Reductional Segregation Research Articles

Meiotic Behavior of Achiasmate Sex Chromosomes in the African Pygmy Mouse Mus mattheyi Offers New Insights into the Evolution of Sex Chromosome Pairing and Segregation in Mammals.

X and Y chromosomes in mammals are different in size and gene content due to an evolutionary process of differentiation and degeneration of the Y chromosome. Nevertheless, these chromosomes usually share a small region of homology, the pseudoautosomal region (PAR), which allows them to perform a partial synapsis and undergo reciprocal recombination during meiosis, which ensures their segregation. However, in some mammalian species the PAR has been lost, which challenges the pairing and segregation of sex chromosomes in meiosis. The African pygmy mouse Mus mattheyi shows completely differentiated sex chromosomes, representing an uncommon evolutionary situation among mouse species. We have performed a detailed analysis of the location of proteins involved in synaptonemal complex assembly (SYCP3), recombination (RPA, RAD51 and MLH1) and sex chromosome inactivation (γH2AX) in this species. We found that neither synapsis nor chiasmata are found between sex chromosomes and their pairing is notably delayed compared to autosomes. Interestingly, the Y chromosome only incorporates RPA and RAD51 in a reduced fraction of spermatocytes, indicating a particular DNA repair dynamic on this chromosome. The analysis of segregation revealed that sex chromosomes are associated until metaphase-I just by a chromatin contact. Unexpectedly, both sex chromosomes remain labelled with γH2AX during first meiotic division. This chromatin contact is probably enough to maintain sex chromosome association up to anaphase-I and, therefore, could be relevant to ensure their reductional segregation. The results presented suggest that the regulation of both DNA repair and epigenetic modifications in the sex chromosomes can have a great impact on the divergence of sex chromosomes and their proper transmission, widening our understanding on the relationship between meiosis and the evolution of sex chromosomes in mammals.

Sex chromosome quadrivalents in oocytes of the African pygmy mouse Mus minutoides that harbors non-conventional sex chromosomes

Eutherian mammals have an extremely conserved sex-determining system controlled by highly differentiated sex chromosomes. Females are XX and males XY, and any deviation generally leads to infertility, mainly due to meiosis disruption. The African pygmy mouse (Mus minutoides) presents an atypical sex determination system with three sex chromosomes: the classical X and Y chromosomes and a feminizing X chromosome variant, called X*. Thus, three types of females coexist (XX, XX*, and X*Y) that all show normal fertility. Moreover, the three chromosomes (X and Y on one side and X* on the other side) are fused to different autosomes, which results in the inclusion of the sex chromosomes in a quadrivalent in XX* and X*Y females at meiotic prophase. Here, we characterized the configurations adopted by these sex chromosome quadrivalents during meiotic prophase. The XX* quadrivalent displayed a closed structure in which all homologous chromosome arms were fully synapsed and with sufficient crossovers to ensure the reductional segregation of all chromosomes at the first meiotic division. Conversely, the X*Y quadrivalents adopted either a closed configuration with non-homologous synapsis of the X* and Y chromosomes or an open chain configuration in which X* and Y remained asynapsed and possibly transcriptionally silenced. Moreover, the number of crossovers was insufficient to ensure chromosome segregation in a significant fraction of nuclei. Together, these findings raise questions about the mechanisms allowing X*Y females to have a level of fertility as good as that of XX and XX* females, if not higher.

Enablers of sustainable municipal solid waste management system in India

The present study moves beyond the traditional focus of municipal solid waste management (MSWM) of collection and disposal to sustainable MSWM that takes a systems view and addresses issues related to waste prevention, waste reduction, and waste segregation. The empirical study was conducted in large cities in North India that have a very high rate of solid waste generation. The study was conducted in two stages - in the first stage, an empirical study with two major stakeholders, the elected and government officials was conducted. In the second stage, interpretive structural modelling (ISM) is applied to evolve a hierarchy-based relationship among the enablers of sustainable MSWM. According to the results of empirical study, there are disagreements on several issues considered as strategic to implement a sustainable municipal solid waste management. Thus, there is a need to bring all the stakeholders agree on common policy issues of sustainable MSWM. Further, the ISM model shows that there exists a group of variables having a high driving power and low dependence requiring maximum attention and are of strategic importance.

An interplay between Shugoshin and Spo13 for centromeric cohesin protection and sister kinetochore mono-orientation during meiosis I in Saccharomyces cerevisiae.

Meiosis is a specialized cell division process by which haploid gametes are produced from a diploid mother cell. Reductional chromosome segregation during meiosis I (MI) is achieved by two unique and conserved events: centromeric cohesin protection (CCP) and sister kinetochore mono-orientation (SKM). In Saccharomyces cerevisiae, a meiosis-specific protein Spo13 plays a role in both these centromere-specific events. Despite genome-wide association of Spo13, we failed to detect its function in global processes such as cohesin loading, cohesion establishment and homologs pairing. While Shugoshin (Sgo1) and protein phosphatase 2A (PP2ARts1) play a central role in CCP, it is not fully understood whether Spo13 functions in the process through a Sgo1- PP2ARts1-dependent or -independent mechanism. To delineate this and to find the relative contribution of each of these proteins in CCP and SKM, we meticulously observed the sister chromatid segregation pattern in the wild type, sgo1Δ, rts1Δ and spo13Δ single mutants and in their respective double mutants. We found that Spo13 protects centromeric cohesin through a Sgo1- PP2ARts1-independent mechanism. To our surprise, we observed a hitherto unknown role of Sgo1 in SKM. Further investigation revealed that Sgo1-mediated recruitment of aurora kinase Ipl1 to the centromere facilitates monopolin loading at the kinetochore during MI. Hence, this study uncovers the role of Sgo1 in SKM and demonstartes how the regulators (Sgo1, PP2ARts1, Spo13) work in a coordinated manner to achieve faithful chromosome segregation during meiosis, the failure of which leads to aneuploidy and birth defects.

Meiosis-like Functions in Oncogenesis: A New View of Cancer.

Cancer cells have many abnormal characteristics enabling tumors to grow, spread, and avoid immunologic and therapeutic destruction. Central to this is the innate ability of populations of cancer cells to rapidly evolve. One feature of many cancers is that they activate genes that are normally associated with distinct developmental states, including germ cell-specific genes. This has historically led to the proposal that tumors take on embryonal characteristics, the so called embryonal theory of cancer. However, one group of germline genes, not directly associated with embryonic somatic tissue genesis, is the one that encodes the specific factors to drive the unique reductional chromosome segregation of meiosis I, which also results in chromosomal exchanges. Here, we propose that meiosis I-specific modulators of reductional segregation can contribute to oncogenic chromosome dynamics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, as meiotic factors are not a feature of most embryonic tissue development. We postulate that some meiotic chromosome-regulatory functions contribute to a soma-to-germline model for cancer, in which activation of germline (including meiosis) functions drive oncogenesis, and we extend this to propose that meiotic factors could be powerful sources of targets for therapeutics and biomonitoring in oncology. Cancer Res; 77(21); 5712-6. ©2017 AACR.

Untimely expression of gametogenic genes in vegetative cells causes uniparental disomy.

Uniparental disomy (UPD), in which an individual contains a pair of homologous chromosomes originating from only one parent, is a frequent phenomenon that is linked to congenital disorders and various cancers. UPD is thought to result mostly from pre- or post-zygotic chromosome missegregation. However, the factors that drive UPD remain unknown. Here we use the fission yeast Schizosaccharomyces pombe as a model to investigate UPD, and show that defects in the RNA interference (RNAi) machinery or in the YTH domain-containing RNA elimination factor Mmi1 cause high levels of UPD in vegetative diploid cells. This phenomenon is not due to defects in heterochromatin assembly at centromeres. Notably, in cells lacking RNAi components or Mmi1, UPD is associated with the untimely expression of gametogenic genes. Deletion of the upregulated gene encoding the meiotic cohesin Rec8 or the cyclin Crs1 suppresses UPD in both RNAi and mmi1 mutants. Moreover, overexpression of Rec8 is sufficient to trigger UPD in wild-type cells. Rec8 expressed in vegetative cells localizes to chromosomal arms and to the centromere core, where it is required for localization of the cohesin subunit Psc3. The centromeric localization of Rec8 and Psc3 promotes UPD by uniquely affecting chromosome segregation, causing a reductional segregation of one homologue. Together, these findings establish the untimely vegetative expression of gametogenic genes as a causative factor of UPD, and provide a solid foundation for understanding this phenomenon, which is linked to diverse human diseases.

Differentiating the roles of microtubule-associated proteins at meiotic kinetochores during chromosome segregation.

