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Peer-reviewedCC BYELife

Bruce suppresses autophagy-regulated caspase activity and wing tissue growth in Drosophila.

  • Natsuki Shinoda1,2
  • Yutaro Hama3,4
  • Nozomi Hanawa1
  • Masayuki Miura1,5,6
6 affiliations
  1. 1Department of Genetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
  2. 2Cellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Japan.
  3. 3Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
  4. 4Institute of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Japan.
  5. 5Laboratory for Cell Vigor Regulation, National Institute for Basic Biology, Okazaki, Japan.
  6. 6Basic Biology Program, The Graduate University for Advanced Studies, SOKENDAI, Okazaki, Japan.
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Abstract

Caspases are cysteine-aspartic proteases that mediate both lethal and non-lethal cellular outcomes, including the promotion of tissue growth. However, the mechanisms underlying the differential regulation of these activities remain unclear. We have previously shown that among the two Drosophila executioner caspases, Dcp-1 and Drice, Dcp-1 promotes tissue growth in a non-lethal manner, independent of canonical apoptotic signaling. Herein, we demonstrated that overexpressed Dcp-1, but not Drice, was activated without canonical apoptosome components. TurboID-based proximity labeling revealed distinct proximal proteomes, among which Sirtuin 1, an Atg8a deacetylase, which promotes autophagy, was specifically required for Dcp-1 activation. Autophagy-related genes, including Bcl-2 family members Debcl and Buffy, are required for Dcp-1 activation. Structure-based prediction using AlphaFold3 further identified Bruce, an autophagy-regulated inhibitor of apoptosis, as a Dcp-1-specific regulator acting outside the apoptosome-mediated pathway. Physiologically, Bruce suppresses wing tissue growth. These findings indicate that non-lethal Dcp-1 activity is governed by the autophagy-Bruce axis, enabling distinct non-lethal functions independent of cell death.

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Cite

BibTeXRIS
BibTeX
@article{shinoda2026bruce,
  title = {{Bruce suppresses autophagy-regulated caspase activity and wing tissue growth in Drosophila.}},
  author = {Natsuki Shinoda and Yutaro Hama and Nozomi Hanawa and Masayuki Miura},
  journal = {ELife},
  year = {2026},
  month = oct,
  doi = {10.7554/elife.109876},
  url = {https://europepmc.org/article/MED/42895886},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Bruce suppresses autophagy-regulated caspase activity and wing tissue growth in Drosophila.
AU  - Natsuki Shinoda
AU  - Yutaro Hama
AU  - Nozomi Hanawa
AU  - Masayuki Miura
PY  - 2026
DA  - 2026/10/19
JO  - ELife
DO  - 10.7554/elife.109876
UR  - https://europepmc.org/article/MED/42895886
AB  - Caspases are cysteine-aspartic proteases that mediate both lethal and non-lethal cellular outcomes, including the promotion of tissue growth. However, the mechanisms underlying the differential regulation of these activities remain unclear. We have previously shown that among the two Drosophila executioner caspases, Dcp-1 and Drice, Dcp-1 promotes tissue growth in a non-lethal manner, independent of canonical apoptotic signaling. Herein, we demonstrated that overexpressed Dcp-1, but not Drice, was activated without canonical apoptosome components. TurboID-based proximity labeling revealed distinct proximal proteomes, among which Sirtuin 1, an Atg8a deacetylase, which promotes autophagy, was specifically required for Dcp-1 activation. Autophagy-related genes, including Bcl-2 family members Debcl and Buffy, are required for Dcp-1 activation. Structure-based prediction using AlphaFold3 further identified Bruce, an autophagy-regulated inhibitor of apoptosis, as a Dcp-1-specific regulator acting outside the apoptosome-mediated pathway. Physiologically, Bruce suppresses wing tissue growth. These findings indicate that non-lethal Dcp-1 activity is governed by the autophagy-Bruce axis, enabling distinct non-lethal functions independent of cell death.
SN  - 2050-084X
ER  -