Physiological cell death is crucial for matching defined cellular populations within the central nervous system. Whereas the time course of developmental cell death in the central nervous system is well analyzed, information about its precise spatial patterning is scarce. Yet, the latter one is needed to appraise its contribution to circuit formation and refinement. Here, we document that during normal cerebellar development, dying Purkinje cells were highly localized within the vermal midline and in a lobule specific, parasagittal pattern along the whole mediolateral axis. In addition, single hot spots of cell death localized to the caudal declive and ventral lobule IX within the posterolateral fissure. These hot spots of dying Purkinje cells partly overlapped with gaps within the Purkinje cell layer which supports the classification of different gaps based on histological and molecular criteria, i.e., midline gap, patchy gaps, and raphes. Areas characterized by a high incidence of Purkinje cell death and gaps colocalize with known molecular and functional boundaries within the cerebellar cortex. Physiological cell death can thus be considered to serve as an important regulator of cerebellar histogenesis.
Mesoderm formation is a hallmark of vertebrate gastrulation and, at the same time, one of the prime examples for epithelio-mesenchymal transformation. Recent advances in experimental embryology and molecular biology have clarified the role of growth factors and genes in this process; however, its microscopic anatomy in higher vertebrates is still far from clear. Therefore, the present study describes the morphology of mesoderm formation in the rabbit embryo, a species which may be representative for both the avian and the mammalian embryo in this respect. Serial semithin sections were correlated with topographical landmarks in surface views of embryonic discs at 6.4, 6.5, and 6.6 days post conceptionem, and selected semithin sections were reembedded for ultrastructural analysis. Mesoderm cells are shown to be generated by ingression of bottle-shaped epiblast cells in the area of the posterior node and the primitive streak. Here, basal endocytotic pits and absence or discontinuity of the basal lamina are taken as suggestive evidence for specific removal of extracellular matrix material. Within the bottle-shaped cells most organelles are concentrated in a narrow apical neck which will subsequently constitute the ‘trailing end’ of the ingressing mesoderm cells. These features support the assumption that most principles of epithelio-mesenchymal transformation seen during primary mesenchyme formation in the sea urchin also apply to mesoderm formation in vertebrates. However, transient tripartite zonula adherens-type junctions are formed apically between ingressing mesoderm cells and the neighboring epiblast cells. They are interpreted here as being responsible for maintaining supracellular integrity of the embryonic disc during the shedding of mesoderm cells in the amniote embryo.
Degenerating prespermatogonial germ cells in the testis of the immature golden hamster [aged 14 days post conceptionem (dpc) to 13 days post partum [dpp)] were studied with regard to their morphology and temporal incidence. Judged by their ultrastructural features, these cells clearly take the form of apoptosis and finally are subjected to phagocytosis by neighboring Sertoli cells; only a few germ cells of a presumably incipient, partly variant degenerative morphology cannot, at present, be assigned to the apoptotic mode of cellular death. Degenerating prespermatogonia occur between the 14th dpc and 3rd dpp and again, after an interval in which no such cells are found, from the 9th dpp onwards. This pattern reveals a striking parallelism to the phases of proliferation of these cells, viz., the appearance of M- and T2-prespermatogonia. Both this obvious temporal association of proliferation and degeneration and the classification of prespermatogonial death as apoptosis suggest some developmental significance of the degenerative phenomena investigated.
The sequence of events and a possible reason for germ cell death during oogenesis in the prenatal ovary were studied in rat and mouse embryos. ED 14-22 rat and ED 14-16 mouse embryos were studied using semithin sections for light microscopy and serial ultrathin sections for electron microscopy. In addition, the rat material was 3H-thymidine labelled for historadioautography and cytospin preparations of freshly obtained gonads were immunohistochemically analysed. During the transition from the proliferating oogonial stage to the meiotic prophase about 16% of the postmitotic oocytes do not pass the initial meiotic checkpoint on ED 18/19 in the rat (ED 15/16 in the mouse). These germ cells first show structural signs of mitosis; the diploid number of 'super-condensed' chromosomes are globally formed and are concentrated in the center of the cell. Although the germ cells show all morphological signs of living cells they never have mitotic spindles; the micro-tubulus-organisation-centres (MTOCs) are found peripherally and become concentrated, forming a single centrosomal body (acentriolar MTOC) as detected by immunohistochemistry for the centrosomal protein MPM2 and gamma-tubulin. EM studies show 25 nm tubule-like profiles within the MTOC bodies. The centrioles frequently lie separate from the MTOC material or are not present at all; the germ cells are apparently arrested in a prophase- or metaphase-like stage when they have reached the postmitotic G2/preleptotenal transition and are unable to enter meiosis. Forty-eight to 72 h after the first mitotically arrested germ cells are found, degeneration is seen in these germ cells. This second event, the germ cell death proper, shows neither criteria of apoptosis (cell shrinkage, marginal condensation of chromatin, DNA fragmentation) nor signs of necrosis (cell swelling, pycnosis, inflammation). Both arrested pro- and metaphase-like stages are found with signs of cell death and phagocytosis. The morphological signs of phagocytosis are found in neighbouring pregranulosa cells. The final heterocytotic bodies contain the remnants of the centrosomal (MTOC) material and DAPI-positive DNA material. The pregranulosa cells are mitotically silent during the phase when mitotic arrest and germ cell degeneration is found. The results suggest the presence of a hypothetical 'anti-spindle' factor, which under normal conditions is necessary for induction of meiotic prophase. The structural events of 'arrested mitosis' is reminiscent of those induced by the antimitotic, tubule-degrading drug colcemid. This type of arrest may inhibit meiosis of more than 33% prenatal germ cells and induce their cell death.
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