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Involvement of Notch and Delta genes in spider segmentation

Abstract

It is currently debated whether segmentation in different animal phyla has a common origin and shares a common genetic mechanism1,2. The apparent use of different genetic networks in arthropods and vertebrates has become a strong argument against a common origin of segmentation. Our knowledge of arthropod segmentation is based mainly on the insect Drosophila, in which a hierarchical cascade of transcription factors controls segmentation3,4. The function of some of these genes seems to be conserved among arthropods, including spiders5,6, but not vertebrates1,6,7,8. The Notch pathway has a key role in vertebrate segmentation (somitogenesis) but is not involved in Drosophila body segmentation1,7,9. Here we show that Notch and Delta genes are involved in segmentation of another arthropod, the spider Cupiennius salei. Expression patterns of Notch and Delta, coupled with RNA interference experiments, identify many similarities between spider segmentation and vertebrate somitogenesis. Our data indicate that formation of the segments in arthropods and vertebrates may have shared a genetic programme in a common ancestor and that parts of this programme have been lost in particular descendant lineages.

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Figure 1: Expression of Notch, Delta-1 and Delta-2 genes during segmentation in the spider C. salei.
Figure 2: Segmentation defects in Notch and Delta RNAi embryos.
Figure 3: The expression of the hairy gene is disturbed in embryos deficient for Notch or Delta.

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Acknowledgements

We thank D, Tautz for support and discussion; S. Roth for comments on the manuscript; T. Klein for discussion; A. Pozhitkov for help with the statistic analysis; and R. Janßen for care of the spider culture. This work was partially supported by the Deutsche Forschungsgemeinschaft.

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Correspondence to Wim G. M. Damen.

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Stollewerk, A., Schoppmeier, M. & Damen, W. Involvement of Notch and Delta genes in spider segmentation. Nature 423, 863–865 (2003). https://doi.org/10.1038/nature01682

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