MarvelD3 regulates the c-Jun N-terminal kinase pathway during eye development in Xenopus.

Barbara Vacca,Shin-Ichi Ohnuma,Noriaki Sasai,Elena Sanchez-Heras,Emily Steed,Karl Matter,Roberto Mayor,Maria S Balda

doi:10.1242/bio.018945

Abstract

ABSTRACTOcular morphogenesis requires several signalling pathways controlling the expression of transcription factors and cell-cycle regulators. However, despite a well-known mechanism, the dialogue between those signals and factors remains to be unveiled. Here, we identify a requirement for MarvelD3, a tight junction transmembrane protein, in eye morphogenesis in Xenopus. MarvelD3 depletion led to an abnormally pigmented eye or even an eye-less phenotype, which was rescued by ectopic MarvelD3 expression. Altering MarvelD3 expression led to deregulated expression of cell-cycle regulators and transcription factors required for eye development. The eye phenotype was rescued by increased c-Jun terminal Kinase activation. Thus, MarvelD3 links tight junctions and modulation of the JNK pathway to eye morphogenesis.

Highlights

Eye morphogenesis is an evolutionarily conserved feature of most organisms to ensure an efficient communication with the environment (Gilbert, 2000)
Structure and expression of MarvelD3 in the eye field Xenopus MD3 (GenBank accession number, BC 068841) encodes a 420 amino acid (AA) protein with an amino-terminal intracellular domain followed by four transmembrane domains, two extracellular loops and an 18 AA cytoplasmic carboxy-terminal domain (Fig. 1A)
We first analysed the spatial distribution of MD3 expression by whole-mount in situ hybridization (WISH) and found that the MD3 transcript is broadly expressed in the animal pole before gastrulation (Fig. S1A,B)

Summary

Introduction

Eye morphogenesis is an evolutionarily conserved feature of most organisms to ensure an efficient communication with the environment (Gilbert, 2000). Eye development is a complex multi-step process, which involves cell proliferation, migration, cell-fate determination, survival and differentiation (Fuhrmann, 2008; Gilbert, 2000; Harada et al, 2007). EFTFs specify a single eye-field in the most anterior region of the neural plate. In this region, inhibition of cell-cycle activators occurs to favour EFTF expression, while duration of the expression of the transcription factors is established by cell-cycle-independent factors (Bilitou and Ohnuma, 2010; Cavodeassi et al, 2005; Gilbert, 2000; Harada et al, 2007; Zuber, 2010).

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Conclusion