Nashville, Tenn. -- A humble aquarium fish may be the key to finding therapies capable of preventing the structural birth defects that account for one out of three infant deaths in the United States today.
That is one of the implications of a new study published online August 8 in the journal Cell Metabolism. The paper describes a number of striking parallels between a rare but fatal human birth defect called Menkes disease and a lethal mutation in a small tropical fish called the zebrafish that has become an important animal model for studying early development.
Zebrafish are easy and inexpensive to raise and lay eggs that are transparent and develop outside the body. Much of the zebrafish genome has been sequenced, allowing researchers to identify human versions of zebrafish genes and vice versa. These qualities make the zebrafish exceptionally handy in studying the complex relationship between genes and nutrition during development, a puzzle that has stood in the way of developing effective treatments for birth defects.
"This is a proof of concept that we can use the zebrafish to finally understand the role that maternal nutrition plays in causing structural birth defects and develop new treatments that can prevent them," said co-author Jonathan Gitlin, the Helene B. Robertson Professor of Pediatrics at Washington University in Saint Louis. Collaborating in the study were Professor of Biological Sciences Lilianna Solnica-Krezel, postdoctoral fellow Thomas P. Wilm and graduate student Chunyue Yin from Vanderbilt University along with Associate Professor of Genetics Stephen L. Johnson and graduate student Bryce A. Mendelsohn from Washington University in St. Louis.
For many years, scientists have relied on the mouse and the frog Xenopus laevis as research models for vertebrates (animals with backbones), but zebrafish have an important advantage for studying early development: It is possible for researchers to watch the ch
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Contact: David F. Salisbury
david.salisbury@vanderbilt.edu
615-343-6803
Vanderbilt University
8-Aug-2006