• Genetical studies on the skeleton of the mouse - XII. the development of undulated

    • Fulltext

       

        Click here to view fulltext PDF


      Permanent link:
      https://www.ias.ac.in/article/fulltext/jgen/052/02/0441-0454

    • Abstract

       

      The anomalies produced by the gene for undulated in the mouse have been traced back to the 11-day stage of embryonic development. On that day, it can be seen that the condensations of mesenchyme cranial to the sclerotomic fissures are smaller than normal. Later on, these condensations continue to lag behind those of normal embryos and are not clearly demarcated from those caudal to the sclerotomic fissures. On the basis of sensenig’s view that, in normal development, the condensations cranial to the fissures fuse with the primitive centra in front of them and thus help to form the vertebrae, and that the fissures themselves correspond in position to the posterior ends of the vertebrae in the adult, the anomalies produced by the undulated gene can be interpreted as follows. The condensations cranial to the sclerotomic fissures, instead of being incorporated with the vertebral material in front of them, are (at least in part) retained by the condensations behind them which form the intervertebral disks. For this reason, the reduction of the vertebrae is accompanied by an increase in size of the intervertebral disks. The material absent from the undulated vertebrae is, in normal development, destined to help in the formation of the centrum, the neural arches, the spinous processes and the transverse processes and ribs; all these structures are reduced to a varying extent in the undulated mouse; the involvement of the ribs is but slight, but can be detected in a tendency of fusions between adjacent sternebrae. Following chondrification, the formation of hyaline matrix is slow at first in undulated embryos, but the cartilage ultimately becomes perfectly normal histologically.

      The work reported in this paper has been supported by grants from the Medical Research Council and from the Rockefeller Foundation, which are gratefully acknowledged. For assistance in various directions I am indebted to my colleague, Dr Gillian M. Truslove. My special thanks are due to Mr A. J. E. Munday (Galton Laboratory, University College) for the microphotographs which illustrate this paper.

    • Author Affiliations

       

      Hans Grüneberg1

      1. University College, London
    • Dates

       
  • Journal of Genetics | News

    • Editorial Note on Continuous Article Publication

      Posted on July 25, 2019

      Click here for Editorial Note on CAP Mode

© 2021-2022 Indian Academy of Sciences, Bengaluru.