The multiple fates of gene duplications: Deletion, hypofunctionalization, subfunctionalization, neofunctionalization, dosage balance constraints, and neutral variation.

The multiple fates of gene duplications: Deletion, hypofunctionalization, subfunctionalization, neofunctionalization, dosage balance constraints, and neutral variation.
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DOI:
10.1093/plcell/koac076
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发表时间:
2022-07-04
期刊:
The Plant cell
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其他
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基因复制长期以来被认为是具有新功能的基因进化的贡献者。基因的多个拷贝可能是串联复制、转座到新染色体或全基因组复制(多倍性)造成的。最常见的结果是,一对中的一个成员被删除,使基因恢复到单态。其他途径涉及两个拷贝的表达减少(功能减退),这两个拷贝以一式两份的形式保持以维持足够量的功能。这两个副本可以分裂功能(子功能化)或可以发散以生成新功能(新功能化)。全基因组加倍导致的重复保留发生在涉及多组分相互作用的基因,如转录因子和信号转导组分。相比之下,这些类别的基因在小片段重复中代表性不足。这种互补的模式表明,相互作用的平衡影响了重复对的命运。我们讨论了不同的机制,保持重复的基因,这可能会随着时间的推移而变化和交叉。重复基因的命运进行了讨论。
Gene duplications have long been recognized as a contributor to the evolution of genes with new functions. Multiple copies of genes can result from tandem duplication, from transposition to new chromosomes, or from whole-genome duplication (polyploidy). The most common fate is that one member of the pair is deleted to return the gene to the singleton state. Other paths involve the reduced expression of both copies (hypofunctionalization) that are held in duplicate to maintain sufficient quantity of function. The two copies can split functions (subfunctionalization) or can diverge to generate a new function (neofunctionalization). Retention of duplicates resulting from doubling of the whole genome occurs for genes involved with multicomponent interactions such as transcription factors and signal transduction components. In contrast, these classes of genes are underrepresented in small segmental duplications. This complementary pattern suggests that the balance of interactors affects the fate of the duplicate pair. We discuss the different mechanisms that maintain duplicated genes, which may change over time and intersect. The fates of duplicate genes are discussed.
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