Abstract

SoxC genes are involved in many developmental processes such as cardiac, lymphoid, and bone development. The SoxC gene family is represented by Sox4, Sox11, and Sox12. Loss of either Sox4 or Sox11 function is lethal during mouse embryogenesis. Here, we demonstrate that sox4 and sox11 are strongly expressed in the developing eye, heart as well as brain in Xenopus laevis. Morpholino oligonucleotide mediated knock-down approaches in anterior neural tissue revealed that interference with either Sox4 or Sox11 function affects eye development. A detailed analysis demonstrated strong effects on eye size and retinal lamination. Neural induction was unaffected upon Sox4 or Sox11 MO injection and early eye field differentiation and cell proliferation were only mildly affected. Depletion of both genes, however, led independently to a significant increase in cell apoptosis in the eye. In summary, Sox4 and Sox11 are required for Xenopus visual system development.

Highlights

  • In Xenopus, eye development starts with the induction of the eye field in the anterior neural plate at the end of gastrulation

  • As we did not detect any significant expression of sox12 in the eye, we subsequently focused on sox4 and sox11 during early Xenopus embryogenesis

  • We showed that (I) the high mobility group (HMG) box transcription factors sox4 and sox11 are expressed in the developing Xenopus eye, (II) depletion of either Sox4 or Sox11 lead to severe malformations of the eye characterized by a decrease in size and disturbed retinal lamination, (III) loss of Sox4 or Sox11 does not affect neural induction, IV) Sox4 and Sox11 have no influence on the primary fate of most retinal cell types and (V) Sox4 or Sox11 downregulation results in increased cellular apoptosis in the eye

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Summary

Introduction

In Xenopus, eye development starts with the induction of the eye field in the anterior neural plate at the end of gastrulation. The eye anlage is characterized by the expression of eye specific marker genes such as rax, pax, and six. Loss of any of these genes leads to strong defects during early eye development [1]. The single eye field splits into two eye anlagen located on either side of the embryo, a process supported by the underlying prechordal mesoderm [2]. At the end of neurulation, two optic vesicles evaginate from the neural tube at the level of the prospective diencephalon towards the overlaying ectoderm. The distal half of the eye vesicles invaginates into the embryo thereby forming a bilayered optic cup

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