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支持一年生脂鲤 Austrofundulus limnaeus 胚胎新型发育应激缓冲的基因表达模式。

Gene expression patterns that support novel developmental stress buffering in embryos of the annual killifish Austrofundulus limnaeus.

机构信息

Department of Biology, Portland State University, P.O. Box 751, Portland, OR 97207 USA.

出版信息

Evodevo. 2015 Jan 21;6:2. doi: 10.1186/2041-9139-6-2. eCollection 2015.

DOI:10.1186/2041-9139-6-2
PMID:25810897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4372997/
Abstract

BACKGROUND

The cellular signaling mechanisms and morphogenic movements involved in axis formation and gastrulation are well conserved between vertebrates. In nearly all described fish, gastrulation and the initial patterning of the embryonic axis occur concurrently with epiboly. However, annual killifish may be an exception to this norm. Annual killifish inhabit ephemeral ponds in South America and Africa and permanent populations persist by the production of stress-tolerant eggs. Early development of annual killifish is unique among vertebrates because their embryonic blastomeres disperse randomly across the yolk during epiboly and reaggregate several days later to form the embryo proper. In addition, annual killifish are able to arrest embryonic development in one to three stages, known as diapause I, II, and III. Little is known about how the highly conserved developmental signaling mechanisms associated with early vertebrate development may have shifted in order to promote the annual killifish phenotype. One of the most well-characterized and conserved transcription factors, oct4 (Pou5f1), may have a role in maintaining pluripotency. In contrast, BMP-antagonists such as chordin, noggin, and follistatin, have been previously shown to establish dorsal-ventral asymmetry during axis formation. Transcription factors from the SOXB1 group, such as sox2 and sox3, likely work to induce neural specification. Here, we determine the temporal expression of these developmental factors during embryonic development in the annual killifish Austrofundulus limnaeus using quantitative PCR and compare these patterns to other vertebrates.

RESULTS

Partial transcript sequences to oct4, sox2, sox3, chordin, noggin-1, noggin-2, and follistatin were cloned, sequenced, and identified in A. limnaeus. We found oct4, sox3, chordin, and noggin-1 transcripts to likely be maternally inherited. Expression of sox2, follistatin, and noggin-2 transcripts were highest in stages following a visible embryonic axis.

CONCLUSIONS

Our data suggest that embryonic cells acquire their germ layer identity following embryonic blastomere reaggregation in A. limnaeus. This process of cellular differentiation and axis formation may involve similar conserved signaling mechanisms to other vertebrates. We propose that the undifferentiated state is prolonged during blastomere dispersal, thus functioning as a developmental stress buffer prior to the establishment of embryonic asymmetry and positional identity among the embryonic cells.

摘要

背景

脊椎动物的轴形成和原肠胚形成过程中的细胞信号机制和形态发生运动是高度保守的。在几乎所有描述的鱼类中,原肠胚形成和胚胎轴的初步模式形成与外包同时发生。然而,一年生的食蚊鱼可能是这一规律的例外。一年生的食蚊鱼栖息在南美洲和非洲的短暂池塘中,通过产生耐受应激的卵来维持永久性种群。一年生食蚊鱼的早期发育在脊椎动物中是独一无二的,因为它们的胚胎分裂球在外包过程中随机分散在卵黄中,几天后重新聚集形成胚胎本身。此外,一年生食蚊鱼能够在一个到三个阶段暂停胚胎发育,称为休眠 I、II 和 III。关于与早期脊椎动物发育相关的高度保守的发育信号机制如何发生变化以促进一年生食蚊鱼表型,人们知之甚少。Oct4(Pou5f1)是最具特征和保守的转录因子之一,可能在维持多能性方面发挥作用。相比之下,BMP 拮抗剂,如 chordin、noggin 和 follistatin,先前已被证明在轴形成过程中建立背腹不对称性。SOXB1 组的转录因子,如 sox2 和 sox3,可能用于诱导神经特化。在这里,我们使用定量 PCR 确定了一年生食蚊鱼 Austrofundulus limnaeus 胚胎发育过程中这些发育因子的时间表达,并将这些模式与其他脊椎动物进行了比较。

结果

克隆、测序并鉴定了 Austrofundulus limnaeus 中的 oct4、sox2、sox3、chordin、noggin-1、noggin-2 和 follistatin 的部分转录本序列。我们发现 oct4、sox3、chordin 和 noggin-1 转录本可能是母系遗传的。sox2、follistatin 和 noggin-2 转录本的表达在可见胚胎轴形成后阶段最高。

结论

我们的数据表明,A. limnaeus 中的胚胎细胞在胚胎分裂球重新聚集后获得其胚层身份。这种细胞分化和轴形成过程可能涉及与其他脊椎动物相似的保守信号机制。我们提出,在胚胎细胞之间建立胚胎不对称性和位置身份之前,细胞分散过程中延长未分化状态,从而作为发育应激缓冲。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/16df60044187/13227_2014_139_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/c045b6671641/13227_2014_139_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/08fc3baf02fa/13227_2014_139_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/93fd0ce59409/13227_2014_139_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/16df60044187/13227_2014_139_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/c045b6671641/13227_2014_139_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/9a82b0c606e7/13227_2014_139_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/08fc3baf02fa/13227_2014_139_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/93fd0ce59409/13227_2014_139_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bb/4372997/16df60044187/13227_2014_139_Fig5_HTML.jpg

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