关键词: Caenorhabditis elegans Pristionchus pacificus PRC2 bioinformatics chromatin comparative analysis epigenetics evo-devo gene loss histones

Mesh : Animals Epigenesis, Genetic Evolution, Molecular Caenorhabditis elegans / genetics Polycomb Repressive Complex 2 / genetics metabolism Histone Methyltransferases / metabolism genetics Nematoda / genetics Helminth Proteins / genetics metabolism

来  源:   DOI:10.1093/genetics/iyae041   PDF(Pubmed)

Abstract:
Comparative approaches have revealed both divergent and convergent paths to achieving shared developmental outcomes. Thus, only through assembling multiple case studies can we understand biological principles. Yet, despite appreciating the conservation-or lack thereof-of developmental networks, the conservation of epigenetic mechanisms regulating these networks is poorly understood. The nematode Pristionchus pacificus has emerged as a model system of plasticity and epigenetic regulation as it exhibits a bacterivorous or omnivorous morph depending on its environment. Here, we determined the \"epigenetic toolkit\" available to P. pacificus as a resource for future functional work on plasticity, and as a comparison with Caenorhabditis elegans to investigate the conservation of epigenetic mechanisms. Broadly, we observed a similar cast of genes with putative epigenetic function between C. elegans and P. pacificus. However, we also found striking differences. Most notably, the histone methyltransferase complex PRC2 appears to be missing in P. pacificus. We described the deletion/pseudogenization of the PRC2 genes mes-2 and mes-6 and concluded that both were lost in the last common ancestor of P. pacificus and a related species P. arcanus. Interestingly, we observed the enzymatic product of PRC2 (H3K27me3) by mass spectrometry and immunofluorescence, suggesting that a currently unknown methyltransferase has been co-opted for heterochromatin silencing. Altogether, we have provided an inventory of epigenetic genes in P. pacificus to compare with C. elegans. This inventory will enable reverse-genetic experiments related to plasticity and has revealed the first loss of PRC2 in a multicellular organism.
摘要:
比较方法揭示了实现共同发展成果的不同和趋同路径。因此,只有通过组合多个案例研究,我们才能理解生物学原理。然而,尽管认识到发展网络的保护或缺乏保护,调节这些网络的表观遗传机制的保守性知之甚少。线虫Pristionchuspacificus已成为可塑性和表观遗传调控的模型系统,因为它根据其环境表现出细菌或杂食性形态。这里,我们确定了可用于P.pacificus的“表观遗传工具包”,作为未来可塑性功能工作的资源,并与秀丽隐杆线虫进行比较,以研究表观遗传机制的保守性。广义上,我们观察到在秀丽隐杆线虫和太平洋疟原虫之间具有类似的表观遗传功能的基因。然而,我们还发现了惊人的差异。最值得注意的是,组蛋白甲基转移酶复合物PRC2似乎在太平洋疟原虫中缺失。我们描述了PRC2基因mes-2和mes-6的缺失/假基因化,并得出结论,这两个基因都在P.pacificus和相关物种P.arcanus的最后一个共同祖先中丢失。有趣的是,我们通过质谱和免疫荧光法观察了PRC2(H3K27me3)的酶产物,表明目前未知的甲基转移酶已被选择用于异染色质沉默。总之,我们提供了pacificus的表观遗传基因清单,以与秀丽隐杆线虫进行比较。该清单将使与可塑性相关的反向遗传实验成为可能,并揭示了多细胞生物中PRC2的首次丢失。
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