An integration of old and new perspectives of mammalian meiotic sterility.
The many events of meiotic prophase can now be viewed as a series of specialized incidents that are monitored by meiotic checkpoints, some of which are similar to their mitotic counterparts, and some of which are probably unique to meiosis. This shift in perspective means that meiotic sterility in mammals must be reexamined and viewed as the result of errors subject to meiotic checkpoint controls. Like their mitotic counterparts, the meiotic checkpoints detect defects and halt normal progression until these mistakes can be repaired. Some of these checkpoints utilize mitotic checkpoint proteins, others may involve meiotic-specific proteins, or splice forms. If repair is impossible, the checkpoints then either trigger immediate apoptosis or cause an arrest of meiotic progression followed by eventual cell death. If a sufficient number of spermatocytes are involved, either alternative results in sterility. Identification of these meiotic checkpoints and delineation of the signal transduction cascades involved has only just begun. While yeast, or other model organisms, may provide clues to some of these pathways, others appears to have arisen during vertebrate evolution. The study of mammalian meiosis has entered a new era and the foundations are being laid for a growing understanding of the many problems that may contribute to sterility.
Ashley
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Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
D000818:Animals; D002453:Cell Cycle / Q000235:genetics / Q000502:physiology; D006801:Humans; D007248:Infertility, Male / Q000235:genetics; D008297:Male; D008322:Mammals / Q000235:genetics / Q000502:physiology*; D008540:Meiosis / Q000235:genetics / Q000502:physiology; D013091:Spermatogenesis / Q000235:genetics / Q000502:physiology; D013573:Synaptonemal Complex / Q000235:genetics / Q000502:physiology