Tanaka Kentaro M, Takahashi Aya, Fuse Naoyuki, Takano-Shimizu-Kouno Toshiyuki
Department of Population Genetics, National Institute of Genetics, Yata 1111, Mishima, Shizuoka, 411-8540, Japan Department of Biological and Medical Sciences, Oxford Brookes University, Gipsy Lane, Oxford, OX3 0BP, United Kingdom
Department of Population Genetics, National Institute of Genetics, Yata 1111, Mishima, Shizuoka, 411-8540, Japan Department of Biological Sciences, Tokyo Metropolitan University, Hachioji, 192-0397, Japan Research Center for Genomics and Bioinformatics, Tokyo Metropolitan University, Hachioji, 192-0397, Japan.
Genetics. 2014 Jun;197(2):739-42. doi: 10.1534/genetics.114.163337. Epub 2014 Mar 25.
Cell death is a mechanism utilized by organisms to eliminate excess cells during development. Here, we describe a novel regulator of caspase-independent cell death, Mabiki (Mabi), that is involved in the repair of the head patterning defects caused by extra copies of bicoid in Drosophila melanogaster. Mabiki functions together with caspase-dependent cell death mechanisms to provide robustness during development.
细胞死亡是生物体在发育过程中用于清除多余细胞的一种机制。在此,我们描述了一种新的不依赖于半胱天冬酶的细胞死亡调节因子,即Mabiki(Mabi),它参与了果蝇中由双尾基因额外拷贝导致的头部模式缺陷的修复。Mabiki与依赖于半胱天冬酶的细胞死亡机制共同发挥作用,以在发育过程中提供稳健性。