1: Dev Biol. 2005 Oct 10; [Epub ahead of print] 

Odd-skipped related 1 (Odd1) is an essential regulator of heart and urogenital
development.

Wang Q, Lan Y, Cho ES, Maltby KM, Jiang R.

Center for Oral Biology and Department of Biomedical Genetics, University of
Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 611,
Rochester, NY 14642, USA.

The Odd-skipped related 1 (Odd1) gene encodes a zinc finger protein homologous
to the Drosophila Odd-skipped class transcription factors that play critical
roles in embryonic patterning and tissue morphogenesis. We have generated mice
carrying a targeted null mutation in the Odd1 gene and show that Odd1 is
essential for heart and intermediate mesoderm development. Odd1(-/-) mutant
mouse embryos fail to form atrial septum, display dilated atria with hypoplastic
venous valves, and exhibit blood backflow from the heart into systemic veins. In
contrast to other transcription factors implicated in atrial septum development,
Odd1 mRNA expression is restricted to the central dorsal domain of the atrial
myocardium during normal heart development. Moreover, expression patterns of
known key regulatory genes of atrial septum development, including Nkx2.5,
Pitx2, and Tbx5, are unaltered in the developing heart in Odd1(-/-) mutants
compared to that of the wild-type littermates. Furthermore, homozygous Odd1(-/-)
mutant embryos exhibit complete agenesis of adrenal glands, metanephric kidneys,
gonads, and defects in pericardium formation. Detailed molecular marker analyses
show that key regulators of early intermediate mesoderm development, including
Lhx1, Pax2, and Wt1, are all down-regulated and nephrogenic mesenchyme undergoes
massive apoptosis, resulting in disruption of nephric duct elongation and
failure of metanephric induction in the Odd1(-/-) mutant embryos. These data
provide new insights into the molecular mechanisms underlying heart
morphogenesis and urogenital development.

PMID: 16223478 [PubMed - as supplied by publisher]


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