Institute for Genome Sciences, Department of Microbiology and Immunology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201
Molecular Evolution, Department of Cell and Molecular Biology, Uppsala University, 75124 Sweden.
G3 (Bethesda). 2018 Jan 4;8(1):373-374. doi: 10.1534/g3.117.300164.
In "Retrotransposons Are the Major Contributors to the Expansion of the Muller F Element," Leung (2017) improved contigs attributed to the Muller F element from the original CAF1 assembly, and used them to conclude that most of the sequence expansion of the fourth chromosome of is due to a higher transposon load than previously thought, but is not due to DNA integrations. While we do not disagree with the first conclusion, the authors base their second conclusion on the lack of homology detected between their improved CAF1 genome assembly attributed to and reference genomes. While the consensus CAF1 genome assembly lacks any sequence similarity to the reference genome of the endosymbiont of (Mel), numerous studies from multiple laboratories provide experimental support for a large lateral/horizontal gene transfer (LGT) of a genome into this line. As such, we strongly suspect that the original whole genome assembly was either constructed after the removal of all reads, or that sequences were directly removed from the contigs in the CAF1 assembly. Hence, Leung (2017) could not have identified the LGT using the CAF1 assembly. This manuscript by Leung (2017) highlights that an assembly of the sequence reads and their mate pairs was erroneously attributed solely to the endosymbiont, albeit before we understood the extent of LGT in As such, we recommend that the sequences deposited at the National Center for Biotechnology Information (NCBI) under PRJNA13365 should not be attributed to endosymbiont of , but should have their taxonomy reclassified by NCBI as "Unclassified sequences." As our knowledge about genome biology improves, we need to reconsider and reanalyze earlier genomes removing the prejudice introduced from now defunct paradigms.
在《逆转录转座子是 Muller F 因子扩张的主要贡献者》一文中,Leung(2017)改进了最初 CAF1 组装中归因于 Muller F 因子的基因序列,并利用这些序列得出结论,认为 第四号染色体的大部分序列扩张是由于转座子负荷比以前认为的要高,而不是由于 DNA 整合。虽然我们不同意第一个结论,但作者的第二个结论是基于他们改进的 CAF1 基因组组装与参考基因组之间没有检测到同源性。虽然共识 CAF1 基因组组装与 共生体的参考基因组缺乏任何序列相似性(Mel),但来自多个实验室的多项研究为一个 基因组大量侧向/水平基因转移(LGT)到这个 系提供了实验支持。因此,我们强烈怀疑最初的全基因组组装是在去除所有 序列后构建的,或者 序列是直接从 CAF1 组装的基因序列中删除的。因此,Leung(2017)不可能使用 CAF1 组装来识别 LGT。Leung(2017)的这篇论文强调,对 序列读取及其配对的组装错误地归因于 共生体,尽管我们还不了解 中的 LGT 程度。因此,我们建议在国家生物技术信息中心(NCBI)下提交的序列(PRJNA13365)不应归因于 共生体,而应由 NCBI 将其分类法重新归类为“未分类序列”。随着我们对基因组生物学的认识的提高,我们需要重新考虑和重新分析早期的基因组,消除现在已经失效的范式带来的偏见。