The gap junction protein Innexin7 is required for cellularization of the Tribolium blastoderm

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• Maurijn van der Zee, University of Leiden
• Wednesday 01 February 2012, 13:00-14:00
• Part II Lecture Theatre, Department of Zoology.

If you have a question about this talk, please contact Matt Benton.

The gap junction protein Innexin7 is required for cellularization of the Tribolium blastoderm

In insects, development starts with a rapid series of nuclear divisions without cytokinesis. The resulting syncytium then undergoes cellularization to form a proper blastoderm. This provides an excellent model to study membrane polarization and junction formation. Blastoderm cellularization has been studied in detail in the fruit fly Drosophila melanogaster, but it is unknown to what extent these details are evolutionary conserved. Furthermore, screens in Drosophila might have missed genes that have a complementary maternal and zygotic mRNA contribution. We set out to describe cellularization in the beetle Tribolium castaneum and performed a small-scale parental RNAi (pRNAi) screen for cell adhesion proteins, knocking down maternal and zygotic gene expression simultaneously.

We found that knock-down of the gap junctional protein Innexin7 leads to a complete breakdown of cellularization. pRNAi prevents the forming cells from closing basally, resulting in detaching nuclei. Using time-lapse movies and immunohistochemistry we show that membrane invagination and recruitment of adherens junctions proceed normally and that only the final basal closure of cells is affected.

Our results unravel a novel function for Innexin7. We propose that it forms basal junctions to seal the nascent cells. pRNAi in Tribolium is a straightforward way to uncover the function of genes that are both maternally and zygotically expressed.

This talk is part of the Evolution and Development Seminar Series series.

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