YRA1 Autoregulation Requires Nuclear Export and Cytoplasmic Edc3p-Mediated Degradation of Its Pre-mRNA
YRA1 Autoregulation Requires Nuclear Export and Cytoplasmic Edc3p-Mediated Degradation of Its Pre-mRNA
Autoregulatory loops often provide precise control of the level of expression of specific genes that encode key regulatory proteins. Here we have defined a pathway by which Yra1p, a yeast mRNA export factor, controls its own expression. We show that YRA1 exon 1 sequences in cis and Yra1p in trans inhibit YRA1 pre-mRNA splicing and commit the pre-mRNA to nuclear export. Mex67p and Crm1p jointly promote YRA1 pre-mRNA export, and once in the cytoplasm, the pre-mRNA is degraded by a 5' to 3' decay mechanism that is dependent on the decapping activator Edc3p and on specific sequences in the YRA1 intron. These results illustrate how common steps in the nuclear processing, export, and degradation of a transcript can be uniquely combined to control the expression of a specific gene and suggest that Edc3p-mediated decay may have additional regulatory functions in eukaryotic cells.
- University of Massachusetts Medical School United States
- Albert Einstein College of Medicine United States
RNA Caps, 570, Nucleocytoplasmic Transport Proteins, RNA Splicing, RNA Stability, Active Transport, Cell Nucleus, Receptors, Cytoplasmic and Nuclear, Karyopherins, Regulatory Sequences, Nucleic Acid, Catalysis, RNA Transport, Gene Expression Regulation, Fungal, RNA Precursors, RNA, Messenger, Molecular Biology, Cell Nucleus, Feedback, Physiological, Nuclear Proteins, RNA-Binding Proteins, RNA, Fungal, Cell Biology, Exons, Gene Deletion
RNA Caps, 570, Nucleocytoplasmic Transport Proteins, RNA Splicing, RNA Stability, Active Transport, Cell Nucleus, Receptors, Cytoplasmic and Nuclear, Karyopherins, Regulatory Sequences, Nucleic Acid, Catalysis, RNA Transport, Gene Expression Regulation, Fungal, RNA Precursors, RNA, Messenger, Molecular Biology, Cell Nucleus, Feedback, Physiological, Nuclear Proteins, RNA-Binding Proteins, RNA, Fungal, Cell Biology, Exons, Gene Deletion
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