PUBLICATION
The hox paradox: more complex(es) than imagined
- Authors
- Prince, V.
- ID
- ZDB-PUB-020911-1
- Date
- 2002
- Source
- Developmental Biology 249(1): 1-15 (Review)
- Registered Authors
- Prince, Victoria E.
- Keywords
- Hox genes; Hox clusters; gene duplication; vertebrate evolution; teleosts; zebrafish; hindbrain
- MeSH Terms
-
- Animals
- Biological Evolution
- Fishes/physiology
- Gene Expression Regulation, Developmental
- Homeodomain Proteins/genetics*
- Homeodomain Proteins/metabolism
- Multigene Family*
- Rhombencephalon/physiology*
- Vertebrates/physiology*
- Zebrafish Proteins/physiology
- PubMed
- 12217314 Full text @ Dev. Biol.
Citation
Prince, V. (2002) The hox paradox: more complex(es) than imagined. Developmental Biology. 249(1):1-15.
Abstract
An understanding of the origin of different body plans requires knowledge of how the genes and genetic pathways that control embryonic development have evolved. The Hox genes provide an appealing starting point for such studies because they play a well-understood causal role in the regionalization of the body plan of all bilaterally symmetric animals. Vertebrate evolution has been characterized by gene, and possibly genome, duplication events, which are believed to have provided raw genetic material for selection to act upon. It has recently been established that the Hox gene organization of ray-finned fishes, such as the zebrafish, differs dramatically from that of their lobe-finned relatives, a group that includes humans and all the other widely used vertebrate model systems. This unusual Hox gene organization of zebrafish is the result of a duplication event within the ray-finned fish lineage. Thus, teleosts, such as zebrafish, have more Hox genes arrayed over more clusters (or "complexes") than do tetrapod vertebrates. Here, I review our understanding of Hox cluster architecture in different vertebrates and consider the implications of gene duplication for Hox gene regulation and function and the evolution of different body plans.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping