PUBLICATION
Molecular basis of left-right asymmetry
- Authors
- Tamura, K., Yonei-Tamura, S., and Belmonte, J.C.
- ID
- ZDB-PUB-000201-25
- Date
- 1999
- Source
- Development, growth & differentiation 41(6): 645-656 (Journal)
- Registered Authors
- Izpisúa Belmonte, Juan Carlos
- Keywords
- none
- MeSH Terms
-
- Animals
- Body Patterning/genetics*
- Embryo, Nonmammalian
- Embryonic and Fetal Development
- Gene Expression Regulation, Developmental
- Humans
- Morphogenesis/genetics
- Mutation
- Viscera/embryology*
- PubMed
- 10646794 Full text @ Dev. Growth Diff.
Citation
Tamura, K., Yonei-Tamura, S., and Belmonte, J.C. (1999) Molecular basis of left-right asymmetry. Development, growth & differentiation. 41(6):645-656.
Abstract
In vertebrates visceral asymmetry is conserved along the left-right axis within the body. Only a small percentage of randomization (situs ambiguus), or complete
reversal (situs inversus) of normal internal organ position and structural asymmetry is found in humans. A breakdown in left-right asymmetry is occasionally associated with severe malformations of the organs, clearly indicating that the regulated asymmetric patterning could have an evolutionary advantage over allowing random placement of visceral organs. Genetic, molecular and cell transplantation experiments in humans, mice, zebrafish, chick and Xenopus have advanced our understanding of how initiation and establishment of left-right asymmetry occurs in the vertebrate embryo. In particular, the chick embryo has served as an extraordinary animal model to manipulate genes, cells and tissues. This chick model system has enabled us to reveal the genetic pathways that occur during left-right development. Indeed, genes with asymmetric expression domains have been identified and well characterized using the chick as a model system. The present review summarizes the molecular and experimental studies employed to gain a better understanding of left-right asymmetry pattern formation from the first split of symmetry in embryos, to the exhibition of asymmetric morphologies in organs.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping