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Results for “Synaptonemal Complex”

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PubMed2003

Dynamic relocation of telomere complexes in mouse meiotic chromosomes.

Telomeric DNA repeats as well as different specific proteins such as TRF1 and Rap1 associate in functional telomere complexes found at chromosome ends. Using spreading techniques, the presence of TRF1 and Rap1 has been reported at mammalian meiotic telomeres during prophase I. In the present study, we have analysed, by fluorescence in-situ hybridization and immunofluorescence, the appearance and location of telomere complexes during both male mouse meiotic divisions. Additionally, we have studied their relationship with different centromere/kinetochore proteins and the synaptonemal complex protein SCP3. Our results show that telomere complexes are not located at condensed meiotic chromosome tips. Therefore, a change in chromosome structure may occur from pachytene up to metaphase I involving the dynamic relocation of telomere complexes in condensed chromosomes. Moreover, we have found that proximal telomere complexes are relocated internally to kinetochores from metaphase I up to anaphase II. We discuss the functional significance of the location of telomere complexes into internal domains of condensed meiotic chromosomes.

Animals↗

PubMed2006

A Role for SUMO in meiotic chromosome synapsis.

During meiotic prophase, homologous chromosomes engage in a complex series of interactions that ensure their proper segregation at meiosis I. A central player in these interactions is the synaptonemal complex (SC), a proteinaceous structure elaborated along the lengths of paired homologs. In mutants that fail to make SC, crossing over is decreased, and chromosomes frequently fail to recombine; consequently, many meiotic products are inviable because of aneuploidy. Here, we have investigated the role of the small ubiquitin-like protein modifier (SUMO) in SC formation during meiosis in budding yeast. We show that SUMO localizes specifically to synapsed regions of meiotic chromosomes and that this localization depends on Zip1, a major building block of the SC. A non-null allele of the UBC9 gene, which encodes the SUMO-conjugating enzyme, impairs Zip1 polymerization along chromosomes. The Ubc9 protein localizes to meiotic chromosomes, coincident with SUMO staining. In the zip1 mutant, SUMO localizes to discrete foci on chromosomes. These foci coincide with axial associations, where proteins involved in synapsis initiation are located. Our data suggest a model in which SUMO modification of chromosomal proteins promotes polymerization of Zip1 along chromosomes. The ubc9 mutant phenotype provides the first evidence for a cause-and-effect relationship between sumoylation and synapsis.

Chromosome Pairing↗

PubMed1992

Synapsis, recombination, and meiotic segregation in the mesquite lizard, Sceloporus grammicus, complex. I. Pericentric inversion heteromorphism of the F5 cytotype.

Chromosomal pairing and recombination were analyzed in male specimens of Sceloporus grammicus heterozygous for a large pericentric inversion of macrochromosome 4. Analysis of silver-stained synaptonemal complexes (SCs) in surface-spread nuclei revealed that homologously paired inversion loops were not formed. Synapsis of the inverted segments proceeded directly to nonhomologous straight pairing. In some nuclei, this resulted in a configuration that could not be distinguished from homozygous bivalents of similar size. Examination of Giemsa- and silver-stained diakinetic nuclei indicated that crossing-over was limited to the noninverted (homologous) portion of the heteromorphic bivalent. Analysis of secondary spermatocytes (metaphase II configurations) revealed normal disjunction and balanced segregation of the elements of the heteromorphic bivalent. These observations indicate that the inversion heteromorphism does not lead to the production of unbalanced gametes.

Animals↗

PubMed1998

Meiosis: Avoiding inappropriate relationships.

Meiosis is distinguished from mitosis by the way double-strand breaks are made and by the synapsis and segregation of homologous chromosomes. Recent studies with the yeast Saccharomyces cerevisiae have identified some of the key players that link homologous recombination to synaptonemal complex formation.

Fungal Proteins↗

PubMed2004

Imposition of crossover interference through the nonrandom distribution of synapsis initiation complexes.

Meiotic crossovers (COs) are nonrandomly distributed along chromosomes such that two COs seldom occur close together, a phenomenon known as CO interference. We have used genetic and cytological methods to investigate interference mechanisms in budding yeast. Assembly of the synaptonemal complex (SC) initiates at a few sites along each chromosome, triggered by a complex of proteins (including Zip2 and Zip3) called the synapsis initiation complex (SIC). We found that SICs, like COs, display interference, supporting the hypothesis that COs occur at synapsis initiation sites. Unexpectedly, we found that SICs show interference in mutants in which CO interference is abolished; one explanation is that these same mutations eliminate the subset of COs that normally occur at SICs. Since SICs are assembled in advance of SC and they are properly positioned even in the absence of SC formation, these data clearly demonstrate an aspect of interference that is independent of synapsis.

