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. 2021 Jul 2;11:13771. doi: 10.1038/s41598-021-93110-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed model of FYCO1 function in lens α-A/B-crystallin quality control. FYCO1 recruits damaged αA/αB-crystallin into autophagosomes and facilitates its degradation in autolysosomes to prevent cataract formation. In the case that wild-type mice FYCO1 positively controls autophagy, it will lead to degrade the aggregated αA-crystallin and αB-crystallin. On the other hand, due to decreased autophagy activity in the case of FYCO1 knockout mice, aggregated αA-crystallin and αB-crystallin accumulate, thereby leading to cataract formation.