Modifiers of the jumonji mutation downregulate cyclin D1 expression and cardiac cell proliferation

• Published in: Biochemical and biophysical research communications Vol. 317; no. 3; pp. 925 - 929
• Main Authors: Ohno, Tadayuki, Nakajima, Kuniko, Kojima, Mizuyo, Toyoda, Masashi, Takeuchi, Takashi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 07-05-2004
• Subjects: Animals; Cardiac myocyte; Cell cycle; Cell Division - genetics; Cyclin D1; Cyclin D1 - genetics; Down-Regulation - physiology; Genetic background; Jumonji; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Modifier; Morphogenesis; Mouse strain; Mutant; Mutation; Myocardium - cytology; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - physiology; Polycomb Repressive Complex 2; Transcription; Morphogenesis; Genetic background; Transcription; Cell cycle; Mutant; Jumonji; Mouse strain; Cardiac myocyte; Cyclin D1; Modifier
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2004.03.131

Cell proliferation is an important factor in various developmental processes in tissue morphogenesis, and is strictly regulated spatiotemporally.
jumonji (
jmj) deficient mice with a C3H/He background show hyperproliferation of cardiac myocytes and die probably of the phenotype around embryonic day 11.5. Analyses of the abnormalities revealed that repression of
cyclin D1 expression by
jmj is necessary for downregulation of cardiac myocyte proliferation. On the other hand,
jmj mutant mice with a BALB/c background die around E14.5, suggesting that genetic background modifies hyperproliferation in the heart and timing of lethality. Here, we demonstrated that the hyperproliferation was not observed, and that cell proliferation and expression of
cyclin D1 were downregulated properly in the cardiac ventricles of
jmj mutant mice with a BALB/c background. These results suggest the modifier(s) of the
jmj mutation can downregulate cardiac cell proliferation by repressing
cyclin D1 expression in the same way as
jmj.