Meiosis is a specialised cell division process for generating gametes. In contrast to mitosis, meiosis involves recombination followed by two consecutive rounds of cell division, meiosis I and II. A vast field of research has been devoted to understanding the differences between mitotic and meiotic cell divisions from the viewpoint of chromosome behaviour. For faithful inheritance of paternal and maternal genetic information to offspring, two events are indispensable: meiotic recombination, which generates a physical link between homologous chromosomes, and reductional segregation, in which homologous chromosomes move towards opposite poles, thereby halving the ploidy. The cytoskeleton and its regulators play specialised roles in meiosis to accomplish these divisions. Recent studies have shown that microtubule-associated proteins (MAPs), including tumour overexpressed gene (TOG), play unique roles during meiosis. Furthermore, the conserved mitotic protein kinase Polo modulates MAP localisation in meiosis I. As Polo is a well-known regulator of reductional segregation in meiosis, the evidence suggests that Polo constitutes a plausible link between meiosis-specific MAP functions and reductional segregation. Here, we review the latest findings on how the localisation and regulation of MAPs in meiosis differ from those in mitosis, and we discuss conservation of the system between yeast and higher eukaryotes.

Germline/meiotic genes in cancer: new dimensions

Intergenerational passage of genetic information in humans is dependent on a complex sexual program which is orchestrated by a large cohort of tissue-specific germline genes. These genes drive a range of germline-specific pathways including spermatogenesis in males and the reductional chromosome segregation of meiosis. In somatic tissues these genes are transcriptionally silenced, but can become activated in cancerous tissue.1-3 Initial interest in these genes was driven by the need to identify new cancer-specific biomarkers that could be used for diagnostics, prognostics and/or immunotherapeutics, and the first group to be discovered became widely known as the cancer/testis antigen (CTA) genes as they were expressed only in the testis and cancerous tissues, but not in healthy somatic cells. Latterly, many of these gene have also been referred to as the cancer germline genes.1,2 Despite the early interest in these genes as clinical biomarkers or targets, recent works have started to reveal another important cancer-associated role, one which has undergone remarkably limited scrutiny. It has emerged from various studies that germline genes can contribute to oncogenesis and can also contribute to tumor maintenance and drug resistance,1,2 potentially revealing this family of proteins as potent new drug targets. The genes that drive and maintain the male germline have a range of distinct functional roles, including germline cell maintenance in mitotically proliferating spermatagonial cell populations, cellular differentiation during spermatogenesis and the chromosomal reduction of meiosis. To date, many of the CTA genes that have been identified are encoded by the X chromosome and their expression is restricted to the spermatagonial germline cells, becoming transcriptionally inactive during the differentiation to meiotic spermatocytes. A recent screen for new cancer germline genes based on the human orthologues of mouse meiotic spermatocyte genes revealed a large number of autosomally encoded cancer germline genes that were transcriptionally activated in a wide range of cancer types.4,5 A number of these human genes have been shown to encode meiosis-specific functions, including the meiosis-specific inter sister chromatid cohesion protein gene RAD21L and the transcriptional activator / meiotic recombination hot spot regulator gene PRDM9.4,5 From this, it was speculated that the activation of such genes could drive oncogenesis and tumor evolution by interfering with normal equational mitotic chromosome segregation programmes, thus driving oncogenic genome instability.4,5 However, while germline genes have been implicated in a number of oncogenic processes, until recently no direct evidence had been offered to implicate meiosis-specific chromosome regulators in oncogenesis or tumor maintenance. This changed when it was discovered that the ALT telomere maintenance pathway used by some telomerease deficient cancer cells to maintain their telomeres was dependent upon 2 meiosis-specific factors, Hop2 and Mnd1, both of which normally drive the mechanism that biases meiotic recombination to establish the inter homolog connections required for correct reductional chromosome segregation during meiosis I.6 This discovery adds a new class of factors to the complex mix of genes that become activated during oncogenesis and highlights the need to explore the functional activity of other human meiotic genes that may contribute to cancer formation, maintenance and evolution.4,5 In addition, it places further importance on the study of basic molecular mechanisms of the meiotic program. Remarkably, given the emerging importance of germline genes and meiosis-specific genes in cancer, very little is known about their transcriptional regulation. Some studies imply that many of these genes are under a similar regulatory pathway, so that when this becomes dysregulated, functionally related groups of genes become active driving inappropriate functional germline/meiotic modules.3 The epigenetic regulation of previously well characterized CTA genes has been relatively well documented with all studied genes being controlled at some level by the methylation of DNA transcriptional regulatory regions. These genes are activated when cells are treated with the DNA methyltransferase inhibitor 5-AzaC. However, a new layer of complexity to this activation has been revealed by a recent study that demonstrated that not all human cancer germline genes are activated by inhibition of DNA methyltransferases, indicating a complex hierarchy of germline, and possibly meiotic, gene activation.7 In this study it was shown that not only did some cancer germline genes fail to become activated upon inhibition of DNA methyltransferase activity, a number were only transiently silenced during exposure to the demethylating agents while others remained more robustly activated following removal of the demethylation agent.7 Altogether, the finding that meiosis-specific factors can contribute to oncogenesis and that the normal somatic silencing of germline genes is controlled by unique, as yet uncharted factors, makes the study of meiotic and germline genes in cancer an emerging and important field, one which impinges directly on a range of clinical applications including diagnostics, patient stratification/prognostics and new therapeutic and drug targeting strategies.

