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PreprintCC BY-NC-NDbioRxiv

Ile35 residue of SOD1 plays a key role in aggregate formation and eye degeneration in a Drosophila model of ALS

  • K. Yano
  • Y. Fujino
  • Y. Nagai
  • N. Fujiwara1
  1. 1Hyogo Medical University
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Abstract

{middle dot}The pathophysiology of ALS caused by mutant SOD1 remains unclear. {middle dot}We previously demonstrated, using the BioID2-EGFP sandwich expression system in cultured cells, that the Ile35 residue of ALS-linked mutant SOD1 promotes its aggregate formation. {middle dot}However, the precise role of the SOD1 Ile35 residue in aggregate formation and neurodegeneration in vivo remained unclear. {middle dot}Drosophila expressing BioID2-G93A-EGFP demonstrated aggregate formation and eye degeneration with reduced eye size, whereas those expressing BioID2-G93A/I35S-EGFP showed less of these phenotypes. {middle dot}These findings highlight the crucial role of the Ile35 residue of ALS-linked SOD1 in aggregate formation and neurodegeneration in vivo.

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Cite

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BibTeX
@misc{yano2026ile35,
  title = {{Ile35 residue of SOD1 plays a key role in aggregate formation and eye degeneration in a Drosophila model of ALS}},
  author = {K. Yano and Y. Fujino and Y. Nagai and N. Fujiwara},
  howpublished = {bioRxiv},
  year = {2026},
  month = sep,
  doi = {10.64898/2026.09.13.751333},
  url = {https://www.biorxiv.org/content/10.64898/2026.09.13.751333v1},
  note = {CC BY-NC-ND},
}
RIS
TY  - UNPB
TI  - Ile35 residue of SOD1 plays a key role in aggregate formation and eye degeneration in a Drosophila model of ALS
AU  - K. Yano
AU  - Y. Fujino
AU  - Y. Nagai
AU  - N. Fujiwara
PY  - 2026
DA  - 2026/09/13
PB  - bioRxiv
DO  - 10.64898/2026.09.13.751333
UR  - https://www.biorxiv.org/content/10.64898/2026.09.13.751333v1
AB  - {middle dot}The pathophysiology of ALS caused by mutant SOD1 remains unclear. {middle dot}We previously demonstrated, using the BioID2-EGFP sandwich expression system in cultured cells, that the Ile35 residue of ALS-linked mutant SOD1 promotes its aggregate formation. {middle dot}However, the precise role of the SOD1 Ile35 residue in aggregate formation and neurodegeneration in vivo remained unclear. {middle dot}Drosophila expressing BioID2-G93A-EGFP demonstrated aggregate formation and eye degeneration with reduced eye size, whereas those expressing BioID2-G93A/I35S-EGFP showed less of these phenotypes. {middle dot}These findings highlight the crucial role of the Ile35 residue of ALS-linked SOD1 in aggregate formation and neurodegeneration in vivo.
ER  -