Relevant bibliographies by topics / Synaptonemal Complex

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Synaptonemal Complex'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Synaptonemal Complex"

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Lake, Cathleen M., and R. Scott Hawley. "Synaptonemal complex." Current Biology 31, no. 5 (March 2021): R225—R227. http://dx.doi.org/10.1016/j.cub.2021.01.015.

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Gillies, C. B. "Synaptonemal complex." Genome 31, no. 1 (January 1, 1989): 439–40. http://dx.doi.org/10.1139/g89-069.

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Heyting, C., A. J. J. Dietrich, P. B. Moens, R. J. Dettmers, H. H. Offenberg, E. J. W. Redeker, and A. C. G. Vink. "Synaptonemal complex proteins." Genome 31, no. 1 (January 1, 1989): 81–87. http://dx.doi.org/10.1139/g89-016.

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Synaptonemal complexes were isolated from rate spermatocytes for the purpose of biochemical and morphological analysis. Several monoclonal antibodies were elicited against purified synaptonemal complexes to study the composition and assembly of these structures. Four classes of antibodies could be discriminated according to the polypeptides that they recognize on Western blots of purified synaptonemal complexes, namely antibodies recognizing (i) a 190-kDa polypeptide; (ii) a 30- and a 33-kDa polypeptide; (iii) two polypeptides with molecular weights of about 120 kDa; and (iv) polypeptides with molecular weights of 66–55 kDa. The localization of these antigens within spermatocytes was analyzed light microscopically, by means of the immunoperoxidase technique and ultrastructurally, by immunogold labelling of surface-spread spermatocytes. The 66-to 55-kDa polypeptides are not confined to synaptonemal complexes; rather, these polypeptides appear to be chromosomal components. The 190-, 30-, and 33-kDa polypeptides make part of the lateral elements of paired as well as unpaired segments of synaptonemal complexes. The 120-kDa polypeptides were localized on the inner edge of the lateral elements, specifically in paired segments of synaptonemal complexes. The distribution of the 190-, 120-, 30-, and 33-kDa polypeptides within the testis was analyzed by immunofluorescence staining of cryostat sections. All these polypeptides turned out to be specific for nuclei of zygotene up to and including diplotene spermatocytes. Only in some early spermatids could the 190-, 30-, and 33-kDa polypeptides be detected, presumably in remnants of synaptonemal complexes. We conclude that the lateral elements of synaptonemal complexes do not arise by rearrangement of pre-existing components in the nucleus, but that their major components are newly synthesized during meiotic prophase.Key words: synaptonemal complex, immunocytochemistry, meiosis.
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Fedotova, Yu S., O. L. Kolomiets, and Yu F. Bogdanov. "Synaptonemal complex transformations in rye microsporocytes at the diplotene stage of meiosis." Genome 32, no. 5 (October 1, 1989): 816–23. http://dx.doi.org/10.1139/g89-516.

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The process of synaptonemal complex degradation during diplotene was studied in spreads of rye microsporocytes stained with silver nitrate at pH 3.5–4.5 and 6.0–8.0. Two different patterns of the synaptonemal complex degradation process have been observed, depending on the two staining procedures used. Progressive synaptonemal complex fragmentation observable at the higher pH appeared to be absent in staining at pH 3.5–4.5: thin connecting threads have been found in the "gaps" between the synaptonemal complex segments. Complete tracing of the synaptonemal complex degradation process was attempted and revealed the following successive steps: (i) local repulsion of lateral elements; (ii) lateral element looping in the regions of repulsion; (iii) extension of the loops; (iv) transformation of the extended loops into coils of irregular shape with a diameter of about 2 μm and a pitch of about 1.2 μm; and (v) formation of paired beanlike thickenings on a gyral coil. In asynaptic mutant sy-9 unpaired lateral elements are transformed without looping into a similar coil but with single beanlike thickenings. We conclude that synaptonemal complex lateral element loops at diplotene are invisible after the routine silver staining of microspreads (at pH about 6 and higher) and look like gaps between discontinuous synaptonemal complex segments, thus simulating the process of synaptonemal complex fragmentation.Key words: synaptonemal complex, diplotene, rye.
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Grishayeva, T. M., and Y. F. Bogdanov. "Dependence on genie balance for synaptonemal complex formation in Drosophila melanogaster." Genome 30, no. 2 (April 1, 1988): 258–64. http://dx.doi.org/10.1139/g88-044.

