2009年7月14日，北京生命科學研究所張宏實驗室在Developmental Biology上在線發表題為「The C. elegans engrailed homolog ceh-16 regulates the self-renewal expansion division of stem cell-like seam cells」的文章，該文章首次報導了線蟲的ceh-16基因通過和Wnt信號通路的相互作用來調節線蟲側線細胞的對稱和不對稱分裂。
我們都知道，幹細胞可以通過對稱分裂來增加本身的數目，也可以通過不對稱分裂產生一系列分化的細胞。但是決定發育過程中幹細胞對稱和不對稱分裂的選擇機制仍不是很清楚。本篇文章以線蟲的側線細胞為模型發現線蟲的engrailed同源基因ceh-16能夠和Wnt信號通路相互作用來決定側線細胞的對稱分裂。在ceh-16功能缺失的突變體中，原本應該進行對稱分裂的側線細胞會異常而進行不對稱分裂，而且如果在ceh-16突變體中導入人的同源基因En2能夠回復這種異常表型，說明ceh-16的這種調節功能在進化過程中是十分保守的。作者還發現Wnt信號通路的成員基因apr-1突變後會產生和ceh-16相反的表型，而且在apr-1； ceh-16雙突變體裡，異常表型就會回復成野生型，這表明ceh-16是通過和Wnt信號通路相互作用來調節線蟲側線細胞的分裂選擇的。此外，ceh-16突變後還會影響線蟲中一個多巴胺神經元的形成，作者還證明這種異常表型也是和側線細胞的不對稱分裂和Wnt信號通路有關。該研究為進一步了解幹細胞的調控機製做出了貢獻。
該文章的第一作者黃鑫欣是北京生命科學研究所和北京師範大學聯合培養的博士生，論文的其他作者還有北京生命科學研究所的田娥和徐豔華，張宏博士為本文的通訊作者。此項研究由科技部863計劃，北京市科委資助，在北京生命科學研究所完成。（生物谷Bioon.com）
生物谷推薦原始出處：
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.