Lens defects in Astyanax mexicanus Cavefish: Evolution of crystallins and a role for alphaA‐crystallin. Issue 5 (4th November 2014)

• Record Type: Journal Article
• Authors: Hinaux, Hélène; Blin, Maryline; Fumey, Julien; Legendre, Laurent; Heuzé, Aurélie; Casane, Didier; Rétaux, Sylvie
• Is Part Of: Developmental neurobiology. Volume 75:Issue 5(2015:May)
• Page Start: 505
• Page End: 521
• Publication Date: 2014-11-04
• Subjects: Neurobiology -- Periodicals; Neurobiology; Neurobiologie -- Périodiques; Neurobiology; Periodicals; Periodicals; 573.838
• DOI: 10.1002/dneu.22239
• Languages: English
• ISSNs: 1932-8451

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <p>The fish <italic>Astyanax mexicanus</italic> presents, within the same species, populations of river‐dwelling surface fish (SF) and blind cave‐living fish. In cavefish (CF), the eyes develop almost normally during embryogenesis. But 40 h after fertilization, the lens enters apoptosis, triggering the progressive degeneration of the entire eye. Before apoptosis, the CF lens expresses early differentiation factors correctly. Here, we searched for possible late differentiation defects that would be causal in CF lens degeneration. We reasoned that crystallins, the major lens structural proteins, could be defective or misregulated. We surveyed the CF and SF transcriptomes and uncovered 14 <italic>Astyanax</italic> 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 CF than in SF, suggesting relaxed selection at these loci in CF. <italic>In situ</italic> hybridizations and qPCR show that <italic>crybb1c</italic>, <italic>crybgx, crygm5</italic> are expressed at much lower levels or are not expressed in the CF lens. For the best crystallin candidates, we tested a potential causal role in CF lens apoptosis. <italic>Crybgx</italic>, <italic>crybb1c</italic> (not expressed in CF from very early on), and <italic>cryaa</italic> (previously shown to be faintly expressed in CF) failed to induce any defect when knocked‐down in zebrafish embryos. However, the anti‐apoptotic <italic>cryaa</italic> protected lens cells from apoptosis when reexpressed by transgenesis in CF, 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 CF. © 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 505–521, 2015</p> </abstract>