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Coordinated Segregation of Sister Chromatids 2419 Staining (To Visualize the SC) and FISH (To Identify the X Chromosome and the Telomeres)

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Coordinated Segregation of Sister Chromatids 2419 Staining (To Visualize the SC) and FISH (To Identify the X Chromosome and the Telomeres) RESEARCH ARTICLE 2417 Coordinating the segregation of sister chromatids during the first meiotic division: evidence for sexual dimorphism Craig A. Hodges, Renée LeMaire-Adkins and Patricia A. Hunt* Department of Genetics and Center for Human Genetics, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio 44106-4955, USA *Author for correspondence (e-mail: [email protected]) Accepted 5 April 2001 Journal of Cell Science 114, 2417-2426 © The Company of Biologists Ltd SUMMARY Errors during the first meiotic division are common in our chromosome at prophase to determine if this factor species, but virtually all occur during female meiosis. The influenced the propensity of the chromosome for self- reason why oogenesis is more error prone than synapsis. We were unable to directly correlate synaptic spermatogenesis remains unknown. Normal segregation of differences with subsequent segregation behavior. homologous chromosomes at the first meiotic division (MI) However, unexpectedly, we uncovered a sexual dimorphism requires coordinated behavior of the sister chromatids that may partially explain sex-specific differences in the of each homolog. Failure of sister kinetochores to act fidelity of meiotic chromosome segregation. Specifically, in cooperatively at MI, or precocious sister chromatid the male remnants of the synaptonemal complex remain segregation (PSCS), has been postulated to be a major associated with the centromeres until anaphase of the contributor to human nondisjunction. To investigate the second meiotic division (MII), whereas in the female, all factors that influence PSCS we utilized the XO mouse, since traces of synaptonemal complex (SC) protein components the chromatids of the single X chromosome frequently are lost from the chromosomes before the onset of the first segregate at MI, and the propensity for PSCS is influenced meiotic division. This finding suggests a sex-specific by genetic background. Our studies demonstrate that the difference in the components used to correctly segregate strain-specific differences in PSCS are due to the actions chromosomes during meiosis, and may provide a reason for of an autosomal trans-acting factor or factors. Since the high error frequency during female meiosis. components of the synaptonemal complex are thought to play a role in centromere cohesion and kinetochore Key words: Meiosis, Nondisjunction, Sister chromatid cohesion, orientation, we evaluated the behavior of the X Synaptonemal complex, XO mouse INTRODUCTION form attachments to the same rather than opposing spindle poles. The second meiotic division (MII) is similar to a mitotic Proper chromosome segregation during mitotic cell division cell division, involving the segregation of sister chromatids. requires at least two chromosome-associated protein However, because MI and MII occur without an intervening S complexes. At the centromere, functional kinetochores must be phase, successful chromosome segregation at MII requires formed on individual sister chromatids to facilitate the a mechanism whereby cohesion is released along the attachment of the chromatids to opposite spindle poles. In chromosome arms at anaphase I but maintained between sister addition, cohesion must be established between the centromeres until anaphase II. centromeres and along the arms of the sister chromatids and It is commonly assumed that the specialized meiotic maintained until anaphase to prevent their precocious cohesion requirements depend upon the unique events of separation. meiotic prophase, e.g. synapsis and recombination. The role of By comparison with mitotic cell division, the segregation recombination in the disjunction of homologous chromosomes behavior of chromosomes during meiotic cell division is at MI is well established (e.g. Carpenter, 1994; reviewed in complex, necessitating modification of both the kinetochore Hassold et al., 2000; Hawley, 1988; Koehler et al., 1996; Lamb and cohesion complexes. Our understanding of these meiotic et al., 1996). The role of synapsis remains less well modifications remains rudimentary. The first meiotic division characterized, but the inferential evidence is compelling: both (MI) involves the segregation of homologs rather than defects in homolog synapsis and the absence of a homologous sister chromatids (Fig. 1A). Thus, successful chromosome partner are associated with an increased frequency of segregation at MI requires specialized cohesion mechanisms premature separation of sister chromatids at MI in a variety of that provide physical connections between homologs (rather species (reviewed in Moore and Orr-Weaver, 