English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  The teleost  Astyanax mexicanus  is a single species consisting of eyed surface-dwelling (surface fish) and blind cave-dwelling (cavefish) morphs. Cavefish eyes are lost through apoptosis of the lens, which in turn promotes the degeneration of other optic tissues. The  αA-crystallin  ( αA-crys ) gene is strongly downregulated in the cavefish lens and is located in a genomic region (QTL) responsible for eye loss. Therefore,  αA-crys  has been proposed as a candidate for regulating cavefish eye degeneration. The purpose of this study was to determine the mechanism of  αA-crys  downregulation and its role in cavefish eye degeneration.    Results  The involvement of  αA-crys  in eye degeneration was confirmed by knocking down its expression in surface fish, which led to apoptosis of the lens. The underlying reason for  αA-crys  downregulation in cavefish was investigated by comparing genomic  αA-crys  DNA sequences in surface fish and cavefish, however, no obvious cis-regulatory factors were discovered. Furthermore, the cavefish  αA-crys  allele is expressed in surface fish x cavefish F1 hybrids, indicating that evolutionary changes in upstream genes are most likely responsible for  αA-crys  downregulation. In other species, Sox2 is one of the transcription factors that regulate lens  crystallin  genes during eye development. Determination of  sox2  expression patterns during surface fish and cavefish development showed that  sox2  is specifically downregulated in the cavefish lens. The upstream regulatory function of Sox2 was demonstrated by knockdown in surface fish, which abolished  αA-crys  expression and induced lens apoptosis.    Conclusions  The results suggest that  αA-crys  is required for normal eye development in cavefish via suppression of lens apoptosis. The regulatory changes involved in  αA-crys  downregulation in cavefish are in trans-acting factors rather than cis-acting mutations in the  αA-crys  gene. Therefore,  αA-crys  is unlikely to be the mutated gene(s) associated with an  Astyanax  eye QTL. The results reveal a genetic pathway leading from  sox2  to  αA-crys  that is required for survival of the lens in  Astyanax  surface fish. Defects in this pathway may be involved in lens apoptosis and thus a cause of cavefish eye degeneration.

The role of a lens survival pathway including sox2 and αA-crystallin in the evolution of cavefish eye degeneration