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First published online August 2, 2004
doi: 10.1242/10.1242/dev.01268

Development 131, 3907-3920 (2004)
Published by The Company of Biologists 2004
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Ribosomal protein L24 defect in Belly spot and tail (Bst), a mouse Minute

Edward R. Oliver1, Thomas L. Saunders2, Susan A. Tarlé2 and Tom Glaser1,2,*

1 Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI 48109, USA
2 Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA

* Author for correspondence (e-mail: tglaser{at}umich.edu)

Accepted 12 May 2004

Ribosomal protein mutations, termed Minutes, have been instrumental in studying the coordination of cell and tissue growth in Drosophila. Although abundant in flies, equivalent defects in mammals are relatively unknown. Belly spot and tail (Bst) is a semidominant mouse mutation that disrupts pigmentation, somitogenesis and retinal cell fate determination. Here, we identify Bst as a deletion within the Rpl24 riboprotein gene. Bst significantly impairs Rpl24 splicing and ribosome biogenesis. Bst/+ cells have decreased rates of protein synthesis and proliferation, and are outcompeted by wild-type cells in C57BLKS{leftrightarrow}ROSA26 chimeras. Bacterial artificial chromosome (BAC) and cDNA transgenes correct the mutant phenotypes. Our findings establish Bst as a mouse Minute and provide the first detailed characterization of a mammalian ribosomal protein mutation.

Key words: Mouse, Genetics, Minute, Ribosome, Cell cycle, Retina, Bst


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Related articles in Development:

Ribosomal insights from Minute mice

Development 2004 131: e1602. [Full Text]  

Ribosomal insights from Minute mice

Development 2004 131: e1602. [Full Text]  



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