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The Wilms' tumor 1 (WT1) gene (+KTS isoform) functions with a CTE to enhance translation from an unspliced RNA with a retained intron

Bor, Yeou Cherng; Hammarskjöld, Marie Louise; Swartz, Jennifer; Morrison, Avril; Rekosh, David; Ladomery, Michael

Authors

Yeou Cherng Bor

Marie Louise Hammarskjöld

Jennifer Swartz

Avril Morrison

David Rekosh



Abstract

The Wilms' tumor 1 (WT1) gene plays an important role in mammalian urogenital development, and dysregulation of this gene is observed in many human cancers. Alternative splicing of WT1 RNA leads to the expression of two major protein isoforms, WT1(+KTS) and WT1(-KTS). Whereas WT1(-KTS) acts as a transcriptional regulator, no clear function has been ascribed to WT1(+KTS), despite the fact that this protein is crucial for normal development. Here we show that WT1(+KTS) functions to enhance expression from RNA possessing a retained intron and containing either a cellular or viral constitutive transport element (CTE). WT1(+KTS) expression increases the levels of unspliced RNA containing a CTE and specifically promotes the association of this RNA with polyribosomes. These studies provide further support for links between different steps in RNA metabolism and for the existence of post-transcriptional operons. © 2006 by Cold Spring Harbor Laboratory Press.

Journal Article Type Article
Publication Date Jun 15, 2006
Journal Genes and Development
Print ISSN 0890-9369
Electronic ISSN 1549-5477
Publisher Cold Spring Harbor Laboratory Press
Peer Reviewed Peer Reviewed
Volume 20
Issue 12
Pages 1597-1608
APA6 Citation Hammarskjöld, M. L., Bor, Y. C., Bor, Y., Swartz, J., Morrison, A., Rekosh, D., …Hammarskjold, M. (2006). The Wilms' tumor 1 (WT1) gene (+KTS isoform) functions with a CTE to enhance translation from an unspliced RNA with a retained intron. Genes and Development, 20(12), 1597-1608. https://doi.org/10.1101/gad.1402306
DOI https://doi.org/10.1101/gad.1402306
Keywords WT1, Wilms’ tumor, CTEconstitutive transport element, RNA export, post-transcriptional regulation, translational regulation
Publisher URL http://dx.doi.org/10.1101/gad.1402306
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