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ABSTRACT: Purpose
HSF4 mutations are responsible for congenital cataract formation. Dysfunction of HSF4 leads to defects in lens terminal differentiation. We aimed to study the mechanism of how HSF4 promotes organelle degradation during lens differentiation.Methods
HSF4del42 mutant mice that developed congenital cataracts were employed. The organelle degradation and autophagic function in lens fibers were detected by immunofluorescence and Immunoblotting. Transcriptome analysis was performed to investigate the differentially expressed genes in HSF4del42 lenses, whereas luciferase report assay and ChIP assay were used to confirm the directly transcriptional regulation of ATG9a by HSF4.Results
HSF4del42 mice displayed delayed organelle clearance and impaired autophagic degradat
SUBMITTER: Zhang J
PROVIDER: S-EPMC10243497 | biostudies-literature | 2023 Jun
REPOSITORIES: biostudies-literature