Polycomblike-2-deficient mice exhibit normal left-right asymmetry

被引:30
作者
Wang, Shusheng
He, Fenglei
Xiong, Wei
Gu, Shuping
Liu, Hongbin
Zhang, Tao
Yu, Xueyan
Chen, Yiping
机构
[1] Ohio State Univ, Med Ctr, Dept Oral Biol, Hlth Sci Ctr, Columbus, OH 43210 USA
[2] Tulane Univ, Dept Cell & Mol Biol, Div Dev Biol, New Orleans, LA 70118 USA
关键词
pcl2; mouse; left-right asymmetry; organogenesis;
D O I
10.1002/dvdy.21070
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Polycomb group (PcG) proteins are required for maintaining the repressed state of developmentally important genes such as homeotic genes. Polycomblike (Pcl), a member of PcG genes with two characteristic PHD finger motifs, was shown to strongly enhance the effects of PcG genes in Drosophila. Three Pcl genes exist in the mouse genome, with their function largely unknown. Our previous studies demonstrate that the chick Pcl2 is essential for the left-right asymmetry by silencing Shh expression in the right side of the node (Wang et al. [2004b] Development 131:4381-4391). To elucidate the in vivo role of mouse Pcl2, we generated Pcl2 mutant mice. Phenotypic analyses indicate the normal development of left-right asymmetry in the Pcl2 mutant mice. However, Pcl2 mutant mice exhibit posterior transformation of axial skeletons and other phenotypic defects, with a relatively low penetrance. These results demonstrate that Pcl2 is dispensable for the normal left-right axis development in mice.
引用
收藏
页码:853 / 861
页数:9
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