ArticleMolecular and cellular biology2005
The distal sequence element of the selenocysteine tRNA gene is a tissue-dependent enhancer essential for mouse embryogenesis.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 19 citations in OpenAlex.
- Compensation for impaired sensing of selenoprotein deficiency by alternative cysteine residues in KEAP1.Redox biology · 2026Article
- The choreography of chromatin in RNA polymerase III regulation.Biochemical Society transactions · 2024Review
- Methylation profile of bovineJournal of integrative agriculture : JIA · 2016Article
- Selenoproteins and cardiovascular stress.Thrombosis and haemostasis · 2015Review
- Queuosine deficiency in eukaryotes compromises tyrosine production through increased tetrahydrobiopterin oxidation.The Journal of biological chemistry · 2011Article
- Tissue-restricted expression of Nrf2 and its target genes in zebrafish with gene-specific variations in the induction profiles.PloS one · 2011Article
- Mouse models targeting selenocysteine tRNA expression for elucidating the role of selenoproteins in health and development.Molecules (Basel, Switzerland) · 2009Review
- Selenoprotein N is dynamically expressed during mouse development and detected early in muscle precursors.BMC developmental biology · 2009Article
- The selenocysteine tRNA STAF-binding region is essential for adequate selenocysteine tRNA status, selenoprotein expression and early age survival of mice.The Biochemical journal · 2009Article
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8 authors at 2 institutions in 1 country.
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Abstract
Appropriate expression of the selenocysteine tRNA (tRNA(Sec)) gene is necessary for the production of an entire family of selenoprotein enzymes. This study investigates the consequence of disrupting an upstream enhancer region of the mouse tRNA(Sec) gene (Trsp) known as the distal sequence element (DSE) by use of a conditional repair gene targeting strategy, in which a 3.2-kb insertion was introduced into the promoter of the gene. In the absence of DSE activity, homozygous mice failed to develop in utero beyond embryonic day 7.5 and had severely decreased levels of selenoprotein transcript. Cre-mediated removal of the selection cassette recovered DSE regulation of Trsp, restoring wild-type levels of tRNA(Sec) expression and allowing the generation of viable rescued mice. Further analysis of targeted heterozygous adult mice revealed that the enhancer activity of the DSE is tissue dependent since, in contrast to liver, heart does not require the DSE for normal expression of Trsp. Similarly, in mouse cell lines we showed that the DSE functions as a cell-line-specific inducible element of tRNA(Sec). Together, our data demonstrate that the DSE is a tissue-dependent regulatory element of tRNA(Sec) expression and that its activity is vital for sufficient tRNA(Sec) production during mouse embryogenesis.
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