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Lectin-binding patterns in the embryonic human paraxial mesenchyme

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Abstract

The paraxial mesenchyme in seven human embryos aged between Carnegie stages 12 and 17 was studied by lectin histochemistry with the lectins AIA, Con A, GSA II, LFA, LTA, PNA, RCA I, SBA, SNA, WGA. The paraxial mesenchyme was found to be segmented into sclerotomes by intersegmental vessels and from late stage 12 by intrasclerotomal clefts dividing each sclerotome into a cranial and caudal half. The lectins Con A, GSA II, LFA, LTA, SBA and SNA did not react at all in the paraxial mesenchyme. Staining for AIA, PNA, RCA I and WGA was found in the developing sclerotomes. However, no differences in the staining pattern between the two sclerotomal halves could be seen. It was striking that in contrast to the chick embryo no differences in binding for PNA between the cranial and caudal sclerotomal parts was observed. These findings reveal that PNA-binding sites do not play the same functional role in segmented axonal outgrowth and neural crest immigration into cranial sclerotomal halves in the human embryo, as found in chick embryonic development. Beginning with the stage 16-embryo, the already condensed caudal sclerotomal halves express Con A-, RCA- and PNA-binding sites. The staining for PNA in particular marked the differentiation of chondrogenous structures developing in this half. From the late stage 12 or stage 13, the walls of intersegmental and other vessels showed binding sites for AIA, PNA, RCA I, SNA and WGA.

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  1. W. Götz

    Present address: Zentrum Anatomie, Abteilung Histologie, Kreuzbergring 36, D-37075, Göttingen, Germany

Authors and Affiliations

  1. Zentrum Anatomie, Abteilung Histologie, Kreuzbergring 36, D-37075, Göttingen, Germany

    D. Frisch & R. Herken

  2. Zentrum Frauenheilkunde, Abteilung Gynäkologie und Geburtshilfe, Klinikum der Universität, Robert-Koch-Str. 40, D-37075, Göttingen, Germany

    R. Osmers

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Götz, W., Frisch, D., Osmers, R. et al. Lectin-binding patterns in the embryonic human paraxial mesenchyme. Anat Embryol 188, 579–585 (1993). https://doi.org/10.1007/BF00187013

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