{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T13:40:18Z","timestamp":1779889218309,"version":"3.53.1"},"reference-count":93,"publisher":"Public Library of Science (PLoS)","issue":"7","license":[{"start":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T00:00:00Z","timestamp":1751846400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000053","name":"National Eye Institute","doi-asserted-by":"crossref","award":["EY031303"],"award-info":[{"award-number":["EY031303"]}],"id":[{"id":"10.13039\/100000053","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000053","name":"National Eye Institute","doi-asserted-by":"crossref","award":["P30-EY03039"],"award-info":[{"award-number":["P30-EY03039"]}],"id":[{"id":"10.13039\/100000053","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.plosone.org"],"crossmark-restriction":false},"short-container-title":["PLoS One"],"abstract":"<jats:p>CRY\u03b2A1-\u0394G91 (\u03b2A3\u0394G91) is a mutational hotspot in CRY\u03b2A1, which causes autosomal dominant congenital nuclear cataract in humans and mice. Previous <jats:italic>in-vitro<\/jats:italic> studies of recombinant \u03b2A3\u0394G91 showed defective folding, decreased solubility, and aberrant oligomerization of \u03b2A3\u0394G91 with other crystallins. Emerging evidence demonstrates an association between autophagy and \u03b2A3\u0394G91-induced congenital cataracts. To gain further understanding of the molecular mechanism of congenital cataract development in \u03b2A3\u0394G91 mice, we examined the \u03b2A3\u0394G91- vs WT- lenses for complete gene profiling, lens epithelial cell (LEC) proliferation and migration, and lens epithelial-fiber cell differentiation. We also determined the changes in crystallin proteomic profiles in water-soluble, water-insoluble-urea-soluble, and water-insoluble-urea-insoluble fractions. Our results show that relative to WT lenses, the \u03b2A3\u0394G91 lenses showed: (A) downregulation of genes associated with LECs proliferation and migration (B) abnormal suture line pattern, (C) significant reduction in proliferation and migration of LECs, (D) abnormal F-actin distribution, (E) increased high molecular weight (HMW) peak, and (F) insolubilization and degradation of crystallins and other lens proteins. Together, these defects contribute to the formation of the lens opacity in \u03b2A3\u0394G91 mice lenses.<\/jats:p>","DOI":"10.1371\/journal.pone.0326305","type":"journal-article","created":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T17:33:07Z","timestamp":1751909587000},"page":"e0326305","update-policy":"https:\/\/doi.org\/10.1371\/journal.pone.corrections_policy","source":"Crossref","is-referenced-by-count":4,"title":["G91-deletion in \u03b2A3\/A1-crystallin induces cellular and molecular changes in mouse lenses leading to congenital cataract development"],"prefix":"10.1371","volume":"20","author":[{"given":"Akosua K.","family":"Boateng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roy","family":"Joseph","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5727-4801","authenticated-orcid":true,"given":"Om 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