4.7 Article

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

Journal

DEVELOPMENT
Volume 131, Issue 16, Pages 3907-3920

Publisher

COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.01268

Keywords

mouse; genetics; Minute; ribosome; cell cycle; retina; Bst

Funding

  1. NEI NIH HHS [R01 EY014259, R01 EY014259-03, EY12994, R01 EY012994, EY14259, R01 EY011729-05] Funding Source: Medline
  2. NICHD NIH HHS [T32 HD007505, HD07505] Funding Source: Medline
  3. NIDDK NIH HHS [P60 DK020572, DK20572, P30 DK020572] Funding Source: Medline
  4. NIGMS NIH HHS [GM067840, T32 GM007863, T32 GM07863, R01 GM067840, R01 GM067840-04] Funding Source: Medline

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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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