Abstract:
:Gemin5 acts as a U1 small nuclear RNA (snRNA)-binding protein in U1 small nuclear ribonucleic protein (snRNP) biogenesis. Here, we report a role for Gemin5 in unassembled U1 snRNP disposal under survival of motor neuron (SMN) protein-deficient conditions. We demonstrate that non-Sm protein-associated U1 snRNA and U1A are enriched in cytoplasmic granules and colocalize to P bodies in SMN-deficient cells. Immunoprecipitation assays show increased associations of the U1 snRNP component U1A with P body components and Gemin5 in SMN-deficient cells. More importantly, Gemin5 knockdown eliminates the unassembled U1 snRNP granules and rescues U1 snRNA levels in SMN-deficient cells. Taken together, our study provides direct evidence that Gemin5 is involved in unassembled-U1 snRNA disposal under conditions of SMN deficiency.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Jiang D,Zou X,Zhang C,Chen J,Li Z,Wang Y,Deng Z,Wang L,Chen Sdoi
10.1002/1873-3468.13031subject
Has Abstractpub_date
2018-04-01 00:00:00pages
1400-1411issue
8eissn
0014-5793issn
1873-3468journal_volume
592pub_type
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