Modifiers of the jumonji mutation downregulate cyclin D1 expression and cardiac cell proliferation.
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.
Ohno
Tadayuki
T
Mitsubishi Kagaku Institute of Life Sciences (MITILS), 11 Minamiooya, Machida, Tokyo 194-8511, Japan.
Nakajima
Kuniko
K
Kojima
Mizuyo
M
Toyoda
Masashi
M
Takeuchi
Takashi
T
D000818:Animals; D002455:Cell Division / Q000235:genetics*; D019938:Cyclin D1 / Q000235:genetics*; D015536:Down-Regulation / Q000502:physiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D009154:Mutation; D009206:Myocardium / Q000166:cytology*; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000502:physiology*; D063151:Polycomb Repressive Complex 2
C093650:Jarid2 protein, mouse; D009419:Nerve Tissue Proteins; D019938:Cyclin D1; D063151:Polycomb Repressive Complex 2