1998; Wolf, than sister chromatids), and impose constraint on the 1993). Moreover studies in corn, yeast and mammals provide centromeres of sister chromatids so that their kinetochores evidence for the involvement of components of the 2418 JOURNAL OF CELL SCIENCE 114 (13) synaptonemal complex (SC), the proteinaceous structure influence the behavior of sister kinetochores at the first meiotic involved in homolog synapsis, in MI segregation. In maize, the division. We report here the results of detailed meiotic studies analysis of a variety of mutants and structural rearrangements that exclude X-chromosome specific differences and suggest provides compelling evidence for a relationship between the that segregation is influenced by the action of an autosomal gene SC and sister chromatid cohesion and suggests a direct or genes. We hypothesized that this trans-acting factor(s) would correlation between synaptic failure in the centromeric region influence the synaptic behavior of the X chromosome, and that and precocious sister chromatid segregation (PSCS) (reviewed failure to undergo self-synapsis involving the centromere of the in Maguire, 1995). In yeast, mutations in the meiosis-specific chromosome would result in the premature separation of X component of the cohesion complex, Rec8, show an increase chromatids at MI. Our observations did not fit this expectation, in PSCS at MI (Watanabe and Nurse, 1999). Finally, in but our studies provide new insight to the complexity of the mammals, two pieces of data implicate the involvement of SC synaptic process and suggest that inferences about subsequent proteins in meiotic sister chromatid cohesion. First, remnants meiotic events based on pachytene analysis may be misleading. of the lateral element persist at the centromere until anaphase More importantly, however, our efforts to correlate segregation II, as revealed by immunolocalization studies using antibodies behavior with the retention of synaptonemal complex proteins to two protein components, SCP3 and SCP2 (Dobson et al., revealed a surprising difference in centromere-associated 1994; Offenberg et al., 1998). Second, studies of the recently proteins between oogenesis and spermatogenesis. Differences identified cohesin components, SMC1 and SMC3, provide in the protein components of the meiotic chromosome cohesion evidence of interactions with SCP3 and SCP2 (Eijpe et al., complex may influence the fidelity of meiotic chromosome 2000). Thus, there is considerable indirect evidence for the segregation, thus this intriguing sexual dimorphism may involvement of SC proteins in the unique behavior of sister provide a partial explanation for the high chromosome error rate kinetochores at MI, in the maintenance of connections between during human female meiosis. homologs, and in the maintenance of cohesion between sister centromeres until anaphase II. However, the mechanistic details remain unclear. MATERIALS AND METHODS These processes are not only of academic interest to students of meiotic cell division but rather have a dramatic impact on Production of XO female mice human life: the meiotic divisions in the human female are XO female mice and XX sibling controls were produced on two extraordinarily error prone. Estimates of the error frequency different inbred strain backgrounds using previously described mating range from one in twenty to one in three human oocytes, schemes involving males prone to meiotic sex chromosome depending upon the age of the woman (reviewed in Hassold et nondisjunction. Specifically, C57BL/6 females were mated to al., 1996). Despite intensive investigation, the reason for the C57BL/6 males carrying the Y* chromosome (Eicher et al., 1982) and high error rate in our species remains unknown. It is clear, C3H females were mated to C3H males carrying the X-linked Paf however, that the majority of errors occur during the first mutation (Lane and Davisson, 1990). Both crosses produce meiotic division, that the propensity for segregation errors is approximately 20% XO females. chromosome-specific, and that the fidelity of chromosome Intercrosses of the two inbred strains were made to generate F1 hybrid females that differed only in the origin of their X chromosome: segregation is influenced by the number and placement of C57BL/6 females were mated to C3H males carrying the Paf mutation recombination events along the chromosome arms (reviewed to produce XO females with a C57BL/6 X chromosome and C3H in Hassold et al., 2000). It has been postulated that PSCS is a females were mated to C57BL/6 males carrying the Y* mutation to major mechanism responsible for the age-related increase in produce XO females with a C3H X chromosome. segregation errors in our species (Angell, 1997; Angell et al., 1994; Wolstenholme and Angell, 2000), and the small amount Oocyte collection, culture and fixation of data available from direct studies of human oocytes are To assess the
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