在哺乳动物和人类的着床前胚胎中，染色质的稳定性与细胞端粒的长度以及修复能力密切相关：在人类早期胚胎中经常存在由正常倍性细胞和非整倍体细胞构成的嵌合体，这被认为是导致胚胎发育的停滞、影响正常妊娠和辅助生殖治疗的重要原因。在前期的研究中，借助转基因小鼠构建的短端粒小鼠胚胎模型，我们发现在哺乳动物着床前胚胎发育中卵裂球端粒存在先变短后延长的过程，且在不同细胞之间具有端粒长度的多态性。同时，我们也发现Aurora Kinase B(AURKB)在着床前胚胎的不同细胞中具有不同的表达水平，且已有研究证明AURKB在成体细胞中能够促进端粒的修复。故我们期望采用已建立的基于少量细胞的的高分辨率端长度和染色质结构检测手段，对不同AURKB表达条件下着床前胚胎细胞端粒长度修复以及染色质的结构的稳定性进行系统性的检测，而对哺乳动物着床前胚胎的发育具有更深入的了解，并为提高辅助生殖临床疗效做出贡献。

In preimplantation embryos of mammals and humans, the stability of chromatin is closely related to the length of telomeres and the ability to repair them. Chimeras consisting of normal ploidy cells and aneuploidy cells are often found in early human embryos, which are considered to be the important reasons leading to the stagnation of embryonic development, affecting normal pregnancy and assisted reproductive therapy. In the previous studies, we found that the telomeres of cleavage spheres first shortened and then prolonged during the development of mammalian pre-implantation embryos, and there was a polymorphism of telomere length between different cells by using the short telomere mouse embryo model constructed by transgenic mice. At the same time, we also found that Aurora Kinase B (AURKB) has different expression levels in different cells of preimplantation embryos, and studies have shown that AURKB can promote telomere repair in adult cells. Therefore, we hope to systematically detect telomere length repair and chromatin structure stability of pre-implantation embryonic cells under different AURKB expression conditions using established high-resolution telomere length and chromatin structure detection methods based on a small number of cells. Thus, we can have a better understanding of the development of mammalian preimplantation embryos and contribute to the improvement of clinical efficacy of assisted reproduction.