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Dissection of FUS domains involved in regulation of SnRNP70 gene expression
Author(s) -
Nakaya Tadashi
Publication year - 2020
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13924
Subject(s) - gene knockdown , rna splicing , gene expression , biology , gene , alternative splicing , amyotrophic lateral sclerosis , mutant , messenger rna , regulation of gene expression , genetics , microbiology and biotechnology , computational biology , rna , pathology , medicine , disease
FUS is one of the causative factors of amyotrophic lateral sclerosis. Loss and/or gain of its physiological functions has been believed to be linked to the pathogenesis of this condition. However, its functions remain incompletely understood. This study dissected the domains of FUS regulating the expression of SnRNP70, which functions in mRNA splicing. Biochemical analysis revealed that all FUS domains except for RGG1 contribute to determining Snrnp70 transcript abundance and thus its protein abundance. RNA‐Seq analysis using the Gly‐rich domain‐deleted mutant coupled with snRNP70 knockdown revealed that FUS has a potential to regulate gene expression in both snRNP70‐dependent and snRNP70‐independent manners through the Gly‐rich domain. These results provide insight into molecular details of the regulation of gene expression by FUS.