Ribosomal protein L24 defect in Belly spot and tail (Bst), a mouse Minute

ER Oliver, TL Saunders, SA Tarlé, T Glaser - 2004 - journals.biologists.com
ER Oliver, TL Saunders, SA Tarlé, T Glaser
2004journals.biologists.com
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 …
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.
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