Chiasmatic and achiasmatic inverted meiosis of plants with holocentric chromosomes

Meiosis is a specialized cell division in sexually reproducing organisms before gamete formation. Following DNA replication, the canonical sequence in species with monocentric chromosomes is characterized by reductional segregation of homologous chromosomes during the first and equational segregation of sister chromatids during the second meiotic division. Species with holocentric chromosomes employ specific adaptations to ensure regular disjunction during meiosis. Here we present the analysis of two closely related plant species with holocentric chromosomes that display an inversion of the canonical meiotic sequence, with the equational division preceding the reductional. In-depth analysis of the meiotic divisions of Rhynchospora pubera and R. tenuis reveals that during meiosis I sister chromatids are bi-oriented, display amphitelic attachment to the spindle and are subsequently separated. During prophase II, chromatids are connected by thin chromatin threads that appear instrumental for the regular disjunction of homologous non-sister chromatids in meiosis II.

Synaptonemal Complex Components Promote Centromere Pairing in Pre-meiotic Germ Cells

Mitosis and meiosis are two distinct cell division programs. During mitosis, sister chromatids separate, whereas during the first meiotic division, homologous chromosomes pair and then segregate from each other. In most organisms, germ cells do both programs sequentially, as they first amplify through mitosis, before switching to meiosis to produce haploid gametes. Here, we show that autosomal chromosomes are unpaired at their centromeres in Drosophila germline stem cells, and become paired during the following four mitosis of the differentiating daughter cell. Surprisingly, we further demonstrate that components of the central region of the synaptonemal complex are already expressed in the mitotic region of the ovaries, localize close to centromeres, and promote de novo association of centromeres. Our results thus show that meiotic proteins and meiotic organization of centromeres, which are key features to ensure reductional segregation, are laid out in amplifying germ cells, before meiosis has started.

Cytogenetic Study in a Mutant of Triatoma infestans (Hemiptera: Reduviidae) Carrying a Spontaneous Autosomal Fusion and an Extra Chromosome

Triatomainfestans (2n = 20 A + XY, male) is a blood-sucking bug and the most important vector of Chagas disease in the Southern Cone countries. A cytogenetic analysis of 14 individuals from the Argentine Gran Chaco has revealed the presence of a naturally heterozygous for an autosomal fusion. The fusion heterozygote (2n = 19 A + 1 extra chromosome + XY, male) presented an autosomal trivalent, 8 bivalents, the X and Y sex univalents, and a minute extra chromosome at meiosis I. The autosomal trivalent divided equationally at first anaphase. At metaphase II, cells had 8 autosomes, X and Y sex chromosomes, and an autosomal pseudo-trivalent composed by 3 different-sized chromatids. The orientation of this pseudo-trivalent led to a reductional segregation. The meiotic behaviour of this new chromosome complement was highly regular. The extra chromosome did not affect the segregation of autosomes and sex chromosomes during both meiotic divisions. We propose that the extra chromosome was originated as a product of an autosomal fusion, and it might become a B chromosome. Many authors suggest that karyotype evolution in Heteroptera has proceeded mainly by fusions and fragmentations. The fact that this rearrangement has been found in a natural population of T. infestans and that it shows a regular meiotic behaviour seems to support the suggested hypothesis.

Finding your pair

The pairing and recombination of homologous chromosomes is crucial for their reductional segregation during meiosis I, but until now it has been unclear how chromosomes recognize their homologous partners. Ding et al. observed that fluorescently tagged sme2 loci, located on Schizosaccharomyces pombe chromosome 2, paired frequently in early meiotic prophase. When the sme2 locus was translocated to another region, robust pairing was seen at this ectopic site, indicating that sme2 is sufficient to induce robust homologous pairing. Furthermore, when two copies of sme2 were present on non-homologous chromosomes, the two loci associated transiently, suggesting that sme2 loci can recognize each other. Importantly, sme2 non-coding RNA transcripts, transcribed from both homologous chromosomes, accumulated at their respective gene loci and were found to be essential for pairing. Whether other pairing sites also exist on chromosome 2 remains to be determined.

