Chromosomes are likely to have assembled from unlinked genes in early evolution. Genetic linkage reduces the assortment load and intragenomic conflict in reproducing protocell models to the extent that chromosomes can go to fixation even if chromosomes suffer from a replicative disadvantage, relative to unlinked genes, proportional to their length. Here we numerically show that chromosomes spread within protocells even if recurrent deleterious mutations affecting replicating genes (as ribozymes) are considered. Dosage effect selects for optimal genomic composition within protocells that carries over to the genic composition of emerging chromosomes. Lacking an accurate segregation mechanism, protocells continue to benefit from the stochastic corrector principle (group selection of early replicators), but now at the chromosome level. A remarkable feature of this process is the appearance of multigene families (in optimal genic proportions) on chromosomes. An added benefit of chromosome formation is an increase in the selectively maintainable genome size (number of different genes), primarily due to the marked reduction of the assortment load. The establishment of chromosomes is under strong positive selection in protocells harboring unlinked genes. The error threshold of replication is raised to higher genome size by linkage due to the fact that deleterious mutations affecting protocells metabolism (hence fitness) show antagonistic (diminishing return) epistasis. This result strengthens the established benefit conferred by chromosomes on protocells allowing for the fixation of highly specific and efficient enzymes.

染色体很可能是在早期进化过程中由非关联基因组装而成的。遗传连锁将复制原始细胞模型中的分类负荷和内部基因组冲突降低到一定程度，即使染色体相对于未连锁的基因而言，复制缺陷不利于染色体，且染色体长度与其成正比，染色体也可以固定。在这里，我们从数字上表明，即使考虑到影响复制基因的反复有害突变（如核酶），染色体也会在原细胞内扩散。剂量效应在原始细胞内选择最佳基因组组成，并延续到新兴染色体的基因组成。缺乏精确的分离机制，原生细胞继续受益于随机校正器原理（早期复制子的组选择），但现在处于染色体水平。该过程的显着特征是在染色体上出现了多基因家族（以最佳基因比例）。染色体形成的另一个好处是可选择性维持的基因组大小（不同基因的数量）的增加，这主要是由于分类负荷的显着降低。在具有未连接基因的原细胞中，染色体的建立处于强烈的正选择之下。由于存在影响原细胞代谢的有害突变（因此适应性）显示出拮抗（递减的）上清的事实，通过连锁将复制的错误阈值提高至更高的基因组大小。该结果增强了染色体赋予原细胞的既定益处，从而允许固定高度特异性和高效的酶。