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Electron microscopic examination of gonads of Drosophila melanogaster with different genotypes, including a metafemale 3X;2A and an intersex XXY;3A, have revealed that the formation of synaptonemal complexes is controlled by the genie balance, i.e., the ratio of X chromosomes to autosomes. The Y chromosome is not involved in the genetic control of the formation of precursors of the central element of synaptonemal complexes in males, nor does it disturb their formation in [Formula: see text] females. Hyperploidy for sections 1 – 3A and 18A – 20 of the X chromosome does not lead to the appearance of synaptonemal complexes in males and does not interfere with their formation in females. Females hyperploid for extensive regions of the X chromosome (sections 1 – 11A, 11A – 20, and 8C – 20) are fertile and show apparently normal formation of synaptonemal complexes. Hyperploidy for sections 8C – 11A of the X results in a sharp decrease in the viability of females, in abnormal differentiation of ovary cells, and in the lack of synaptonemal complexes. These data suggest a possible important role for the sections 8C – 11A in the genic balance controlling the formation of synaptonemal complexes in D. melanogaster. The lack of synaptonemal complexes in hypoploid females may be the result of abnormal cell differentiation in gonads.Key words: Drosophila melanogaster, synaptonemal complex, sex chromosomes, genic balance.
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Wallace, B. M. N., and H. Wallace. "Synaptonemal complex karyotype of zebrafish." Heredity 90, no. 2 (February 2003): 136–40. http://dx.doi.org/10.1038/sj.hdy.6800184.

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Loidl, J., and G. H. Jones. "Synaptonemal complex spreading in Allium." Chromosoma 93, no. 5 (April 1986): 420–28. http://dx.doi.org/10.1007/bf00285824.

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Benavente, Ricardo. "The synaptonemal complex—50 years." Chromosoma 115, no. 3 (February 11, 2006): 151. http://dx.doi.org/10.1007/s00412-006-0050-z.

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Greenbaum, Ira F., David W. Hale, Philip D. Sudman, and Eviatar Nevo. "Synaptonemal complex analysis of mole rats (Spalax ehrenbergi): unusual polymorphisms of chromosome." Genome 33, no. 6 (December 1, 1990): 898–902. http://dx.doi.org/10.1139/g90-135.

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Two unusual structural polymorphisms in the largest chromosomal pair of the Israeli mole rat, Spalax ehrenbergi, were analyzed from surface-spread and silver-stained preparations of synaptonemal complexes. A C-band negative polymorphism for the length of the 1p arm was visible as axial length differences during late zygonema and early pachynema. This region underwent synaptic adjustment resulting in a fully paired, mid-pachytene synaptonemal complex with equalized axial lengths. The somatically variable and nonargentophilic secondary constriction in the 1q arm was evident as a distinct silver-stained thickening along the synaptonemal complex. Presence of this structure on the synaptonemal complex varied both among individuals and among cells within individuals. The intraindividual variation of this region is hypothesized to represent differential biochemical activity with its cellular visualization being regulated in a manner similar to that of nucleolus organizer regions.Key words: mole rats, synaptonemal complex, chromosomal polymorphism.
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Sherman, Jamie D., Stephen M. Stack, and Lorinda K. Anderson. "Two-dimensional spreads of synaptonemal complexes from solanaceous plants. IV. Synaptic irregularities." Genome 32, no. 5 (October 1, 1989): 743–53. http://dx.doi.org/10.1139/g89-507.

