Essential mesenchymal role of small GTPase Rac1 in interdigital programmed cell death during limb development

Essential mesenchymal role of small GTPase Rac1 in interdigital programmed cell death during limb development
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DOI:
10.1016/j.ydbio.2009.09.014
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发表时间:
2009-11-15
影响因子:
2.7
通讯作者:
Kamijo, Ryutaro
Kamijo, Ryutaro
中科院分区:
生物学3区
文献类型:
--
作者:
Suzuki, Dai;Yamada, Atsushi;Kamijo, Ryutaro

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发育中的脊椎动物肢体经常被用作研究模式形成和形态发生细胞死亡的模型。在此,我们报告,Rac1,Rho家族的蛋白质的成员,在小鼠肢芽间充质中的条件性缺失导致骨骼畸形的autopod和软组织并指,后者所造成的完全没有的趾间程序性细胞死亡。此外,缺乏趾间程序性细胞死亡和相关的并指与Bmp2,Bmp7的基因表达下调。Msx1和Msx2,已知它们促进趾间充质细胞凋亡。我们从Rac1条件突变体的研究结果表明,Rac1在肢芽形态发生,特别是趾间程序性细胞死亡的关键作用。(C)2009 Elsevier Inc. All rights reserved.
Developing vertebrate limbs are often utilized as a model for studying pattern formation and morphogenetic cell death. Herein, we report that conditional deletion of Rac1, a member of the Rho family of proteins, in mouse limb bud mesenchyme led to skeletal deformities in the autopod and soft tissue syndactyly, with the latter caused by a complete absence of interdigital programmed cell death. Furthermore, the lack of interdigital programmed cell death and associated syndactyly was related to down-regulated gene expression of Bmp2, Bmp7. Msx1, and Msx2, which are known to promote apoptosis in the interdigital mesenchyme. Our findings from Rac1 conditional mutants indicate crucial roles for Rac1 in limb bud morphogenesis, especially interdigital programmed cell death. (C) 2009 Elsevier Inc. All rights reserved.