PUBLICATION
Negative charge correlates with neural expression in vertebrate aldolase isozymes
- Authors
- Merritt, T.J. and Quattro, J.M.
- ID
- ZDB-PUB-030115-30
- Date
- 2002
- Source
- Journal of molecular evolution 55(6): 674-683 (Journal)
- Registered Authors
- Quattro, Joseph M.
- Keywords
- Fructose bisphosphate aldolase, Gene duplication, Neural expression, Teleost fish
- MeSH Terms
-
- Amino Acid Sequence
- Animals
- Base Sequence
- DNA, Complementary
- Fructose-Bisphosphate Aldolase/chemistry
- Fructose-Bisphosphate Aldolase/metabolism*
- Humans
- Isoenzymes/chemistry
- Isoenzymes/metabolism*
- Molecular Sequence Data
- Phylogeny
- Sequence Homology, Amino Acid
- Zebrafish
- PubMed
- 12486526 Full text @ J. Mol. Evol.
Citation
Merritt, T.J. and Quattro, J.M. (2002) Negative charge correlates with neural expression in vertebrate aldolase isozymes. Journal of molecular evolution. 55(6):674-683.
Abstract
Electrophoretic studies suggest that negatively charged neural proteins are a general feature of jawed vertebrates. In an apparent example of this, teleost fish express three aldolase isozymes, one of which is expressed predominantly in neural tissues and is more negatively charged than its more generally expressed paralogues. We characterized three aldolase isozymes from a single species of teleost fish, zebrafish (Danio rerio). These sequences indicated that the correlation of net negative charge and neural expression suggested in other species by gel electrophoresis was supported by sequence analysis. When aldolase sequences from the databases were included in phylogenetic analyses, the negative charge/neural expression phenomenon was observed across the gnathostome vertebrate sequences examined. We found no evidence for a period of positive Darwinian selection resulting in an accumulation of negatively charged amino acids during the evolution of the neural aldolase isozymes. This is likely attributable, however, to limitations associated with the age of the duplication responsible for the neural isozyme and the reconstruction of ancestral sequences.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping