The emergence of new protein-coding genes in a specific lineage or species provides raw materials for evolutionary adaptations. Until recently, the biology of new genes emerging particularly from non-genic sequences remained unexplored. Although the new genes are subjected to variable selection pressure and face rapid deletion, some of them become functional and are retained in the gene pool. To acquire functional novelties, new genes often get integrated into the pre-existing ancestral networks. However, the mechanism by which young proteins acquire novel interactions remains unanswered till date. Since structural orientation contributes hugely to the mode of proteins' physical interactions, in this regard, we put forward an interesting question – Do new genes encode proteins with stable folds? Addressing the question, we demonstrated that the intrinsic disorder inversely correlates with the evolutionary gene ages – i.e. young proteins are richer in intrinsic disorder than the ancient ones. We further noted that young proteins, which are initially poorly connected hubs, prefer to be structurally more disordered than well-connected ancient proteins. The phenomenon strikingly defies the usual trend of well-connected proteins being highly disordered in structure. We justified that structural disorder might help poorly connected young proteins to undergo promiscuous interactions, which provides the foundation for novel protein interactions. The study focuses on the evolutionary perspectives of young proteins in the light of structural adaptations.

中文翻译：

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蛋白质内在疾病与不同真核细胞谱系的基因年龄负相关

在特定谱系或物种中新的蛋白质编码基因的出现为进化适应提供了原材料。直到最近，特别是从非基因序列中出现的新基因的生物学仍未得到开发。尽管新基因承受着可变的选择压力并面临快速缺失，但其中一些变得有功能并保留在基因库中。为了获得功能上的新颖性，通常将新基因整合到先前存在的祖先网络中。然而，迄今为止，年轻蛋白质获得新相互作用的机理尚未得到解答。由于结构取向在很大程度上影响蛋白质的物理相互作用方式，因此，我们提出了一个有趣的问题–新基因是否编码具有稳定折叠的蛋白质？解决这个问题即年轻的蛋白质比古代的蛋白质在固有疾病中的含量更高。我们还注意到，最初是连接不紧密的集线器的年轻蛋白质比结构良好的古老蛋白质更倾向于在结构上更加无序。这种现象显着地克服了良好连接的蛋白质在结构上高度无序的通常趋势。我们证明结构紊乱可能有助于连接不良的年轻蛋白质进行混杂相互作用，这为新型蛋白质相互作用提供了基础。该研究着眼于结构适应性的年轻蛋白质的进化观点。