生物遗传的基础是DNA复制，如果这一复制机制不起作用，其结果可能是细胞缺失或是获得额外的遗传物质，这些是大多数出生缺陷和癌症基因组不稳定的特点。
北卡罗来纳大学医学院的科学家们已经发现CDT1是DNA复制所必需的，CDT1在细胞周期后期很重要，CDT1在有丝分裂中起着重要的作用。这一发现为解释癌症具有不只是基因组不稳定的特征提供了一个可能的原因。
这项新的研究刊登在Nature Cell Biology杂志上，该研究首次明确证实这样一个DNA复制蛋白的双重作用。
UNC学校药理和生物化学和生物物理学研究助理教授Jean Cook博士说
细胞周期中的一系列事件导致细胞其生长、复制和分裂成两个子细胞。它由四个不同的阶段组成：G1期、S（DNA合成）期，有丝分裂和G2。Cook的研究主要集中在G1期。
一旦研究人员知道CDT1在有丝分裂中发挥作用，他们希望弄清楚其中关键的过程。Cook说，CDT1异常的细胞像肿瘤细胞，在复制和有丝分裂中会遇到问题。目前一个临床试验试图提高CDT1在癌细胞中的数量，将肿瘤细胞推到一个已经岌岌可危致命的位置。（生物谷：Bioon.com）
doi:10.1038/ncb2489
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Recruitment of the human Cdt1 replication licensing protein by the loop domain of Hec1 is required for stable kinetochore–microtubule attachment
Dileep Varma,Srikripa Chandrasekaran,Lynsie J. R. Sundin,Karen T. Reidy,Xiaohu Wan,Dawn A. D. Chasse,Kathleen R. Nevis,Jennifer G. DeLuca,E. D. Salmon& Jeanette Gowen Cook
Cdt1, a protein critical for replication origin licensing in G1 phase, is degraded during S phase but re-accumulates in G2 phase. We now demonstrate that human Cdt1 has a separable essential mitotic function. Cdt1 localizes to kinetochores during mitosis through interaction with the Hec1 component of the Ndc80 complex. G2-specific depletion of Cdt1 arrests cells in late prometaphase owing to abnormally unstable kinetochore–microtubule (kMT) attachments and Mad1-dependent spindle-assembly-checkpoint activity. Cdt1 binds a unique loop extending from the rod domain of Hec1 that we show is also required for kMT attachment. Mutation of the loop domain prevents Cdt1 kinetochore localization and arrests cells in prometaphase. Super-resolution fluorescence microscopy indicates that Cdt1 binding to the Hec1 loop domain promotes a microtubule-dependent conformational change in the Ndc80 complex in vivo. These results support the conclusion that Cdt1 binding to Hec1 is essential for an extended Ndc80 configuration and stable kMT attachment.
