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Molecular and Cellular Biology, October 2006, p. 7258-7268, Vol. 26, No. 19
0270-7306/06/$08.00+0     doi:10.1128/MCB.00183-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

DRONC Coordinates Cell Death and Compensatory Proliferation{ddagger}

Shu Kondo,1,2,3,4,5 Nanami Senoo-Matsuda,1,{dagger} Yasushi Hiromi,2,3,4* and Masayuki Miura1,4*

Department of Genetics, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan,1 Division of Developmental Genetics, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan,2 Department of Genetics, SOKENDAI, 1111 Yata, Mishima, Shizuoka 411-8540, Japan,3 CREST, Japan Science and Technology, 4-1-8 Honcho, Kawaguchi-shi, Saitama 332-0012, Japan,4 Division of Morphology and Organogenesis, Institute of DNA Medicine, The Jikei University School of Medicine, 3-25-8, Nishi-Shinbashi, Minato-ku, Tokyo 105-8461, Japan5

Received 1 February 2006/ Returned for modification 7 March 2006/ Accepted 17 July 2006

Accidental cell death often leads to compensatory proliferation. In Drosophila imaginal discs, for example, {gamma}-irradiation induces extensive cell death, which is rapidly compensated by elevated proliferation. Excessive compensatory proliferation can be artificially induced by "undead cells" that are kept alive by inhibition of effector caspases in the presence of apoptotic stimuli. This suggests that compensatory proliferation is induced by dying cells as part of the apoptosis program. Here, we provide genetic evidence that the Drosophila initiator caspase DRONC governs both apoptosis execution and subsequent compensatory proliferation. We examined mutants of five Drosophila caspases and identified the initiator caspase DRONC and the effector caspase DRICE as crucial executioners of apoptosis. Artificial compensatory proliferation induced by coexpression of Reaper and p35 was completely suppressed in dronc mutants. Moreover, compensatory proliferation after {gamma}-irradiation was enhanced in drice mutants, in which DRONC is activated but the cells remain alive. These results show that the apoptotic pathway bifurcates at DRONC and that DRONC coordinates the execution of cell death and compensatory proliferation.

* Corresponding author. Mailing address for Masayuki Miura: Department of Genetics, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. Phone: 81-3-5841-4860. Fax: 81-3-5841-4867. E-mail: miura{at}mol.f.u-tokyo.ac.jp. Mailing address for Yasushi Hiromi: Division of Developmental Genetics, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan. Phone: 81-55-981-6809. Fax: 81-55-981-6868. E-mail: yhiromi{at}lab.nig.ac.jp.

{ddagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{dagger} Present address: Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, 701 West 168th St., New York, NY 10032.

Molecular and Cellular Biology, October 2006, p. 7258-7268, Vol. 26, No. 19
0270-7306/06/$08.00+0     doi:10.1128/MCB.00183-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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