ric, Pfeffer Peter L

机构信息

AgResearch Ruakura, 10 Bisley Road, Hamilton 3214, New Zealand.

AgResearch Ruakura, 10 Bisley Road, Hamilton 3214, New Zealand; School of Biological Sciences, Victoria University of Wellington, PO Box 600, Wellington 6140, New Zealand.

出版信息

Dev Biol. 2015 Jan 1;397(1):77-88. doi: 10.1016/j.ydbio.2014.10.011. Epub 2014 Oct 23.

DOI:10.1016/j.ydbio.2014.10.011

Abstract

The ETS superfamily transcription factors Elf5 and Ets2 have both been implicated in the maintenance of the extraembryonic ectoderm (ExE) of the mouse embryo. While homozygous mutants of either gene result in various degrees of ExE tissue loss, heterozygotes are without phenotype. We show here that compound heterozygous mutants exhibit a phenotype intermediate to that of the more severe Elf5-/- and the milder Ets2-/- mutants. Functional redundancy is shown via commonalities in expression patterns, in target gene expression, and by partial rescue of Elf5-/- mutants through overexpressing Ets2 in an Elf5-like fashion. A model is presented suggesting the functional division of the ExE region into a proximal and distal domain based on gene expression patterns and the proximal to distal increasing sensitivity to threshold levels of combined Elf5 and Ets2 activity.

摘要

ETS超家族转录因子Elf5和Ets2都与维持小鼠胚胎的胚外外胚层（ExE）有关。虽然这两个基因的纯合突变体都会导致不同程度的ExE组织缺失，但杂合子没有表型。我们在此表明，复合杂合突变体表现出的表型介于更严重的Elf5-/-和较轻的Ets2-/-突变体之间。通过表达模式的共性、靶基因表达的共性以及以类似Elf5的方式过表达Ets2对Elf5-/-突变体的部分挽救，显示了功能冗余。本文提出了一个模型，该模型基于基因表达模式以及从近端到远端对Elf5和Ets2联合活性阈值水平的敏感性增加，将ExE区域功能划分为近端和远端结构域。