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Intron loss in interferon genes follows a distinct set of stages, and may confer an evolutionary advantage

机译：干扰素基因中的内含子损失遵循不同的阶段，并可能赋予进化优势

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The promoter-intron-exon structure of genes evolve. While the structures of some IFN genes (e.g., piscine and amphibian Type I IFNs, most tetrapod IFN-X, genes) resemble those of other class II cytokines (e.g., interleukins-10, 19, 20, 22, 24, 26), the structures of other IFN genes differ significantly. Although all bony vertebrate IFN-gamma genes lack the canonical third intron, and all amniote Type I IFN genes lack introns, only some IFN-lambda, genes lost their introns. Interestingly, these intronless IFN-X genes are not preferentially related to one another nor are they clustered with canonical multi-intron IFN-X. genes. Hypothesizing that intronless IFN-2., genes repeatedly and independently evolved and transposed throughout the genome, we sought to understand the genetic processes involved in their intron loss and genomic migration. Utilizing the high conservation of the promoters, the UTRs and the ORFs of the IFN-X genes, we collected data from two families of intronless IFN-lambda genes, and developed a model supported by these data to explain how intronless IFN-lambda,, genes evolved. (1) A cytoplasmic IFN-lambda, cDNA generated by reverse transcriptional activity enters the nucleus and attempts to recombine with its multi-exon progenitor. (2) Nuclear DNA synthesis at the 5' and 3' ends within recombination intermediates affixes the promoter onto the cDNA and preserves its 3' UTR. (3) Resolution of the recombination complex releases the promoter-associated cDNA. (4) The released intronless gene co-integrates with a highly duplicated sequence undergoing transposition. We propose that this process explains not only the evolution of the gene structure of IFN genes, but also the increased transposition of intronless genes in genomes, and may confer an evolutionary advantage. (C) 2016 Elsevier Ltd. All rights reserved.
机译：基因的启动子-内含子-外显子结构进化。虽然某些IFN基因的结构（例如鱼和两栖类I型IFN，大多数四足动物IFN-X基因）类似于其他II类细胞因子（例如白介素10、19、20、22、24、26），其他IFN基因的结构差异很大。尽管所有骨质脊椎动物IFN-γ基因均缺乏规范的第三内含子，而所有羊膜I型IFN基因均缺乏内含子，但只有部分IFN-λ基因丢失了其内含子。有趣的是，这些无内含子的IFN-X基因彼此之间没有优先关联，也不与典型的多内含子的IFN-X成簇。基因。假设无内含子的IFN-2基因反复独立地进化和转座整个基因组，我们试图了解涉及其内含子缺失和基因组迁移的遗传过程。利用IFN-X基因的启动子，UTR和ORF的高度保守性，我们收集了两个无内含子IFN-λ基因家族的数据，并开发了一个模型，这些数据支持了该模型来解释无内含子的IFN-λ，基因进化了。 （1）细胞质IFN-λ，由逆转录活性产生的cDNA进入细胞核，并试图与其多外显子祖细胞重组。 （2）重组中间体内5'和3'端的核DNA合成将启动子固定在cDNA上并保留其3'UTR。 （3）重组复合体的分离释放了启动子相关的cDNA。 （4）释放的无内含子基因与经历转座的高度重复的序列共整合。我们提出，该过程不仅解释了IFN基因的基因结构的进化，而且解释了基因组中无内含子基因转座的增加，并且可能赋予了进化优势。 （C）2016 Elsevier Ltd.保留所有权利。

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