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钼辅因子的生物学、进化与缺乏症

Molybdenum cofactor biology, evolution and deficiency.

作者信息

Mayr Simon J, Mendel Ralf-R, Schwarz Guenter

机构信息

Institute of Biochemistry, Department of Chemistry, Center for Molecular Medicine, University of Cologne, Zuelpicher Str. 47, 50674 Koeln, Germany.

Institute of Plant Biology, Braunschweig University of Technology, Humboldtstr. 1, 38106 Braunschweig, Germany.

出版信息

Biochim Biophys Acta Mol Cell Res. 2021 Jan;1868(1):118883. doi: 10.1016/j.bbamcr.2020.118883. Epub 2020 Oct 2.

DOI:10.1016/j.bbamcr.2020.118883
PMID:33017596
Abstract

The molybdenum cofactor (Moco) represents an ancient metal‑sulfur cofactor, which participates as catalyst in carbon, nitrogen and sulfur cycles, both on individual and global scale. Given the diversity of biological processes dependent on Moco and their evolutionary age, Moco is traced back to the last universal common ancestor (LUCA), while Moco biosynthetic genes underwent significant changes through evolution and acquired additional functions. In this review, focused on eukaryotic Moco biology, we elucidate the benefits of gene fusions on Moco biosynthesis and beyond. While originally the gene fusions were driven by biosynthetic advantages such as coordinated expression of functionally related proteins and product/substrate channeling, they also served as origin for the development of novel functions. Today, Moco biosynthetic genes are involved in a multitude of cellular processes and loss of the according gene products result in severe disorders, both related to Moco biosynthesis and secondary enzyme functions.

摘要

钼辅因子(Moco)是一种古老的金属硫辅因子,在个体和全球范围内作为催化剂参与碳、氮和硫循环。鉴于依赖钼辅因子的生物过程的多样性及其进化年代,钼辅因子可追溯到最后的共同祖先(LUCA),而钼辅因子生物合成基因在进化过程中经历了重大变化并获得了额外功能。在本综述中,我们聚焦于真核生物的钼辅因子生物学,阐明基因融合对钼辅因子生物合成及其他方面的益处。虽然最初基因融合是由生物合成优势驱动的,如功能相关蛋白质的协调表达和产物/底物通道化,但它们也成为新功能发展的起源。如今,钼辅因子生物合成基因参与多种细胞过程,相应基因产物的缺失会导致严重疾病,这些疾病既与钼辅因子生物合成有关,也与二级酶功能有关。

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