Author
Listed:
- Kenta Yashiro
(Developmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1–3 Yamada-oka, Suita, Osaka 565-0871, Japan
CREST, Japan Science and Technology Corporation (JST), 1–3 Yamada-oka, Suita, Osaka 565-0871, Japan
Present address: Translational Cardiovascular Therapeutics, William Harvey Research Institute, Barts and The London, Queen Mary’s School of Medicine and Dentistry, University of London, Charterhouse Square, London EC1M 6BQ, UK)
- Hidetaka Shiratori
(Developmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1–3 Yamada-oka, Suita, Osaka 565-0871, Japan
CREST, Japan Science and Technology Corporation (JST), 1–3 Yamada-oka, Suita, Osaka 565-0871, Japan)
- Hiroshi Hamada
(Developmental Genetics Group, Graduate School of Frontier Biosciences, Osaka University, 1–3 Yamada-oka, Suita, Osaka 565-0871, Japan
CREST, Japan Science and Technology Corporation (JST), 1–3 Yamada-oka, Suita, Osaka 565-0871, Japan)
Abstract
Asymmetries of the heart In the past decade there has been remarkable progress in understanding the mechanism of left–right patterning. However, the cellular and molecular basis of asymmetric morpho-genesis remains largely unknown. Now, Yashiro et al. show that the transcription factor Pitx2 induces a dynamic morphological change in the outflow tract of the heart, which results in asymmetric blood supply to the branchial arch artery system. The uneven blood distribution results in differential signalling responses which cause the asymmetric remodelling of the great arteries.
Suggested Citation
Kenta Yashiro & Hidetaka Shiratori & Hiroshi Hamada, 2007.
"Haemodynamics determined by a genetic programme govern asymmetric development of the aortic arch,"
Nature, Nature, vol. 450(7167), pages 285-288, November.
Handle:
RePEc:nat:nature:v:450:y:2007:i:7167:d:10.1038_nature06254
DOI: 10.1038/nature06254
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