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Mice bearing a targeted inactivation of nBmp2 show decreased muscle strength
Author(s) -
Schmidt Alina D,
Loganathan Sampath K,
Adam Mike M,
Nichols Caitlin A,
Mayo Jaime L,
Felin Jenny E,
Capecchi Mario R,
Barrow Jeffery R,
Bridgewater Laura C
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.685.2
Subject(s) - growth differentiation factor , nucleus , biology , microbiology and biotechnology , mitochondrion , skeletal muscle , bone morphogenetic protein , sarcopenia , wild type , mutant , bone morphogenetic protein 2 , translation (biology) , muscle hypertrophy , anatomy , genetics , endocrinology , gene , messenger rna , in vitro
An important growth factor in the body, bone morphogenetic protein (Bmp2) contributes to mesoderm formation, heart development, neurogenesis, skeletal development, and axis formation. We have recently discovered a novel variant of this protein in the nucleus (nBmp2). This protein is produced by translation from a downstream alternative start codon and is localized to the nucleus by means of a bipartite nuclear localization signal. To determine the function of nBmp2, a mouse was engineered in which the conventional Bmp2 growth factor is still expressed normally, but the nuclear variant, nBmp2, cannot be translocated to the nucleus. The mice appear phenotypically normal at birth and are fertile. A series of flexed limb‐hang strength tests, however, revealed that mutant mice have significantly reduced strength compared to wild type mice. Western blot analysis performed on mitochondrial extracts showed increased amounts of cytochrome C in mutant compared to wild type muscle mitochondria. These results suggest that nBmp2 may affect muscle strength by playing a role in mitochondrial function. This work was supported by NIH grant AR48839 and by an award from the Fulton Family Foundation to promote undergraduate research.