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An unpaired mouse centromere passes consistently through male meiosis and does not significantly compromise spermatogenesis
Authors:P.?Joseph?Mee  author-information"  >  author-information__contact u-icon-before"  >  mailto:P.J.Mee@ed.ac.uk"   title="  P.J.Mee@ed.ac.uk"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Ming?Hong?Shen,Austin?G.?Smith,William?R.?A.?Brown
Affiliation:(1) Institute for Stem Cell Research, The University of Edinburgh, King"rsquo"s Buildings, West Mains Road, Edinburgh , EH9 3JQ, UK;(2) MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK;(3) Institute of Genetics, Queen"rsquo"s Medical Centre, Nottingham University, Nottingham, NG7 2UH, UK
Abstract:ST1 is an artificial mini-chromosome approximately 4.5 Mb in size containing mouse minor and major satellite DNA, human alphoid DNA and sequences derived from interval 5 of the human Y chromosome. Here we have measured the mitotic and meiotic transmission of ST1 and have used the mini-chromosome to define the ability of mice to monitor the presence of unpaired centromeres during meiosis. ST1 is mitotically stable, remaining intact and autonomous in mice for many generations. Female mice efficiently transmit ST1 to their offspring at a frequency approaching 50%. Male mice also reliably transmit the mini-chromosome, though to only 20% of their offspring. Presence of ST1 in males is not associated with any compromise in the output of the seminiferous epithelium nor with histological or immunocytochemical evidence of increased apoptosis, outcomes predicted for a synapsis checkpoint. These data indicate that the presence of an unpaired centromere is not sufficient to arrest male meiosis, implying that univalents are normally eliminated by a mechanism other than a tension-sensitive spindle checkpoint.P.J. Mee and M.M. Shen contributed equally to this article
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