| First Author | Satoh K | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 13771 |
| PubMed ID | 34215815 | Mgi Jnum | J:313730 |
| Mgi Id | MGI:6740002 | Doi | 10.1038/s41598-021-93110-1 |
| Citation | Satoh K, et al. (2021) Loss of FYCO1 leads to cataract formation. Sci Rep 11(1):13771 |
| abstractText | Autophagy is a degradation process of cytoplasmic proteins and organelles trafficked to degradation vesicles known as autophagosomes. The conversion of LC3-I to LC3-II is an essential step of autophagosome formation, and FYCO1 is a LC3-binding protein that mediates autophagosome transport. The p62 protein also directly binds to LC3 and is degraded by autophagy. In the present study, we demonstrated that disrupting the FYCO1 gene in mice resulted in cataract formation. LC3 conversion decreased in eyes from FYCO1 knockout mice. Further, FYCO1 interacted with alphaA- and alphaB-crystallin, as demonstrated by yeast two-hybrid screening and immunoprecipitation analyses. In eyes from knockout mice, the soluble forms of alphaA- and alphaB-crystallin, the lens's major protein components, decreased. In addition, p62 accumulated in eyes from FYCO1 knockout mice. Collectively, these findings suggested that FYCO1 recruited damaged alpha-crystallin into autophagosomes to protect lens cells from cataract formation. |
