Along with errors in meiosis, mitotic errors during post-zygotic cell division contribute to pervasive aneuploidy in human embryos. Relatively little is known, however, about the genesis of these errors or their fitness consequences. Rapid technological advances are helping to close this gap, revealing diverse molecular mechanisms contributing to mitotic error. These include altered cell cycle checkpoints, aberrations of the centrosome, and failed chromatid cohesion, mirroring findings from cancer biology. Recent studies are challenging the idea that mitotic error is abnormal, emphasizing that the fitness impacts of mosaicism depend on its scope and severity. In light of these findings, technical and philosophical limitations of various screening approaches are discussed, along with avenues for future research.

除减数分裂的错误外，合子后细胞分裂过程中的有丝分裂错误也导致人类胚胎中普遍的非整倍性。但是，对于这些错误的起因或适用性后果知之甚少。快速的技术进步正在帮助缩小这一差距，揭示出导致有丝分裂错误的多种分子机制。这些包括改变的细胞周期检查点，中心体畸变和染色单体内聚力失败，这反映了癌症生物学的发现。最近的研究对有丝分裂错误是异常的观点提出了挑战，强调镶嵌性的适应性影响取决于其范围和严重性。根据这些发现，讨论了各种筛选方法的技术和哲学局限性，以及未来研究的途径。