title: Contractile apparatus of the normal and abortive cytokinetic cells during mouse male meiosis.
abstract: Mouse male meiotic cytokinesis was studied using immunofluorescent probes against various elements of cytokinetic apparatus and electron microscopy. In normal mice, some spermatocytes fail to undergo cytokinesis after meiotic I or II nuclear divisions, forming syncytial secondary spermatocytes and spermatids. Abnormal cytokinetic cells develop sparse and dispersed midzone spindles during the early stage. However, during late stages, single and compact midzone spindles are formed as in normal cells, but localize asymmetrically and attach to the cortex. Myosin and f-actin were observed in the midzone spindle and midbody regions of normally cleaving cells as well as in those cells that failed to develop a cytokinetic furrow, implying that cytokinetic failure is unlikely to be due to defect in myosin or actin assembly. Depolymerization of microtubules by nocodazole resulted in the loss of the midbody-associated f-actin and myosin. These observations suggest that actin-myosin localization in the midbody could be a microtubule-dependent process that may not play a direct role in cytokinetic furrowing. Anti-centrin antibody labels the putative centrioles while anti-(gamma)-tubulin antibody labels the minus-ends of the midzone spindles of late-stage normal and abnormal cytokinetic cells, suggesting that the centrosome and midzone spindle nucleation in abnormal cytokinetic cells is not different from those of normally cleaving cells. Possible use of mouse male meiotic cells as a model system to study cytokinesis has been discussed.
authors.affiliation: Departments of Obstetrics & Gynecology and Cell & Developmental Biology, Oregon Regional Primate Research Center, Oregon Health Sciences University, Beaverton, OR 97006, USA.
authors.forename: G
authors.initials: G
authors.lastname: Manandhar
authors.forename: R D
authors.initials: RD
authors.lastname: Moreno
authors.forename: C
authors.initials: C
authors.lastname: Simerly
authors.forename: K
authors.initials: K
authors.lastname: Toshimori
authors.forename: G
authors.initials: G
authors.lastname: Schatten
mesh_terms: D000199:Actins / Q000032:analysis / Q000378:metabolism; D000818:Animals; D000918:Antibody Specificity; D000970:Antineoplastic Agents / Q000494:pharmacology; D019556:COS Cells; D002455:Cell Division / Q000502:physiology; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism; D008297:Male; D008540:Meiosis / Q000502:physiology*; D051379:Mice; D008813:Mice, Inbred ICR; D018613:Microscopy, Confocal; D008854:Microscopy, Electron; D018995:Myosin Heavy Chains / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D009218:Myosins / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D015739:Nocodazole / Q000494:pharmacology; D012708:Sertoli Cells / Q000166:cytology; D013090:Spermatocytes / Q000737:chemistry / Q000378:metabolism* / Q000648:ultrastructure; D008941:Spindle Apparatus / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D015662:Trimethoprim, Sulfamethoxazole Drug Combination / Q000378:metabolism; D014404:Tubulin / Q000378:metabolism
chemical_list: D000199:Actins; D000970:Antineoplastic Agents; D014404:Tubulin; D015662:Trimethoprim, Sulfamethoxazole Drug Combination; D018995:Myosin Heavy Chains; D009218:Myosins; D015739:Nocodazole