School of Biological Sciences, Monash University, Clayton, Victoria, Australia.
Monash Bioinformatics Platform, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
Mol Ecol. 2022 Aug;31(16):4319-4331. doi: 10.1111/mec.16583. Epub 2022 Jul 10.
After gastrulation, oviductal hypoxia maintains turtle embryos in an arrested state prior to oviposition. Subsequent exposure to atmospheric oxygen upon oviposition initiates recommencement of embryonic development. Arrest can be artificially extended for several days after oviposition by incubation of the egg under hypoxic conditions, with development recommencing in an apparently normal fashion after subsequent exposure to normoxia. To examine the transcriptomic events associated with embryonic arrest in green sea turtles (Chelonia mydas), RNA-sequencing analysis was performed on embryos from freshly laid eggs and eggs incubated in either normoxia (oxygen tension ~159 mmHg) or hypoxia (<8 mmHg) for 36 h after oviposition (n = 5 per group). The patterns of gene expression differed markedly among the three experimental groups. Normal embryonic development in normoxia was associated with upregulation of genes involved in DNA replication, the cell cycle, and mitosis, but these genes were commonly downregulated after incubation in hypoxia. Many target genes of hypoxia inducible factors, including the gene encoding insulin-like growth factor binding protein 1 (igfbp1), were downregulated by normoxic incubation but upregulated by incubation in hypoxia. Notably, some of the transcriptomic effects of hypoxia in green turtle embryos resembled those reported to be associated with hypoxia-induced embryonic arrest in diverse taxa, including the nematode Caenorhabditis elegans and zebrafish (Danio rerio). Hypoxia-induced preovipositional embryonic arrest appears to be a unique adaptation of turtles. However, our findings accord with the proposition that the mechanisms underlying hypoxia-induced embryonic arrest per se are highly conserved across diverse taxa.
在原肠胚形成后，输卵管缺氧使海龟胚胎在产卵前处于停滞状态。随后，在产卵时暴露于大气氧会启动胚胎发育的重新开始。通过在缺氧条件下孵育卵，可以人为地将停滞时间延长数天，随后在暴露于正常氧后，发育会以一种明显正常的方式重新开始。为了研究绿海龟（Chelonia mydas）胚胎停滞相关的转录组事件，对刚产下的卵和在产卵后 36 小时内分别在常氧（氧张力约 159mmHg）或缺氧（<8mmHg）条件下孵育的卵中的胚胎进行了 RNA 测序分析（每组 5 个样本）。这三个实验组之间的基因表达模式差异显著。在常氧下正常的胚胎发育与参与 DNA 复制、细胞周期和有丝分裂的基因上调有关，但这些基因在缺氧孵育后通常下调。缺氧诱导因子的许多靶基因，包括编码胰岛素样生长因子结合蛋白 1（igfbp1）的基因，在常氧孵育下下调，但在缺氧孵育下上调。值得注意的是，绿海龟胚胎中的一些转录组效应与在包括线虫秀丽隐杆线虫和斑马鱼在内的多种生物中与缺氧诱导胚胎停滞相关的报道相似。缺氧诱导的产卵前胚胎停滞似乎是海龟的一种独特适应。然而，我们的发现与以下观点一致，即缺氧诱导胚胎停滞本身的机制在不同生物中高度保守。
