Cytoplasmic vinculin in the mouse oocyte

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ULTRASTRUCTURE OF GONADS IN SEX-REVERSED MICE CARRYING THE TI6H/XSxr MUTATION. S.K. Grund, A. McLaren 2 and L.J. Pelliniemi. Laboratory of Electron Microscopy,_. University of Turku, SF-20520 Turku. Finland and 2MRC Mammalian Development Unit, Wolfson House, University College London, London NWI 2HE, United Kingdom. The variations in the histological and ultrastructural organization of abnormal gonads in two adult TI6H/XSxr mice were studied by light and electron microscopy and compared with testis and ovary of normal mice. In the first Sxr mouse the gonad contained fetal type cords and some follicle-like structures. No germ cells were present. Instead of a basal lamina there was a surface coat which covered the cords and the follicles. Its thickness varied in comparison with the lamina densa and it was composed of dense fine granular material. Several negatively stained collagen fibers were seen in the interstitium. The interstitial cells contained various vesicles with lipid-like contents. The second mouse was a true hermaphrodite with an ovary on one side and a testis on the other. The overy contained different types of follicles with oogonia. The follicles were outlined by a surface coat which was for the most part organized like a normal basal lamina. The interstitial cells contained many vesicles with irregular shape and lipid-like contents with a halo or negatively stained needles of crystal-like material. In the testis the seminiferous tubules resembled those in the Sertoli cell-only syndrome with the specific Sertoli cell junctions. The Leydig cells were hyperplastic. The surface c o a t of the tubuli consisted of flocculent basement membrane-like material. The present analysis showed structural differences which indicate that the expression of the mutation varies within different individuals. The gonads develop to different developmental stages according to either sex, and the testis often remains sterile. Steroid metabolism is apparently disturbed in both sexes. (Supported by Sigrid Jus@lius Foundation)

Role of vitamin A in differentiation of spermatogonia. A.M.M. van Pelt and D.G. de Rooij Department of Cell Biology, State University Utrecht Vitamin A-deficiency causes deterioration of spermatogenesis. In the rat the seminiferous tubules were found only to contain Sertoli cells, undifferentiated spermatogonia and a few spermatocytes. Retinol or retinoie acid was given to study the effect on differentiation and proliferation of undifferentiated spermatogonia. Within 30 hours after administration of retinol, spermatogonia did undergo differentiation and the first division took place. The seminiferous epithelium also became synchronized. Although it is generally thought that retinoic acid is not able to reinitiate spermatogenesis in vitamin Adeficient rats, we found a high proliferative activity of spermatogonia already 24 hours after administration. Also differentiation of spermatogonia was found. In conclusion, vitamin A-deficiency arrests spermatogenesis at the level of undifferentiated spermatogonia and both retinol and retinoic acid induce differentiation of undifferentiated spermatogonia in vitamin Adeficient rats.

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