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First published online January 26, 2007
doi: 10.1242/10.1242/dev.02777
1 Division of Mammalian Development, National Institute of Genetics, 1111 Yata,
Mishima Shizuoka 411-8540, Japan.
2 Department of Genetics, The Graduate University for Advanced studies, 1111
Yata, Mishima Shizuoka 411-8540, Japan.
3 Department of Pediatric Cardiology, The Heart Institute of Japan, Tokyo
Women's Medical University, 8-1 Kawada-cho, Shinjyuku-ku, Tokyo 162-8666,
Japan.
4 National Institute for Basic Biology, 38 Nishigonaka, Myodaiji, Okazaki Aichi
444-8585 Japan.
* Authors for correspondence (e-mail: hkokubo{at}lab.nig.ac.jp; ysaga{at}lab.nig.ac.jp)
Accepted 6 December 2006
The establishment of chamber specificity is an essential requirement for cardiac morphogenesis and function. Hesr1 (Hey1) and Hesr2 (Hey2) are specifically expressed in the atrium and ventricle, respectively, implicating these genes in chamber specification. In our current study, we show that the forced expression of Hesr1 or Hesr2 in the entire cardiac lineage of the mouse results in the reduction or loss of the atrioventricular (AV) canal. In the Hesr1-misexpressing heart, the boundaries of the AV canal are poorly defined, and the expression levels of specific markers of the AV myocardium, Bmp2 and Tbx2, are either very weak or undetectable. More potent effects were observed in Hesr2-misexpressing embryos, in which the AV canal appears to be absent entirely. These data suggest that Hesr1 and Hesr2 may prevent cells from expressing the AV canal-specific genes that lead to the precise formation of the AV boundary. Our findings suggest that Tbx2 expression might be directly suppressed by Hesr1 and Hesr2. Furthermore, we find that the expression of Hesr1 and Hesr2 is independent of Notch2 signaling. Taken together, our data demonstrate that Hesr1 and Hesr2 play crucial roles in AV boundary formation through the suppression of Tbx2.
Key words: Hesr1 (Hey1), Hesr2 (Hey2), Heart, Notch signaling
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