The Tetrahymena meiotic chromosome bouquet is organized by centromeres and promotes interhomolog recombination

In order to form crossovers and to undergo reductional segregation during meiosis, homologous chromosomes must pair. In Tetrahymena, meiotic prophase nuclei elongate immensely, and, within the elongated nucleus, chromosomes are arranged with telomeres assembled at one pole and centromeres at the opposite pole. This organisation is an exaggerated form of the bouquet, a meiotic chromosome arrangement that is widely conserved among eukaryotes. We show that centromere function is crucial for the formation of Tetrahymena's stretched bouquet and, thereby, for homologue pairing. This finding adds to previous reports of the importance of centromeres in chromosome pairing in budding yeast and in Drosophila. Tetrahymena's bouquet is an ataxia telangiectasia- and RAD3-related (ATR)-dependent meiotic DNA damage response that is triggered by meiotic DNA double-strand breaks (DSBs), suggesting that the bouquet is needed for DSB repair. However, in the present study we show that although homologous pairing is impeded in the absence of the bouquet, DSB repair takes place nevertheless. Moreover, recombinational DSB repair, as monitored by bromodeoxyuridine incorporation, takes place only after exit from the bouquet stage. Therefore, we conclude that the bouquet is not required for DSB repair per se, but may be necessary for the alignment of homologous loci in order to promote homologous crossovers over alternative repair pathways.

Homologous pairing and the role of pairing centers in meiosis

Homologous pairing establishes the foundation for accurate reductional segregation during meiosis I in sexual organisms. This Commentary summarizes recent progress in our understanding of homologous pairing in meiosis, and will focus on the characteristics and mechanisms of specialized chromosome sites, called pairing centers (PCs), in Caenorhabditis elegans and Drosophila melanogaster. In C. elegans, each chromosome contains a single PC that stabilizes chromosome pairing and initiates synapsis of homologous chromosomes. Specific zinc-finger proteins recruited to PCs link chromosomes to nuclear envelope proteins--and through them to the microtubule cytoskeleton--thereby stimulating chromosome movements in early prophase, which are thought to be important for homolog sorting. This mechanism appears to be a variant of the 'telomere bouquet' process, in which telomeres cluster on the nuclear envelope, connect chromosomes through nuclear envelope proteins to the cytoskeleton and lead chromosome movements that promote homologous synapsis. In Drosophila males, which undergo meiosis without recombination, pairing of the largely non-homologous X and Y chromosomes occurs at specific repetitive sequences in the ribosomal DNA. Although no other clear examples of PC-based pairing mechanisms have been described, there is evidence for special roles of telomeres and centromeres in aspects of chromosome pairing, synapsis and segregation; these roles are in some cases similar to those of PCs.

Initiation of Meiotic Recombination in Mammals

Meiotic recombination is initiated by the induction of programmed DNA double strand breaks (DSBs). DSB repair promotes homologous interactions and pairing and leads to the formation of crossovers (COs), which are required for the proper reductional segregation at the first meiotic division. In mammals, several hundred DSBs are generated at the beginning of meiotic prophase by the catalytic activity of SPO11. Currently it is not well understood how the frequency and timing of DSB formation and their localization are regulated. Several approaches in humans and mice have provided an extensive description of the localization of initiation events based on CO mapping, leading to the identification and characterization of preferred sites (hotspots) of initiation. This review presents the current knowledge about the proteins known to be involved in this process, the sites where initiation takes place, and the factors that control hotspot localization.

From meiosis to postmeiotic events: Alignment and recognition of homologous chromosomes in meiosis

Recombination of homologous chromosomes is essential for correct reductional segregation of homologous chromosomes, which characterizes meiosis. To accomplish homologous recombination, chromosomes must find their homologous partners and pair with them within the spatial constraints of the nucleus. Although various mechanisms have developed in different organisms, two major steps are involved in the process of pairing: first, alignment of homologous chromosomes to bring them close to each other for recognition; and second, recognition of the homologous partner of each chromosome so that they can form an intimate pair. Here, we discuss the various mechanisms used for alignment and recognition of homologous chromosomes in meiosis.

