Lateral Elements Of Synaptonemal Complex Research Articles

Multiple reorganizations of the lateral elements of the synaptonemal complex facilitate homolog segregation in Bombyx mori oocytes.

Although Lepidopteran females build a synaptonemal complex (SC) in pachytene, homologs do not crossover, necessitating an alternative method of homolog conjunction. In Bombyx mori oocytes, the SC breaks down at the end of pachytene, and homolog associations are maintained by a large oocyte-specific structure, which we call the bivalent bridge (BB), connecting paired homologs. The BB is derived from at least some components of the SC lateral elements (LEs). It contains the HORMAD protein HOP1 and the LE protein SYCP2 and is formed by the fusion of the two LE derivatives. As diplotene progresses, the BB increases in width and acquires a layered structure with a thick band of HOP1 separating two layers of SYCP2. The HOP1 interacting protein, PCH2, joins the BB in mid-diplotene, and by late-diplotene, it lies in the middle of the HOP1 filament. This structure is maintained through metaphase I. SYCP2 and PCH2 are lost at anaphase I, and the BB no longer connects the separating homologs. However, a key component of the BB, HOP1, remains at the metaphase I plate. These changes in organization of the BB occur simultaneously with the movement of the kinetochore protein, DSN1, from within the BB at mid-diplotene to the edge of the homologs facing the poles by metaphase I. We view these data in context of models in which SC components and regulators can be repurposed to achieve different functions, a fascinating example of evolution achieving homolog conjunction in an alternative way with recycling of SC proteins.

A small RNA system ensures accurate homologous pairing and unpaired silencing of meiotic chromosomes.

During meiosis, chromosomes with homologous partners undergo synaptonemal complex (SC)-mediated pairing, while the remaining unpaired chromosomes are heterochromatinized through unpaired silencing. Mechanisms underlying homolog recognition during SC formation are still unclear. Here, we show that the Caenorhabditis elegans Argonaute proteins, CSR-1 and its paralog CSR-2, interacting with 22G-RNAs, are required for synaptonemal complex formation with accurate homology. CSR-1 in nuclei and meiotic cohesin, constituting the SC lateral elements, were associated with nonsimple DNA repeats, including minisatellites and transposons, and weakly associated with coding genes. CSR-1-associated CeRep55 minisatellites were expressing 22G-RNAs and long noncoding (lnc) RNAs that colocalized with synaptonemal complexes on paired chromosomes and with cohesin regions of unpaired chromosomes. CeRep55 multilocus deletions reduced the efficiencies of homologous pairing and unpaired silencing, which were supported by the csr-1 activity. Moreover, CSR-1 and CSR-2 were required for proper heterochromatinization of unpaired chromosomes. These findings suggest that CSR-1 and CSR-2 play crucial roles in homology recognition, achieving accurate SC formation between chromosome pairs and condensing unpaired chromosomes by targeting repeat-derived lncRNAs.

Sex chromosome differentiation via changes in the Y chromosome repeat landscape in African annual killifishes Nothobranchius furzeri and N. kadleci.

Homomorphic sex chromosomes and their turnover are common in teleosts. We investigated the evolution of nascent sex chromosomes in several populations of two sister species of African annual killifishes, Nothobranchius furzeri and N. kadleci, focusing on their under-studied repetitive landscape. We combined bioinformatic analyses of the repeatome with molecular cytogenetic techniques, including comparative genomic hybridization, fluorescence in situ hybridization with satellite sequences, ribosomal RNA genes (rDNA) and bacterial artificial chromosomes (BACs), and immunostaining of SYCP3 and MLH1 proteins to mark lateral elements of synaptonemal complexes and recombination sites, respectively. Both species share the same heteromorphic XY sex chromosome system, which thus evolved prior to their divergence. This was corroborated by sequence analysis of a putative master sex determining (MSD) gene gdf6Y in both species. Based on their divergence, differentiation of the XY sex chromosome pair started approximately 2 million years ago. In all populations, the gdf6Y gene mapped within a region rich in satellite DNA on the Y chromosome long arms. Despite their heteromorphism, X and Y chromosomes mostly pair regularly in meiosis, implying synaptic adjustment. In N. kadleci, Y-linked paracentric inversions like those previously reported in N. furzeri were detected. An inversion involving the MSD gene may suppress occasional recombination in the region, which we otherwise evidenced in the N. furzeri population MZCS-121 of the Limpopo clade lacking this inversion. Y chromosome centromeric repeats were reduced compared with the X chromosome and autosomes, which points to a role of relaxed meiotic drive in shaping the Y chromosome repeat landscape. We speculate that the recombination rate between sex chromosomes was reduced due to heterochiasmy. The observed differences between the repeat accumulations on the X and Y chromosomes probably result from high repeat turnover and may not relate closely to the divergence inferred from earlier SNP analyses.

Aurora B and C kinases regulate chromosome desynapsis and segregation during mouse and human spermatogenesis.

Precise control of chromosome dynamics during meiosis is critical for fertility. A gametocyte undergoing meiosis coordinates formation of the synaptonemal complex (SC) to promote efficient homologous chromosome recombination. Subsequent disassembly of the SC occurs prior to segregation of homologous chromosomes during meiosis I. We examined the requirements of the mammalian Aurora kinases (AURKA, AURKB and AURKC) during SC disassembly and chromosome segregation using a combination of chemical inhibition and gene deletion approaches. We find that both mouse and human spermatocytes fail to disassemble SC lateral elements when the kinase activity of AURKB and AURKC are chemically inhibited. Interestingly, both Aurkb conditional knockout and Aurkc knockout mouse spermatocytes successfully progress through meiosis, and the mice are fertile. In contrast, Aurkb, Aurkc double knockout spermatocytes fail to coordinate disassembly of SC lateral elements with chromosome condensation and segregation, resulting in delayed meiotic progression. In addition, deletion of Aurkb and Aurkc leads to an accumulation of metaphase spermatocytes, chromosome missegregation and aberrant cytokinesis. Collectively, our data demonstrate that AURKB and AURKC functionally compensate for one another ensuring successful mammalian spermatogenesis.This article has an associated First Person interview with the first author of the paper.

Multiple Sex Chromosome System X1X2Y in African Killifish Genera Nothobranchius and Fundulosoma (Cyprinodontiformes)

Multiple Sex Chromosome System X1X2Y in African Killifish Genera Nothobranchius and Fundulosoma (Cyprinodontiformes)

Spiral cores of synaptonemal complex lateral elements at the diplotene stage in rye include the ASY1 protein

After completing their functioning, synaptonemal complexes (SCs) degrade during the diplotene stage. In the pollen mother cells of rye Secale cereal L., this occurs through the formation of gaps in lateral elements of the SCs and the shortening of fragments of SCs until their complete disappearance. However, when contrasting SCs with silver nitrate solution at a pH of 3.5-4.5, these gaps appear to be filled with threads associated with SC lateral elements. As the diplotene stage proceeds and gradual degradation of SC fragments continues, these threads turn into submicroscopic spirals. In this study, we found that the threads and spirals associated with degrading synaptonemal complexes are stained by antibodies to the ASY1 protein ofArabidopsis thaliana lateral elements and thus are degradation products of the lateral elements of SCs.

Meiotic Crossover Control by Concerted Action of Rad51-Dmc1 in Homolog Template Bias and Robust Homeostatic Regulation

During meiosis, repair of programmed DNA double-strand breaks (DSBs) by recombination promotes pairing of homologous chromosomes and their connection by crossovers. Two DNA strand-exchange proteins, Rad51 and Dmc1, are required for meiotic recombination in many organisms. Studies in budding yeast imply that Rad51 acts to regulate Dmc1's strand exchange activity, while its own exchange activity is inhibited. However, in a dmc1 mutant, elimination of inhibitory factor, Hed1, activates Rad51's strand exchange activity and results in high levels of recombination without participation of Dmc1. Here we show that Rad51-mediated meiotic recombination is not subject to regulatory processes associated with high-fidelity chromosome segregation. These include homolog bias, a process that directs strand exchange between homologs rather than sister chromatids. Furthermore, activation of Rad51 does not effectively substitute for Dmc1's chromosome pairing activity, nor does it ensure formation of the obligate crossovers required for accurate homolog segregation. We further show that Dmc1's dominance in promoting strand exchange between homologs involves repression of Rad51's strand-exchange activity. This function of Dmc1 is independent of Hed1, but requires the meiotic kinase, Mek1. Hed1 makes a relatively minor contribution to homolog bias, but nonetheless this is important for normal morphogenesis of synaptonemal complexes and efficient crossing-over especially when DSB numbers are decreased. Super-resolution microscopy shows that Dmc1 also acts to organize discrete complexes of a Mek1 partner protein, Red1, into clusters along lateral elements of synaptonemal complexes; this activity may also contribute to homolog bias. Finally, we show that when interhomolog bias is defective, recombination is buffered by two feedback processes, one that increases the fraction of events that yields crossovers, and a second that we propose involves additional DSB formation in response to defective homolog interactions. Thus, robust crossover homeostasis is conferred by integrated regulation at initiation, strand-exchange and maturation steps of meiotic recombination.

The Cohesion Protein SOLO Associates with SMC1 and Is Required for Synapsis, Recombination, Homolog Bias and Cohesion and Pairing of Centromeres in Drosophila Meiosis

Cohesion between sister chromatids is mediated by cohesin and is essential for proper meiotic segregation of both sister chromatids and homologs. solo encodes a Drosophila meiosis-specific cohesion protein with no apparent sequence homology to cohesins that is required in male meiosis for centromere cohesion, proper orientation of sister centromeres and centromere enrichment of the cohesin subunit SMC1. In this study, we show that solo is involved in multiple aspects of meiosis in female Drosophila. Null mutations in solo caused the following phenotypes: 1) high frequencies of homolog and sister chromatid nondisjunction (NDJ) and sharply reduced frequencies of homolog exchange; 2) reduced transmission of a ring-X chromosome, an indicator of elevated frequencies of sister chromatid exchange (SCE); 3) premature loss of centromere pairing and cohesion during prophase I, as indicated by elevated foci counts of the centromere protein CID; 4) instability of the lateral elements (LE)s and central regions of synaptonemal complexes (SCs), as indicated by fragmented and spotty staining of the chromosome core/LE component SMC1 and the transverse filament protein C(3)G, respectively, at all stages of pachytene. SOLO and SMC1 are both enriched on centromeres throughout prophase I, co-align along the lateral elements of SCs and reciprocally co-immunoprecipitate from ovarian protein extracts. Our studies demonstrate that SOLO is closely associated with meiotic cohesin and required both for enrichment of cohesin on centromeres and stable assembly of cohesin into chromosome cores. These events underlie and are required for stable cohesion of centromeres, synapsis of homologous chromosomes, and a recombination mechanism that suppresses SCE to preferentially generate homolog crossovers (homolog bias). We propose that SOLO is a subunit of a specialized meiotic cohesin complex that mediates both centromeric and axial arm cohesion and promotes homolog bias as a component of chromosome cores.

Damage to synaptonemal complex structure and peculiarities of selection of mouse spermatocytes I at response to drug administration

Using immunocytochemistry methods, the structure of synaptonemal complexes (SC) of chromosomes in spread nuclei of primary spermatocytes of mice at 1, 10, and 36 days after the 10-day intraperitoneal administration of antibacterial preparations of three pharmacological groups: furacilin, an antiseptic derivative of nitrofuran; cifran, an antibiotic from the group of fluoroquinolones; and sextaphage, a polyvalent piobacteriophage was investigated. The maximal number of disturbances in the structure and behavior of synaptonemal complex was revealed on the first day after the end of preparation administration. On days 10 and 36, the total number of disturbances in SC structure decreased gradually. On the first day after the end of the administration of cifran and sextaphage in 41.8 and 25% of nuclei, respectively, the fragmentation of synaptonemal complexes was revealed and, in males to whom furacilin had been administered, the fragmentation of synaptonemal complexes was identified in 100% of nuclei. Multiple chromosome fragmentation is a meiotic disaster and results in the degeneration of cells without enabling the mechanism ofpachytene arrest. The features of pachytene arrest were revealed in the nuclei of primary spermatocytes with the disturbances of chromosomes pairing. After the administration of sextaphage, circle structures released from the lateral elements of SC and are dyed with antibodies to SCP3 protein.

Morphological manifestation of unique DNA segments in human meiotic prophase I

The commercial sample of human DNA fragment from the choromosome 17 was used as the probe for FISH to study of the mode of its attachment to the lateral elements of synaptonemal complex (SC) in human spermatocytes. It was a 160 kb probe from the band 17p1.2, containing RAI1 gene with D17S620 marker (the probe for deletion causing Smith-Magenis syndrome). The probe made lateral chromatin protrusions, contacting with SC stained with anty-SYCP3. Different morphological configuration of lateral chromatin protrusions where observed. They depended on substages of meiotic prophase I. At zygotene, FISH probe form two sticks, c. a. 6 micro long, which was perpendicular to SC longitudinal axe, one stick at each SC side. At early pachytene, each stick transforms into a globule, one globule at each SC side again. At late pachytene each globule transformed into two crumbly globules containing short threads and clumps. At diplotene, globules finally transformed into thin DNA (chromatin) loops up to 10 micro long from the base to top with periodical thickenings (beads) along their length. As the result of this dynamics of transformation, two chromatin loops with beads were found on each side of SC of the chromosome 17. These loops most probably were the loops of sister chromatides, the full set of chromatide loops at the particular SC (bivalent) site being four in number, i. e. representing of two pair of chromatides. This study is the first one in which lateral chromatin loops in human mail meiotic prophase I are visualized as true open loop instead of that usually postulated "loops" after observation of condensed road-like or brush-like chromatin protrusion attached to the lateral elements of synaptonemal complexes. Open configuration of the loops, presumably, depends on activation of transcription during late pachytene-early diplotene. They resemble lateral loops of mini lampbrush chromosomes.

A Comparative Analysis of the Mole Vole Sibling Species Ellobius tancrei and E. talpinus (Cricetidae, Rodentia) through Chromosome Painting and Examination of Synaptonemal Complex Structures in Hybrids

A comparative genomic analysis was carried out in the mole vole sibling species Ellobius tancrei and E. talpinus. Performing fluorescent in situ hybridisation (Zoo-FISH) using chromosome paints from the field vole Microtus agrestis showed no differences in the allocation of syntenic groups in the karyotypes of these sibling species. The only difference between their karyotypes was the position of the centromere in one pair of chromosomes, which is assumed to be the result of an inversion. To verify this hypothesis, we analysed chromosome synapsis in prophase I of meiosis. We utilised a synaptonemal complex (SC) surface-spreading technique to visualise the process of chromosome synapsis in the spermatocytes and oocytes of first-generation hybrids and back-crosses of these sibling species. In prophase I of meiosis, immunocytochemical and electron microscopy analyses revealed that all bivalents had been fully adjusted. Even in the case of a submetacentric-acrocentric bivalent with different centromere locations, synapsis of SC lateral elements was fulfilled along the entire length of the chromosomes and the formation of an inversion loop was not observed. We hypothesise that a possible mechanism leading to the change in centromere position is the repositioning and/or generation of a neocentromere. Despite the great similarity in the karyotypes of these sibling species, they exhibited significant genomic diversification, which manifested as hybrid sterility and parous female death.

Asynaptic meiosis in fission yeast?

Meiotic prophase has been studied by both light and electron microscopy in diploid cell lines (h+/h-) of Schizosaccharomyces pombe. One wild-type and one mutant strain were used, the latter (mei4-B2) being blocked after premeiotic DNA synthesis and after commitment to meiosis. Meiosis and sporulation were induced in liquid culture by a shift to a sporulation medium devoid of a nitrogen source. The time course was determined from light-microscopic preparations; most cells passing through meiotic prophase between 5 and 8 h after the shift. In samples from that interval, ca. 20% of the nuclei were elongate in shape, containing strands of chromatin in rough alignement with the long axis of the nucleus. This stage was found to accumulate in the mutant. A bundle of microtubules, just outside of the spindle plaque, apparently stabilized the elongated shape of the nuclei. Linear electron-dense structures were observed to populate these nuclei. They resembled unpaired lateral elements of synaptonemal complexes in other organisms. Yet, at no times did we observe a tripartite complex or any other sign of chromosomal pairing in our material.

Meiotic failure in male mice lacking an X-linked factor

Meiotic silencing of sex chromosomes may cause their depletion of meiosis-specific genes during evolution. Here, we challenge this hypothesis by reporting the identification of TEX11 as the first X-encoded meiosis-specific factor in mice. TEX11 forms discrete foci on synapsed regions of meiotic chromosomes and appears to be a novel constituent of meiotic nodules involved in recombination. Loss of TEX11 function causes chromosomal asynapsis and reduced crossover formation, leading to elimination of spermatocytes, respectively, at the pachytene and anaphase I stages. Specifically, TEX11-deficient spermatocytes with asynapsed autosomes undergo apoptosis at the pachytene stage, while those with only asynapsed sex chromosomes progress. However, cells that survive the pachytene stage display chromosome nondisjunction at the first meiotic division, resulting in cell death and male infertility. TEX11 interacts with SYCP2, which is an integral component of the synaptonemal complex lateral elements. Thus, TEX11 promotes initiation and/or maintenance of synapsis and formation of crossovers, and may provide a physical link between these two meiotic processes.

Expression and Inheritance of a desynaptic phenotype with impaired homologous synapsis in rye

The cytological phenotype was studied in a desynaptic form isolated from a population of rye cultivar Vyatka. The primary defect of desynaptic plants was identified as nonhomologous (heterologous) chromosome synapsis, which was observed by electron microscopy of synaptonemal complexes (SCs) in meiotic prophase I. Synapsis defects involved switches of synapsing axial elements to nonhomologous partners, asynapsis in the switching region, and foldbacks formed by the SC lateral elements. Defective bivalent formation was observed at later stages: the univalent number varied and multivalent chromosome associations were observed in single cells in metaphase I. The desynaptic phenotype was controlled by two recessive genes, sy8a and sy8b, which acted and were inherited independently. In a hybrid combination with line Ku-2/63, the desynaptic phenotype was suppressed by the dominant allele of a third gene for inhibitor I; the segregation in hybrid families corresponded to 57:7.

Expression of two testis-specific genes, TSGA10 and SYCP3, in different cancers regarding to their pathological features

Background Cancer–testis genes are a group of genes expressed in testicular germinal cells and a range of human cancers. Testis-specific gene A10 (TSGA10) is expressed in testis and actively dividing and fetal differentiating tissues. Mouse homologue (Tsga10) mRNA is translated to a 65 kDa protein and appears to be processed to a major fibrous sheath protein of sperm tail. SYCP3 gene is supposed to be a testis-specific gene and constitutes the core of the lateral elements of synaptonemal complex. It has role in regulating DNA binding to the chromatid axis, sister chromatid cohesion, synapsis, and recombination. Methods In this study expression of TSGA10 and SYCP3 were investigated in different cancers (156 tumor samples) using RT-PCR. Diagnosis of cancer was based on histopathological reports. The association with histopathological characteristics of tumors was analyzed using statistical programs. Results TSGA10 expression was observed in 83% of brain tumors, 66% of breast cancers, 58% of gastrointestinal tumors, 66% of skin tumors and 53% of soft tissue tumors. But, SYCP3 transcripts were found in four tumor samples (moderately differentiated gemistocytic astrocytoma, pituitary adenoma, glioma and an ovarian tumor). Conclusion These results may get further insight into TSGA10, but not SYCP3, potential role as a cancer marker and a cancer testis gene implicated in tumorogenesis of cancers.

In Silico Identification and Characterization of Meiotic DNA: AluJb Possibly Participates in the Attachment of Chromatin Loops to Synaptonemal Complex

Earlier, using bioinformatic methods, we reported the identification of repeated DNA sequences (RS), presumably responsible for the attachment of chromatin loops to the lateral elements of synaptonemal complex in meiotic chromosomes. In the present study, consensus sequences for this class of RS were identified. It was demonstrated that at least part of these sequences belonged to the AluJb subfamily of Alu sequences. The Alu copies distribution along the major human histocompatibility complex (MHC) and their spatial separation from the sites of meiotic recombination was examined. It was demonstrated that simple sequences, like (GC/CA)n, were flanking meiotic recombination sites. A model of the RS organization in meiotic chromosome, most efficiently linking experimental data on the meiotic recombination in MHC and the in silico data on the RS localization (the coefficient of multiple correlation, r = 0.92) is suggested.

Meiotic mutations in rye Secale cereale L.

Spontaneous meiotic mutations of winter rye Secale cereale L. (2n = 14) were revealed in inbred F₂ progenies, which were obtained by self-pollination of F₁ hybrids resulting from crosses of individual plants of cultivar Vyatka or weedy rye with plants of self-fertile inbred lines. The mutations cause partial or complete sterility, and are maintained in heterozygote condition. Six types of mutations were distinguished as the result of cytological analysis of meiosis and genetic analysis. (1) Plants with nonallelic asynaptic mutations sy1 and sy9 lacked bivalents in 96.8 and 67.0% metaphase I cells, respectively, formed only axial elements but not the mature synaptonemal complex (SC), and had defects in telomere clustering in early prophase I. (2) Weak asynaptic mutant sy3 showed incomplete synapsis at the start of SC degradation at diplotene and lower chiasma number; yet only 2% meiocytes lacked bivalents in MI. (3) Mutations sy2, sy6, sy7, sy8, sy10, and sy19 caused nonhomologous synapsis; i.e., a varying number of univalents and occasional multivalents were observed in MI, which was preceded by switches of pairing partners and fold-back synapsis at mid-prophase I. (4) Mutation mei6 led to the formation of protrusions and minor branched structures of the SC lateral elements. (5) Allelic mutations mei8 and mei8-10 caused irregular chromatin condensation along the chromosome length in prophase I, which was accompanied by chromosome sticking and fragmentation in MI. (6) Allelic mutations mei5 and mei10 determined chromosome supercondensation, caused the disturbance of meiotic spindle assembly, arrested meiosis at various stages but did not affect formation of the pollen wall, thus arrested meiocytes got covered with the pollen wall. Analysis of double mutants revealed recessive epistatic interactions for some mutations; the epistatic group was sy9 > sy1 > sy3 > sy19. This reflects the sequence of meiotic events controlled by the corresponding genes. The expression of sy2 and sy19 proved to be modified by additional genes. Most meiotic mutations found in rye have analogs in other plants.

S. pombe meiotic linear elements contain proteins related to synaptonemal complex components.

The fission yeast Schizosaccharomyces pombe does not form synaptonemal complexes (SCs) in meiotic prophase nuclei. Instead, thin threads, the so-called linear elements (LEs), are observed at the corresponding stages by electron microscopy. Here, we demonstrate that S. pombe Rec10 is a protein related to the Saccharomyces cerevisiae SC protein Red1 and that it localizes to LEs. Moreover, a homologue to S. cerevisiae Hop1 does exist in S. pombe and we show by in situ immunostaining that it, and the kinase Mek1 (a homologue of which is also known to be associated with SCs), localizes to LEs. These observations indicate the evolutionary relationship of LEs with the lateral elements of SCs and suggest that these structures might exert similar functions in S. cerevisiae and S. pombe.

Localization of DNA Sequences Tightly Associated with the Synaptonemal Complex in Compositional Fractions of the Golden Hamster Genome*

Synaptonemal complex (SC) isolated from spermatocyte nuclei after their exhaustive hydrolysis by DNase II contains DNA sequences tightly associated with it (SCAR DNA). Here, the compositional properties of a cloned family of golden hamster SCAR DNA were studied. For this purpose, 27 SCAR DNA clones were hybridized with compositionally fractionated golden hamster genomic DNA. The sequences of the SCAR DNA family were mainly localized in the GC-poor isochore families L1 and L2, which accounted for 63% of hybridization signals. The remaining 37% of signals pertained to the GC-rich isochore families H1 and H2. Thus, SCAR DNA proved to be distributed throughout the genome, irrespective of differences in density and sequence type between isochore families. Moreover, the SCAR DNA sequences containing the regions of homology with LINE/SINE repeats were found in all the isochore families. The compositional localization of SCAR DNA is in agreement with the hypothesis that the SC and SCAR DNA participate in chromatin reorganization during meiosis prophase I, which should result in the attachment of chromatin loops to the lateral elements of SC throughout its length.

Meiotic sister chromatid cohesion in holocentric sex chromosomes of three heteropteran species is maintained in absence of axial elements.

It has been suggested that in species with monocentric chromosomes axial element (AE) components may be responsible for sister chromatid cohesion during meiosis. To test this hypothesis in species with holocentric chromosomes we selected three heteropteran species with different sex-determining mechanisms. We observed in surface-spreads and sections using transmission electron microscopy that the univalent sex chromosomes form neither AEs nor synaptonemal complexes (SCs) during pachytene. We also found that a polyclonal antibody recognizing SCP3/Cor1, a protein present at AEs and SC lateral elements of rodents, labels the autosomal SCs but not AEs or SC stretches corresponding to the sex chromosomes. Cytological analysis of the segregational behaviour of the sex univalents demonstrates that although these chromosomes segregate equationally during anaphase I they never show precocious separation of sister chromatids during late prophase I or metaphase I. These results suggest that AEs are not responsible for sister cohesion in sex chromosomes. The segregational behaviour of these chromosomes during both meiotic divisions also indicates that different achiasmate modes of chromosome association exist in heteropteran species.