2009年7月14日，北京生命科学研究所张宏实验室在Developmental Biology上在线发表题为“The C. elegans engrailed homolog ceh-16 regulates the self-renewal expansion division of stem cell-like seam cells”的文章，该文章首次报道了线虫的ceh-16基因通过和Wnt信号通路的相互作用来调节线虫侧线细胞的对称和不对称分裂。
我们都知道，干细胞可以通过对称分裂来增加本身的数目，也可以通过不对称分裂产生一系列分化的细胞。但是决定发育过程中干细胞对称和不对称分裂的选择机制仍不是很清楚。本篇文章以线虫的侧线细胞为模型发现线虫的engrailed同源基因ceh-16能够和Wnt信号通路相互作用来决定侧线细胞的对称分裂。在ceh-16功能缺失的突变体中，原本应该进行对称分裂的侧线细胞会异常而进行不对称分裂，而且如果在ceh-16突变体中导入人的同源基因En2能够回复这种异常表型，说明ceh-16的这种调节功能在进化过程中是十分保守的。作者还发现Wnt信号通路的成员基因apr-1突变后会产生和ceh-16相反的表型，而且在apr-1； ceh-16双突变体里，异常表型就会回复成野生型，这表明ceh-16是通过和Wnt信号通路相互作用来调节线虫侧线细胞的分裂选择的。此外，ceh-16突变后还会影响线虫中一个多巴胺神经元的形成，作者还证明这种异常表型也是和侧线细胞的不对称分裂和Wnt信号通路有关。该研究为进一步了解干细胞的调控机制做出了贡献。
该文章的第一作者黄鑫欣是北京生命科学研究所和北京师范大学联合培养的博士生，论文的其他作者还有北京生命科学研究所的田娥和徐艳华，张宏博士为本文的通讯作者。此项研究由科技部863计划，北京市科委资助，在北京生命科学研究所完成。（生物谷Bioon.com）
生物谷推荐原始出处：
Developmental Biology doi:10.1016/j.ydbio.2009.07.005
The C. elegans engrailed homolog ceh-16 regulates the self-renewal expansion division of stem cell-like seam cells
Xinxin Huanga, b, E Tianb, Yanhua Xub and Hong Zhangb,
aCollege of Life Sciences, Beijing Normal University, Beijing, 100875, PR China
bNational Institute of Biological Sciences, No. 7 Science Park Road, Zhongguancan Life Science Park Beijing, 102206, PR China
Stem cells undergo symmetric and asymmetric division to maintain the dynamic equilibrium of the stem cell pool and also to generate a variety of differentiated cells. The homeostatic mechanism controlling the choice between self-renewal and differentiation of stem cells is poorly understood. We show here that ceh-16, encoding the C. elegans ortholog of the transcription factor Engrailed, controls symmetric and asymmetric division of stem cell-like seam cells. Loss of function of ceh-16 causes certain seam cells, which normally undergo symmetric self-renewal expansion division with both daughters adopting the seam cell fate, to divide asymmetrically with only one daughter retaining the seam cell fate. The human engrailed homolog En2 functionally substitutes the role of ceh-16 in promoting self-renewal expansion division of seam cells. Loss of function of apr-1, encoding the C. elegans homolog of the Wnt signaling component APC, results in transformation of self-renewal maintenance seam cell division to self-renewal expansion division, leading to seam cell hyperplasia. The apr-1 mutation suppresses the seam cell division defect in ceh-16 mutants. Our study reveals that ceh-16 interacts with the Wnt signaling pathway to control the choice between self-renewal expansion and maintenance division and also demonstrates an evolutionarily conserved function of engrailed in promoting cell proliferation.
