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Roles of AML1 in Duchenne muscular dystrophy and in myogenesis
Author(s) -
Shi Rongye,
Chen YiWen
Publication year - 2007
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.21.6.a993-b
Subject(s) - duchenne muscular dystrophy , myogenesis , transfection , biology , muscular dystrophy , haematopoiesis , transgene , c2c12 , cancer research , microbiology and biotechnology , myocyte , gene , stem cell , genetics
AML1 (acute myelogenous leukemia 1) was originally cloned from the breakpoint of chromosome 21 in t(8;21)(q22;q22), and is one of the most frequent targets of leukemia‐associated gene aberrations. AML1 is a transcription regulator of a number of haematopoietic genes. The function of AML1 in skeletal muscle is not clear. Based on expression profiling data of muscles of non‐symptomatic DMD patients (10m infants), symptomatic patients (5–12yr), and mdx mice, we hypothesized that AML1 may play an important role in the successful remodeling of muscles in DMD infants and mdx mice. To study the potential function of AML1 in muscle, we transfected C2C12 cells with an expression vector carrying AML1, and showed that the transgene facilitated myotube formation, while the transgene did not affect cell proliferation rate. Fusion index was significantly higher in AML1 transfected cells compared to insertless‐vector transfected controls (P<0.0001). By expression profiling C2C12 cells transfected with AMLl, we further identified up‐regulation of genes involved in myogenesis. The findings suggested that AML1 might be directly regulating genes involved in myogenesis and participating in compensatory responses in Duchenne muscular dystrophy.