Carrier Proteins↗

PubMed2004

A constitutional complex chromosome rearrangement involving meiotic arrest in an azoospermic male: case report.

Complex chromosome rearrangements are rare aberrations that frequently lead to reproductive failure and that may hinder assisted reproduction. A 25-year-old azoospermic male was studied cytogenetically with synaptonemal complex analysis of spermatocytes from a testicular biopsy and fluorescence in situ hybridization (FISH) of lymphocytes. The spermatocytes showed a pentavalent plus a univalent chromosome. Cell death occurred mainly at advanced pachytene stages. The sex chromosomes were involved in the multiple, as shown by their typical axial excrescences. Two autosomal pairs, including an acrocentric chromosome (15), were also involved in the multiple. FISH allowed the definite identification of all the involved chromosomes. An inverted chromosome 12 is translocated with most of one long arm of chromosome 15, while the centromeric piece of this chromosome 15 is translocated with Yqh, forming a small marker chromosome t(15;Y). The euchromatic part of the Y chromosome is joined to the remaining piece of chromosome 12, forming a neo-Y chromosome. The patient shows azoospermia and a normal phenotype. The disruption of spermatogenesis is hypothetically due to the extent of asynaptic segments and to sex-body association during pachytene. This CCR occurred 'de novo' during paternal spermatogenesis. Meiotic analysis and FISH are valuable diagnostic tools in these cases.

Adult↗

PubMed2002

Differential association of SMC1alpha and SMC3 proteins with meiotic chromosomes in wild-type and SPO11-deficient male mice.

SMC proteins are components of cohesin complexes that function in chromosome cohesion. We determined that SMC1alpha and SMC3 localized to wild-type mouse meiotic chromosomes, but with distinct differences in their patterns. Anti-SMC3 coincided with axial elements of the synaptonemal complex, while SMC1alpha was observed mainly in regions where homologues were synapsed. This pattern was especially visible in pachytene sex vesicles where SMC1alpha localized only weakly to the asynapsed regions. At diplotene, SMC3, but not SMC1alpha, remained bound along axial elements of desynapsed chromosomes. SMC1alpha and SMC3 were also found to localize along meiotic chromosome cores of Spo11 null spermatocytes, in which double-strand break formation required for DNA recombination and homologous pairing were disrupted. In Spo11 -/- cells, SMC1alpha localization differed from SMC3 again, confirming that SMC1alpha is mainly associated with homologous or non-homologous synapsed regions, whereas SMC3 localized throughout the chromosomes. Our results suggest that the two cohesin proteins may not always be associated in a dimer and may function as separate complexes in mammalian meiosis, with SMC1alpha playing a more specific role in synapsis. In addition, our results indicate that cohesin cores can form independently of double-strand break formation and homologous pairing.

3T3 Cells↗

PubMed2006

Saccharomyces cerevisiae Mer2, Mei4 and Rec114 form a complex required for meiotic double-strand break formation.

In budding yeast, at least 10 proteins are required for formation of the double-strand breaks (DSBs) that initiate meiotic recombination. Spo11 is the enzyme responsible for cleaving DNA and is found in a complex that also contains Ski8, Rec102, and Rec104. The Mre11/Rad50/Xrs2 complex is required for both DSB formation and DSB processing. In this article we investigate the functions of the remaining three proteins--Mer2, Mei4, and Rec114--with particular emphasis on Mer2. The Mer2 protein is present in vegetative cells, but it increases in abundance and becomes phosphorylated specifically during meiotic prophase. Mer2 localizes to distinct foci on meiotic chromosomes, with foci maximally abundant prior to the formation of synaptonemal complex. If DSB formation is blocked (e.g., by a spo11 mutation), dephosphorylation of Mer2 and its dissociation from chromosomes are delayed. We have also found that the Mei4 and Rec114 proteins localize to foci on chromosomes and these foci partially colocalize with each other and with Mer2. Furthermore, the three proteins co-immunoprecipitate. Mer2 does not show significant colocalization with Mre11 or Rec102 and Mer2 does not co-immunoprecipitate with Rec102. We propose that Mer2, Mei4, and Rec114 form a distinct complex required for DSB formation.

Chromosome Breakage↗

PubMed2003

Meiotic condensin is required for proper chromosome compaction, SC assembly, and resolution of recombination-dependent chromosome linkages.

