PUBLICATION
Lens defects in Astyanax mexicanus cavefish: evolution of crystallins and a role for alphaA-crystallin
- Authors
- Hinaux, H., Blin, M., Fumey, J., Legendre, L., Heuzé, A., Casane, D., Rétaux, S.
- ID
- ZDB-PUB-141029-5
- Date
- 2015
- Source
- Developmental Neurobiology 75(5): 505-21 (Journal)
- Registered Authors
- Blin, Maryline, Casane, Didier
- Keywords
- apoptosis, cryaa, gene expression, molecular evolution, phylogeny
- MeSH Terms
-
- Animals
- Apoptosis/physiology
- Cell Differentiation/physiology
- Cell Survival/physiology
- Evolution, Molecular*
- Gene Expression Regulation, Developmental/physiology*
- Lens, Crystalline/abnormalities
- Lens, Crystalline/metabolism*
- Transcriptome/physiology
- Zebrafish/embryology
- Zebrafish/genetics
- Zebrafish/metabolism*
- alpha-Crystallins/metabolism*
- PubMed
- 25348293 Full text @ Dev. Neurobiol.
Citation
Hinaux, H., Blin, M., Fumey, J., Legendre, L., Heuzé, A., Casane, D., Rétaux, S. (2015) Lens defects in Astyanax mexicanus cavefish: evolution of crystallins and a role for alphaA-crystallin. Developmental Neurobiology. 75(5):505-21.
Abstract
The fish Astyanax mexicanus presents, within the same species, populations of river-dwelling surface fish and blind cave-living fish. In cavefish, the eyes develop almost normally during embryogenesis. But 40 hours after fertilization, the lens enters apoptosis, triggering the progressive degeneration of the entire eye. Before apoptosis, the cavefish lens expresses early differentiation factors correctly. Here we searched for possible late differentiation defects that would be causal in cavefish lens degeneration. We reasoned that crystallins, the major lens structural proteins, could be defective or mis-regulated. We surveyed the cavefish and surface fish transcriptomes and uncovered 14 Astyanax crystallins from the beta, gamma, lambda, mu and zeta families. These proteins are less polymorphic and accumulate more fixed mutations, some at highly conserved positions, in cavefish than in surface fish, suggesting relaxed selection at these loci in cavefish. In situ hybridizations and qPCR show that crybb1c, crybgx, crygm5 are expressed at much lower levels or are not expressed in the cavefish lens. For the best crystallin candidates, we tested a potential causal role in cavefish lens apoptosis. Crybgx, crybb1c (not expressed in CF from very early on) and cryaa (previously shown to be faintly expressed in CF) failed to induce any defect when knocked-down in zebrafish embryos. However, the anti-apoptotic cryaa protected lens cells from apoptosis when re-expressed by transgenesis in cavefish, suggesting a cell-autonomous effect of cryaa on lens cell survival. Altogether, these data suggest that crystallin sequence evolution and expression defects may contribute to the loss of eyes in cavefish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping