Cardiac abnormalities cause early lethality of jumonji mutant mice

• Published in: Biochemical and biophysical research communications Vol. 324; no. 4; pp. 1319 - 1323
• Main Authors: Takahashi, Miho, Kojima, Mizuyo, Nakajima, Kuniko, Suzuki-Migishima, Rika, Motegi, Yoshiko, Yokoyama, Minesuke, Takeuchi, Takashi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 26-11-2004
• Subjects: Animals; Cardiac morphogenesis; Cardiac myocyte; Embryo, Mammalian - pathology; Embryonic lethality; Gene trap; Genes, Lethal; Heart Defects, Congenital - etiology; Heart Defects, Congenital - metabolism; Heart Defects, Congenital - pathology; jumonji; Mice; Mice, Mutant Strains; Mice, Transgenic; Mutant mouse; Myocardium - metabolism; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Polycomb Repressive Complex 2; Transcriptional repressor; Transgenic mouse; Cardiac morphogenesis; Embryonic lethality; Gene trap; Transgenic mouse; Cardiac myocyte; Mutant mouse; Transcriptional repressor; jumonji
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2004.09.203

jumonji (
jmj) mutant mice, obtained by a gene trap strategy, showed several morphological abnormalities including neural tube and cardiac defects, and died in utero around embryonic day 11.5 (E11.5). It is unknown what causes the embryonic lethality. Here, we demonstrate that exogenous expression of
jmj gene in the heart of
jmj mutant mice rescued the morphological phenotypes in the heart, and these embryos survived until E13.5. These results suggest that there are at least two lethal periods in
jmj mutant mice, and that cardiac abnormalities may cause the earlier lethality. In addition, the rescue of the cardiac abnormalities by the
jmj transgene provided solid evidence that the cardiac abnormalities resulted from mutation of the
jmj gene.