Condensin is an evolutionarily conserved protein complex that helps mediate chromosome condensation and segregation in mitotic cells. Here, we show that condensin has two activities that contribute to meiotic chromosome condensation in Saccharomyces cerevisiae. One activity, common to mitosis, helps mediate axial length compaction. A second activity promotes chromosome individualization with the help of Red1 and Hop1, two meiotic specific components of axial elements. Like Red1 and Hop1, condensin is also required for efficient homologue pairing and proper processing of double strand breaks. Consistent with these functional links condensin is necessary for proper chromosomal localization of Red1 and Hop1 and the subsequent assembly of the synaptonemal complex. Finally, condensin has a Red1/Hop1-independent role in the resolution of recombination-dependent linkages between homologues in meiosis I. The existence of distinct meiotic activities of condensin (axial compaction, individualization, and resolution of recombination-dependent links) provides an important framework to understand condensin's role in both meiotic and mitotic chromosome structure and function.

Adenosine Triphosphatases↗

PubMed2001

Checkpoint and DNA-repair proteins are associated with the cores of mammalian meiotic chromosomes.

Meiotic checkpoints are manifested through protein complexes capable of detecting an abnormality in chromosome metabolism and signaling it to effector molecules that subsequently delay or arrest the progression of meiosis. Some checkpoints act during the first meiotic prophase to monitor the repair of chromosomal DSBs, predominantly by meiotic recombination, or to ensure the correct establishment of synapsis and its well-timed dissolution. In mammals, a number of checkpoint and repair proteins localize to the meiotic chromosomal cores, sometimes in the context of the synaptonemal complex (SC). Here we discuss possible functions of these proteins in the accomplishment of meiotic recombination and normal progression of the meiotic pathway. Also, we present arguments for a structural role of cores and SCs in the assembly of the repair and checkpoint protein complexes on the chromosomes.

Animals↗

PubMed2006

Two distinct surveillance mechanisms monitor meiotic chromosome metabolism in budding yeast.

Meiotic recombination is initiated by Spo11-generated DNA double-strand breaks (DSBs) . A fraction of total DSBs is processed into crossovers (CRs) between homologous chromosomes, which promote their accurate segregation at meiosis I (MI) . The coordination of recombination-associated events and MI progression is governed by the "pachytene checkpoint", which in budding yeast requires Rad17, a component of a PCNA clamp-like complex, and Pch2, a putative AAA-ATPase . We show that two genetically separable pathways monitor the presence of distinct meiotic recombination-associated lesions: First, delayed MI progression in the presence of DNA repair intermediates is suppressed when RAD17 or SAE2, encoding a DSB-end processing factor , is deleted. Second, delayed MI progression in the presence of aberrant synaptonemal complex (SC) is suppressed when PCH2 is deleted. Importantly, ZIP1, encoding the central element of the SC , is required for PCH2-dependent checkpoint activation. Analysis of the rad17Deltapch2Delta double mutant revealed a redundant function regulating interhomolog CR formation. These findings suggest a link between the surveillance of distinct recombination-associated lesions, control of CR formation kinetics, and regulation of MI timing. A PCH2-ZIP1-dependent checkpoint in meiosis is likely conserved among synaptic organisms from yeast to human .

Cell Cycle Proteins↗

PubMed2001

Memory and DNA.

A model is presented for the storage of long-term memory. In our model consolidation takes place by specific DNA sequences. These DNA sequences are obtained by the recombination of DNA in a similar way to that during meiosis and the production of immunological antibodies. DNA has the potential of the production of large numbers of specific DNA sequences. These sequences can be attached to images of neural networks. The following considerations lead to the theory: (1)Most of the DNA is not used: approximately 3% of our DNA is used. (2)There are no cell divisions in the brain after adulthood is reached. Structural DNA arrangements will not be altered nor disrupted as a consequence of cell division and mitosis. (3)Chromosomal pairing is demonstrated in the brain, which could indicate the exchange of DNA. In addition, in our first survey experiments we found a positive reaction of components of the synaptonemal complex (SC) in the nuclei of brain cells. The SC is highly meiosis specific and plays a major role in genetic recombination.

Adult↗

PubMed2001

Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway.

