A Tlx2-Cre mouse line uncovers essential roles for hand1 in extraembryonic and lateral mesoderm

Hand1 regulates development of numerous tissues within the embryo, extraembryonic mesoderm, and trophectoderm. Systemic loss of Hand1 results in early embryonic lethality but the cause has remained unknown. To determine if Hand1 expression in extraembryonic mesoderm is essential for embryonic surviv...

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Published inGenesis (New York, N.Y. : 2000) Vol. 48; no. 8; pp. 479 - 484
Main Authors Maska, Emily L., Cserjesi, Peter, Hua, Lisa L., Garstka, Meghan E., Brody, Heather M., Morikawa, Yuka
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.08.2010
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Summary:Hand1 regulates development of numerous tissues within the embryo, extraembryonic mesoderm, and trophectoderm. Systemic loss of Hand1 results in early embryonic lethality but the cause has remained unknown. To determine if Hand1 expression in extraembryonic mesoderm is essential for embryonic survival, Hand1 was conditionally deleted using the HoxB6‐Cre mouse line that expresses Cre in extraembryonic and lateral mesoderm. Deletion of Hand1 using HoxB6‐Cre resulted in embryonic lethality identical to systemic knockout. To determine if lethality is due to Hand1 function in extraembryonic mesoderm or lateral mesoderm, we generated a Tlx2‐Cre mouse line expressing Cre in lateral mesoderm but not extraembryonic tissues. Deletion of Hand1 using the Tlx2‐Cre line results in embryonic survival with embryos exhibiting herniated gut and thin enteric smooth muscle. Our results show that Hand1 regulates development of lateral mesoderm derivatives and its loss in extraembryonic mesoderm is the primary cause of lethality in Hand1‐null embryos. genesis 48:479–484, 2010. © 2010 Wiley‐Liss, Inc.
Bibliography:AHA
ark:/67375/WNG-29HD8DRJ-J
istex:66FE9F59F2ABD06E805F62E1C568E6EDEA27AE95
NSF - No. IOS-0529746; No. MCB-0529746
ArticleID:DVG20644
NIH - No. NS15547
Emily L. Maska and Peter Cserjesi contributed equally to this work.
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These authors contributed equally.
ISSN:1526-954X
1526-968X
1526-968X
DOI:10.1002/dvg.20644