Developmental constraint shaped genome evolution and erythrocyte loss in Antarctic fishes following paleoclimate change.
Developmental constraint shaped genome evolution and erythrocyte loss in Antarctic fishes following paleoclimate change.
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DOI：
10.1371/journal.pgen.1009173
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发表时间：
2020-10
期刊：
影响因子：
4.5
通讯作者：
Detrich HW 3rd
中科院分区：
文献类型：
--
作者：
Daane JM;Auvinet J;Stoebenau A;Yergeau D;Harris MP;Detrich HW 3rd
在寒冷，富氧的南大洋（SO），南极冰鱼（鱼科; Notothenioidei）进化的生存能力，而不产生红细胞和血红蛋白，几乎所有的脊椎动物的氧气运输系统。在这里，我们将古气候记录与广泛的Notothenioid鱼类基因组数据集相结合，以了解与气候变化相关的性状丧失的演变。相反，浮力适应在这个分支，我们发现宽松的选择控制红细胞生成的遗传区域进化后，才持续冷却的SO。这种模式不仅见于冰鱼，而且也独立地发生在其他高纬度的背银鱼类中。我们发现，一个物种的红血龙鱼进化出一个球形红细胞贫血症，表型模仿人类患者通过orthopathic突变与这种疾病。SO气候变化的基因组印记偏向于红细胞相关的保守非编码元件（CNEs），而不是编码区，这在很大程度上是通过多效性保存。CNE的漂移在红细胞生成后期优先表达的基因附近特异性富集。此外，我们发现，造血骨髓的冰鱼物种保留proerythroblasts，这表明早期红细胞发育保持完整。我们的研究结果为理解发育与基因组在塑造物种对气候变化的反应方面的相互作用提供了一个框架。我们的气候正在迅速变化。为了更好地了解物种如何适应主要的气候扰动，我们回顾了过去一组经历了剧烈气候剧变并蓬勃发展的鱼类：南极鱼。特别是，我们专注于冰鱼，它失去了在南大洋寒冷的环境中产生红细胞的能力。通过将过去的气候记录与南极鱼类的大型遗传数据集相结合，我们发现红细胞的损失仅发生在南大洋持续冷却之后。随着冷却持续到现代，我们发现即使是冰鱼的一些“红血”亲属也显示出红细胞损失的早期遗传和形态学迹象。这一冷却事件在冰鱼的基因组上留下了非随机的印记。除了少数例外，红细胞发育的遗传工具包在冰鱼中保持完整，因为许多“红细胞”基因在其他组织中发挥重要作用。相反，突变已经积累在基因调控区附近的基因控制终端红细胞成熟，使冰鱼继续产生红细胞祖细胞，但不成熟的红细胞。这些结果表明，调节胚胎发育的遗传限制塑造了这一鱼类群体对气候变化的进化反应。
In the frigid, oxygen-rich Southern Ocean (SO), Antarctic icefishes (Channichthyidae; Notothenioidei) evolved the ability to survive without producing erythrocytes and hemoglobin, the oxygen-transport system of virtually all vertebrates. Here, we integrate paleoclimate records with an extensive phylogenomic dataset of notothenioid fishes to understand the evolution of trait loss associated with climate change. In contrast to buoyancy adaptations in this clade, we find relaxed selection on the genetic regions controlling erythropoiesis evolved only after sustained cooling in the SO. This pattern is seen not only within icefishes but also occurred independently in other high-latitude notothenioids. We show that one species of the red-blooded dragonfish clade evolved a spherocytic anemia that phenocopies human patients with this disease via orthologous mutations. The genomic imprint of SO climate change is biased toward erythrocyte-associated conserved noncoding elements (CNEs) rather than to coding regions, which are largely preserved through pleiotropy. The drift in CNEs is specifically enriched near genes that are preferentially expressed late in erythropoiesis. Furthermore, we find that the hematopoietic marrow of icefish species retained proerythroblasts, which indicates that early erythroid development remains intact. Our results provide a framework for understanding the interactions between development and the genome in shaping the response of species to climate change. Our climate is rapidly changing. To better understand how species can adapt to major climate disturbance, we looked back into the past at a group of fishes that have encountered dramatic climate upheavals and thrived: Antarctic notothenioid fishes. In particular, we focus on the icefishes, which lost the ability to produce red blood cells in the frigid environment of the Southern Ocean. By integrating past climate records with a large genetic dataset of Antarctic fishes, we show that the loss of red blood cells occurred only after sustained cooling of the Southern Ocean. As cooling continued into the modern era, we discover that even some of the “red-blooded” relatives of the icefishes show early genetic and morphological signs of erythrocyte loss. This cooling event left a non-random imprint on the genome of icefishes. With few exceptions, the genetic toolkit underlying red cell development has remained intact in icefishes because many “erythroid” genes perform important functions in other tissues. Rather, mutations have accumulated in gene regulatory regions near genes that control terminal erythroid maturation, such that icefishes continue to produce red cell progenitors but not mature erythrocytes. These results show that the genetic constraints regulating embryonic development shaped the evolutionary response of this fish group to climate change.
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影响因子：
20.3
作者：
CATTON, WT
通讯作者：
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影响因子：
16.8
作者：
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DOI：
10.1016/0034-5687(84)90093-8
发表时间：
1984-01-01
期刊：
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