A new molecule that regulates embryonic heart and muscle development in mice has been identified, according to a paper in the 04 Nov 2004 issue of Nature (Vol. 432, No. 7013, pp. 107-112). This finding may suggest a new way that genes are controlled during organ formation, and provide a clue to how birth defects occur in humans.
During embryonic development, tightly coiled DNA must be partially unwound to allow access of gene-copying proteins. Baf60c is part of a group of enzymes that are responsible for this modeling and during early embryonic development it is active mainly at the poles of the heart. Benoit G. Bruneau and his colleagues found that a large reduction in the molecule's activity disrupts top-to-bottom development and the formation of the heart's chambers. Smaller reductions in Baf60c levels affect the formation of the body's major blood vessels. Something similar is also seen to happen in congenital heart defects in humans.
Birth defects are the leading cause of infant mortality in most developed countries. Of these, cardiovascular defects are the most common, affecting approximately 1 in 115 live births.
Benoit G. Bruneau (The Hospital for Sick Children, Toronto, Canada)
Tel +1 416 813 6349, E-mail: email@example.com
Dr. Janet Rossant (Co-Author) Mount Sinai Hospital, Toronto, Canada)
Tel +1 416 586-8267, E-mail: firstname.lastname@example.org
(C) Nature press release.
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