Fanconi anemia (FA) is a human autosomal recessive cancer susceptibility disorder characterized by cellular sensitivity to mitomycin C and ionizing radiation. Although six FA genes (for subtypes A, C, D2, E, F, and G) have been cloned, their relationship to DNA repair remains unknown. In the current study, we show that a nuclear complex containing the FANCA, FANCC, FANCF, and FANCG proteins is required for the activation of the FANCD2 protein to a monoubiquitinated isoform. In normal (non-FA) cells, FANCD2 is monoubiquitinated in response to DNA damage and is targeted to nuclear foci (dots). Activated FANCD2 protein colocalizes with the breast cancer susceptibility protein, BRCA1, in ionizing radiation-induced foci and in synaptonemal complexes of meiotic chromosomes. The FANCD2 protein, therefore, provides the missing link between the FA protein complex and the cellular BRCA1 repair machinery. Disruption of this pathway results in the cellular and clinical phenotype common to all FA subtypes.

Active Transport, Cell Nucleus↗

PubMed2003

Dynamic relocalization of the chromosomal passenger complex proteins inner centromere protein (INCENP) and aurora-B kinase during male mouse meiosis.

INCENP and aurora-B kinase are two chromosomal passenger proteins that are thought to play key roles in coordinating chromosome segregation with cytokinesis in somatic cells. Here we have analyzed their subcellular distribution, and that of phosphorylated histone H3, and the timing of their relative appearance in mouse spermatocytes during both meiotic divisions. Our results show that in mitotic spermatogonial cells, INCENP and aurora-B show the same pattern of distribution as they do in cultured somatic cells. INCENP labels the synaptonemal complex central element from zygotene up to late pachytene when it begins to relocalize to heterochromatic chromocentres. Aurora-B first appears at chromocentres in late diplotene before the initial phosphorylation of histone H3. INCENP and aurora-B concentrate at centromeres during diakinesis and appear during metaphase I as T-shaped signals at their inner domains, just below associated sister kinetochores. During late anaphase I both proteins relocalize to the spindle midzone. Both proteins colocalize at a connecting strand traversing the centromere region and joining sister kinetochores, in metaphase II centromeres. This strand disappears at the metaphase II/anaphase II transition and relocalizes to the spindle midzone. We discuss the complex dynamic relocalization of the chromosomal passenger complex during prophase I. Additionally, we suggest that this complex may regulate sister-chromatid centromere cohesion during both meiotic divisions.

3T3 Cells↗

PubMed1985

Identification of the meiotic division of malarial parasites.

Zygotes of Plasmodium berghei were cultured 15-25 h in vitro to yield mature infective ookinetes. Samples taken in the first 5 h of culture were examined by electron microscopy. Meiotic figures were detected in the nuclei of the zygotes. Threadlike leptotene chromatids (chromosomes) condensed from attachment plaques on the nuclear envelope; chromatid pairing followed (zygotene), with synaptonemal complexes subsequently appearing (pachytene). These complexes persisted into metaphase but dissociated when the chromatids rapidly decondensed during anaphase. At telophase of the first meiotic division the kinetochores were retracted toward two small spindle complexes, which were found at widely separated poles in the nuclear envelope. The observations are consistent with a haploid genome of 8-10 chromosomes.

Anaphase↗

PubMed1987

Nonhomologous synapsis of the XY during early pachynema in In(X)1H male mice.

It has been previously supposed that meiotic synapsis is restricted to homology during early, but not late pachynema. The synaptic behavior of an inverted X chromosome, In(X)1H as reflected in the synaptonemal complexes of the sex chromosomes has been examined in microspread spermatocytes by electron microscopy and evidence of extensive nonhomologous synapsis between the X and Y during early pachynema has been obtained.

Animals↗

PubMed1996

Effect of X-rays on germ cells in female fetuses of Rattus norvegicus irradiated at three different times of gestation.

We analyzed the effect of X-rays on the number of recoverable germ cells in female rat fetuses irradiated at three different times of gestation: 14 days (oogonia), 16 days (leptotene) and 18 days (zygotene). Our results show that irradiation significantly decreases the number of germ cells, and increases the incidence of synaptonemal complex fragmentation. The different sensitivity of the germ cells to irradiation could depend on the meiotic stage at the time of irradiation.

Animals↗

PubMed1989

Colcemid effects on homologue pairing and crossing over during fetal mouse oogenesis.

Colcemid was administered to gestational day 13 female mice to test effects on homologue pairing, synapsis and recombination of fetal oogenesis. Pairing abnormalities were detected in pachytene oocytes by light and electron microscopy examination of bivalents and synaptonemal complexes. Reduction of total chiasmata per treated diplotene oocyte (22.74) compared to controls (31.07) was found.

Animals↗