端粒的延长和维持在胚胎发育、器官的稳态维持、体细胞重编程、肿瘤发生等过程中发挥着重要作用。不依赖于端粒酶的端粒延长机制（alternative lengthening of telomeres，ALT）是早期胚胎端粒快速延长的主要方式，然而其发生的分子机制却不清楚。近期的研究表明理解早期胚胎ALT机制可能会极大改善现有的诱导型重编程技术，并且可能为肿瘤发生过程中的ALT机制研究提供帮助。我们在前期研究中，收集了从受精卵到囊胚不同发育时期的数万枚胚胎并借助定量质谱技术首次获得了早期胚胎蛋白质组，经生物信息学分析，我们发现了一些可能与ALT发生或者端粒调控相关的蛋白分子，其中很多分子的具体功能有待深入研究。我们将利用早期胚胎发育（包括体细胞核移植胚胎）和iPS诱导系统深入研究这些基因在ALT过程中的作用机制。我们的研究不仅可以揭示早期胚胎ALT机制，还将为改善iPS技术提供重要的理论基础。

Telomeres play vital roles in early embryo development, organ homeostasis, somatic cell reprogramming and tumorigenesis. Telomeres lengthen significantly in preimplantation embryos via alternative lengthening of telomeres (ALT) mechanism. However, the molecular mechanism of ALT in early embryos remains unknown. Importantly, a strong association between ALT and tumorigenesis has been implicated in recent studies. In the past a few years, ALT mechanism in abnormal situations has been intensively studied while how it works in early embryo has been unclear due to the limit of small amount of samples. However, increasing evidence indicates that understanding of ALT mechanism in early embryo will benefit the improvement of induced pluripotent stem cells (iPS) and the research of ALT in tumors. We will use the proteomic technique and embryo micromanipulation technique to study ALT mechanism in early embryos. Embryos at different stage have been collected and the proteomic information has been obtained by mass spectrometry analysis. We have identified some candidate genes might closely related to ALT and telomere regulation. However, these genes’ function in ALT need to be further validated. We will further understand the function of these genes in the process of embryo development and iPS cells induction. Overall, our research will greatly benifit the understanding of the molecular mechanism of ALT in early embryos and provide invaluable information for iPS improvement and cancer therapy.