Chromosomes of Theridiidae spiders (Entelegynae): interspecific karyotype diversity in Argyrodes and diploid number intraspecific variability in Nesticodes rufipes

Theridiidae is a derived family within the Araneoidea clade. In contrast to closely related groups, the 2n(male) = 20+X1 X 2 with acro/telocentric chromosomes is the most widespread karyotype among the theridiid spiders. In this work, the cytogenetic analysis of Argyrodes elevatus revealed original chromosome features different from those previously registered for Theridiidae, including the presence of 2n(male) = 20+X with meta/submetacentric chromosomes. Most individuals of Nesticodes rufipes showed family conserved karyotype characteristics. However, one individual had a 2n(male) = 24 due to the presence of an extra chromosome pair, which exhibited regular behavior and reductional segregation during meiosis. After silver staining, mitotic cells exhibited NORs localized on the terminal regions of the short arms of pairs 2, 3, and 4 of A. elevatus and on the terminal regions of long arms of pair 4 of N. rufipes. The comparative analysis with data from phylogenetically related species allowed the clarification of the origin of the interspecific and intraspecific chromosome variability observed in Argyrodes and in N. rufipes, respectively.

Cdc7-Dbf4 RegulatesNDT80Transcription as Well as Reductional Segregation during Budding Yeast Meiosis

In budding yeast, as in other eukaryotes, the Cdc7 protein kinase is important for initiation of DNA synthesis in vegetative cells. In addition, Cdc7 has crucial meiotic functions: it facilitates premeiotic DNA replication, and it is essential for the initiation of recombination. This work uses a chemical genetic approach to demonstrate that Cdc7 kinase has additional roles in meiosis. First, Cdc7 allows expression of NDT80, a meiosis-specific transcriptional activator required for the induction of genes involved in exit from pachytene, meiotic progression, and spore formation. Second, Cdc7 is necessary for recruitment of monopolin to sister kinetochores, and it is necessary for the reductional segregation occurring at meiosis I. The use of the same kinase to regulate several distinct meiosis-specific processes may be important for the coordination of these processes during meiosis.

Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis

During meiosis the programmed induction of DNA double-stranded breaks (DSB) leads to crossover (CO) and non-crossover products (NCO). One key role of CO is to connect homologs before metaphase I and thus to ensure the proper reductional segregation. This role implies an accurate regulation of CO frequency with the establishment of at least one CO per chromosome arm. Current major challenges are to understand how CO and NCO formation are regulated and what is the role of NCO. We present here the current knowledge about CO and NCO and their regulation in mammals. CO density varies widely along chromosomes and their distribution is not random as they are subject to positive interference. As documented in the mouse and human, a significant excess of DSB are generated relative to the number of CO. In fact, evidence has been obtained for the formation of NCO products, for regulation of the choice of DSB repair towards CO or NCO and for a CO specific pathway. We discuss the roles of Msh4, Msh5 and Sycp1 which affect DSB repair and probably not only the CO pathway. We suggest that, in mammals, the regulation of NCO differs from that described in Saccharomyces cerevisiae.

An Analysis of Univalent Segregation in Meiotic Mutants ofArabidopsis thaliana: A Possible Role for Synaptonemal Complex

During first meiotic prophase, homologous chromosomes are normally kept together by both crossovers and synaptonemal complexes (SC). In most eukaryotes, the SC disassembles at diplotene, leaving chromosomes joined by chiasmata. The correct co-orientation of bivalents at metaphase I and the reductional segregation at anaphase I are facilitated by chiasmata and sister-chromatid cohesion. In the absence of meiotic reciprocal recombination, homologs are expected to segregate randomly at anaphase I. Here, we have analyzed the segregation of homologous chromosomes at anaphase I in four meiotic mutants of Arabidopsis thaliana, spo11-1-3, dsy1, mpa1, and asy1, which show a high frequency of univalents at diplotene. The segregation pattern of chromosomes 2, 4, and 5 was different in each mutant. Homologous univalents segregated randomly in spo11-1-3, whereas they did not in dsy1 and mpa1. An intermediate situation was observed in asy1. Also, we have found a parallelism between this behavior and the synaptic pattern displayed by each mutant. Thus, whereas spo11-1-3 and asy1 showed low amounts of SC stretches, dsy1 and mpa1 showed full synapsis. These findings suggest that in Arabidopsis there is a system, depending on the SC formation, that would facilitate regular disjunction of homologous univalents to opposite poles at anaphase I.