Central Role for the Lens in Cave Fish Eye Degeneration

Abstract

Astyanax mexicanus is a teleost with eyed surface-dwelling and eyeless cave-dwelling forms. Eye formation is initiated in cave fish embryos, but the eye subsequently arrests and degenerates. The surface fish lens stimulates growth and development after transplantation into the cave fish optic cup, restoring optic tissues lost during cave fish evolution. Conversely, eye growth and development are retarded following transplantation of a surface fish lens into a cave fish optic cup or lens extirpation. These results show that evolutionary changes in an inductive signal from the lens are involved in cave fish eye degeneration.

The role of the posterior ciliary body in the biosynthesis of vitreous humour

“…22 At present, the nature of the inducing molecule(s) produced by the lens is also unknown although induction of Tgfb1i4 and Ptmb4 can be achieved in a simple cell culture system where the lens is placed in juxtaposition to the retina. 22 That the lens (and presumably macromolecules secreted by the lens) play a central role in development of the posterior chamber including the retina is clearly demonstrated by experiments involving lens transplantation in blind cave fish 50 and by inhibition specifically of lens development in the mouse eye. [51][52][53] Furthermore, the blood vessels of the tunica vasculosa lentis appear to be dependent upon vascular endothelial growth factor secretion by the lens as decreased expression levels are associated with regression of this system at embryonic day 17.5 in the mouse.…”

Pleiotropy and eye degeneration in cavefish

“…This is held in contrast to the alternative viewpoint that the lens alone controls optic degeneration events, which was allegedly concluded from partial recovery of eye development after a normal surface fish lens was transplanted into a cavefish optic cup during embryogenesis (Yamamoto and Jeffery, 2000). However, no such claim is made in this or subsequent lens transplantation studies, which instead conclude that at least two processes govern eye regression, one centered in the lens and another in the optic cup (possibly the pigment epithelium; Strickler et al, 2007).…”

“…As shown by Strickler et al (2007), the lens is necessary to prevent cell death in the retina, including its photoreceptor cells, which gradually turn over and are replaced in the normal and degenerating retina. The recovery of photoreceptor cells in cavefish hosts containing a transplanted surface fish lens, observed by Yamamoto and Jeffery (2000) and Strickler et al (2007), cannot be explained by variability in eye phenotypes within the cavefish population, as also claimed by Wilkens (2010), because replaced photoreceptor cells are not seen in the opposite (degenerating) eye of the same host, which did not receive a lens transplant. In summary, the genetic and developmental data are not conflicting on this point.…”

Zebrafish dou yan mutation causes patterning defects and extensive cell death in the retina

“…Furthermore, in addition to the small eye phenotype, malfunction of these gene products also causes other defects. For example, disruption of Rab11-FIP4 and Mcm5 genes leads to extensive cell death not only in the retina but also in the brain (Ryu et al, 2005;Muto et al, 2006); the small heart mutation causes malformation of the heart and a curled body axis (Yuan and Joseph, 2004); disruption of the PITX3 gene function, which is required for lens development, likely has an indirect effect on retinal development as a consequence of disrupted interactions between lens and retina (Yamamoto and Jeffery, 2000;Shi et al, 2005); in no tectal neuron, the small eye phenotype does not appear Fig. 9.…”