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Genetic Basis For Some Birth Defects Uncovered
ScienceDaily (Nov. 12, 2008) — A multidisciplinary research team at Case
Western Reserve University led by Gary Landreth, Ph.D., a professor in the
School of Medicine's Department of Neurosciences, has uncovered a common
genetic pathway for a number of birth defects that affect the development of
the heart and head.
Abnormal development of the jaw, palate, brain and heart are relatively common
congenital defects and frequently arise due to genetic errors that affect a key
Landreth, also the senior author of the study, developed a mouse model of these
disorders by removing a gene central to this developmental pathway, called
ERK2. He, together with Dr. William Snider at the University of North Carolina,
discovered that the mice missing the gene for ERK2 in neural crest cells had
developmental defects resembling those of human patients with a deletion that
includes this gene. The patients have features that are similar to DiGeorge
syndrome, which is associated with cardiac and palate defects. Interestingly,
the ERK2 gene is central to a well-known pathway already associated with a
different distinct group of cardiac and craniofacial syndromes that include
Noonan, Costello, Cardiofaciocutaneous syndrome, and LEOPARD syndrome.
Landreth enlisted the help of Michiko Watanabe, Ph.D., professor of Pediatrics
at Case Western Reserve University School of Medicine to look at the mouse
hearts. She and her team found that they had characteristic heart defects
resembling those seen in the patients with ERK2 deletions.
"Given Dr. Watanabe's findings, we determined that we had in fact developed
animal models that mimicked the human deletion syndrome," said Landreth. "This
work sheds light on how these developmental errors occur."
Remarkably, Dr. Sulagna Saitta, a human geneticist at Children's Hospital of
Philadelphia had identified children who had comparable heart defects as well
as subtle facial differences. These children were all missing a very small
region of chromosome 22 that contained the ERK2 gene.
Saitta agreed that the similarity in the anatomic structures affected in the
mice and those in the patients who have lost one copy of this gene suggest that
ERK2 and its pathway members are essential for normal development and might
lead to these birth defects. These findings link together several distinct
syndromes that are each characterized by cardiac and craniofacial abnormalities
and show that they can result from perturbations of the ERK cascade.
Landreth and his team will take these findings back to the lab and find out
exactly why cells need ERK2 during embryogenesis.
Funding was provided by the National Institutes of Health, the National Science
Foundation, the National Heart Lung Blood Institue and a National Research
1. Jason Newbern et al. Mouse and human phenotypes indicate a critical
conserved role for ERK2 signaling in neural crest development. PNAS,
105:17115-17120; published ahead of print October 24, 2008 DOI:
Adapted from materials provided by Case Western Reserve University, via
EurekAlert!, a service of AAAS.
Need to cite this story in your essay, paper, or report? Use one of the
Case Western Reserve University (2008, November 12). Genetic Basis For Some
Birth Defects Uncovered. ScienceDaily. Retrieved November 12, 2008, from
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