A Novel Cell Death Gene Acts to Repair Patterning Defects in Drosophila Melanogaster
NOTE A Novel Cell Death Gene Acts to Repair Patterning Defects in Drosophila melanogaster Kentaro M. Tanaka,*,†,1 Aya Takahashi,*,‡,§ Naoyuki Fuse,** and Toshiyuki Takano-Shimizu-Kouno*,††,1 *Department of Population Genetics, National Institute of Genetics, Yata 1111, Mishima, Shizuoka, 411-8540, Japan, †Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, OX3 0BP, United Kingdom, ‡Department of Biological Sciences and §Research Center for Genomics and Bioinformatics, Tokyo Metropolitan University, Hachioji, 192-0397, Japan, **Department of Biophysics, Kyoto University, Kitashirakawa-Oiwake-cho, Sakyo-ku, Kyoto, 606-8502, Japan, and ††Drosophila Genetic Resource Center, Kyoto Institute of Technology, Saga Ippongi-cho, Ukyo-ku, Kyoto, 616-8354, Japan ABSTRACT 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. RGANISMS are surprisingly robust to various stresses and embryos. However, the mechanism leading to this compensa- Operturbations. Elimination of undesirable cells is one tory cell death remains largely unexplored. mechanism that ensures robust development. For example, To identify genes involved in this repair, we first screened compensatory cell death is observed in the expanded prospec- a panel of 152 autosomal deficiencies for those with signifi- tive head region of embryos from mothers carrying extra (six) cantly lower viability in 6xbcd than in normal (2xbcd)condi- copies of bicoid (6xbcd)inDrosophila melanogaster.
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