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