The C. elegans engrailed homolog ceh-16 regulates the self-renewal expansion division of stem cell-like seam cells
The C. elegans engrailed homolog ceh-16 regulates the self-renewal expansion division of stem cell-like seam cells
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DOI：
10.1016/j.ydbio.2009.07.005
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发表时间：
2009-09-15
影响因子：
2.7
通讯作者：
Zhang, Hong
中科院分区：
文献类型：
--
作者：
Huang, Xinxin;Tian, E.;Zhang, Hong
干细胞进行对称和不对称分裂，以维持干细胞库的动态平衡，并产生多种分化细胞。人们对控制干细胞自我更新和分化之间选择的稳态机制知之甚少。我们在此表明，编码转录因子 Engrailed 的秀丽隐杆线虫直系同源物的 ceh-16 控制干细胞样接缝细胞的对称和不对称分裂。 ceh-16功能丧失会导致某些接缝细胞发生不对称分裂，这些接缝细胞通常会进行对称的自我更新扩张分裂，两个子细胞都采用接缝细胞的命运，而只有一个子细胞保留接缝细胞的命运。人类engrailed同源物En2在功能上替代了ceh-16在促进seam细胞自我更新扩张分裂中的作用。编码秀丽隐杆线虫Wnt信号成分APC同源物的apr-1的功能丧失，导致自我更新维持seam细胞分裂转变为自我更新扩张分裂，导致seam细胞增生。 apr-1 突变抑制了 ceh-16 突变体中的接缝细胞分裂缺陷。我们的研究揭示了ceh-16与Wnt信号通路相互作用来控制自我更新扩张和维持分裂之间的选择，并且还证明了engrailed在促进细胞增殖方面的进化保守功能。 (C) 2009 Elsevier Inc. 保留所有权利。
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. (C) 2009 Elsevier Inc. All rights reserved.