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Irregularities in the structure of synaptonemal complexes have been reported in a wide variety of organisms, but so far there has been no study concentrating on synaptic irregularities per se. We have used a hypotonic bursting technique to spread synaptonemal complexes from autotetraploid Solanum tuberosum (potato) and diploid, tetraploid, and trisomic Lycopersicon esculentum (tomato). In this study we observed most of the synaptic irregularities that have been reported in other organisms as well as an irregularity that has not been illustrated previously (lateral element buckles containing additional synaptonemal complex components). These observations have been used to provide partial answers to the following questions about the formation of the synaptonemal complex. (i) In what way does homology affect synapsis? (ii) What controls multiple synapsis? (iii) What is the relationship of synaptonemal complex components to chromatin and to each other? (iv) Do lateral elements have structural or functional polarity?Key words: synaptonemal complexes, synapsis, synaptic irregularities, solanaceous plants.
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Dissertations / Theses on the topic "Synaptonemal Complex"

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Jones, Marion. "Synaptonemal complex formation in Avena." Thesis, Cardiff University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278231.

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Yuan, Li. "Meiotic chromosome segregation : molecular analysis of the synaptonemal complex /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4078-9/.

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Eichinger, Christian. "Coordination of synaptonemal complex formation and pachytene checkpoint signaling in meiosis." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-103668.

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Ahuja, Jasvinder Singh. "A ROLE OF THE PROTEASOME IN RECOMBINATION AND SYNAPTONEMAL COMPLEX MORPHOGENESIS." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1418175456.

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Campos, Ramos Rafael. "The synaptonemal complex and analysis of sex chromosomes in the genus Oreochromis." Thesis, University of Stirling, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249166.

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Newnham, Louise Joanna. "Regulation and function of the Synaptonemal Complex during meiosis in Saccharomyces cerevisiae." Thesis, University of Sussex, 2010. http://sro.sussex.ac.uk/id/eprint/2421/.

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The Synaptonemal Complex (SC) is a proteinaceous structure that connects homologous chromosomes lengthwise during meiotic prophase. In budding yeast, the SC consists of two parallel axes that become connected by the central element protein, Zip1 that extends along the chromosome axes (Sym, Engebrecht et al. 1993). Extension of the SC is coordinated to crossover formation by a group of proteins known as the ‘ZMM's (Zip1, Zip2, Zip3, Zip4, Msh4, Msh5 and Mer3) (Borner, Kleckner et al. 2004). Work outlined here demonstrates a role for the mismatch repair paralogue, Msh4 in preventing SC extension from being de-coupled from crossover formation. Furthermore, increased temperature serves as a positive effector for this decoupling. These findings suggest that SC extension is highly regulated to ensure that it is coupled with crossing over. As well as its role in crossover formation (Storlazzi, Xu et al. 1996), the work outlined here demonstrates an independent role for Zip1 in promoting the segregation of non-exchange chromosome pairs (NECs). Zip1 pairs the centromeres of NECs in pachytene through to metaphase I, where it aids their segregation at the first meiotic division. The localisation and function of Zip1 at the centromeres of non-exchange chromosomes depends on Zip3 and Zip2, respectively. Zip1 is observed at the centromeres of all chromosomes following SC disassembly through to the first meiotic division, where it promotes the segregation of exchange pairs also. A model is suggested whereby Zip1 promotes the segregation of both non-exchange and exchange chromosome pairs by tethering homologous centromeres throughout meiotic prophase. Finally, a parallel pathway for NEC segregation is also described that depends upon the spindle checkpoint component, Mad3. When both ZIP1 and MAD3 are deleted, NECs segregate at random.
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Prugar, Evelyn. "Synaptonemal complex disassembly activates Rad51-mediated double strand break repair during budding yeast meiosis." Thesis, State University of New York at Stony Brook, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10170526.

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Meiosis is a highly conserved specialized cell division that occurs in many organisms, including budding yeast and mammals. Meiosis divides the chromosome number of the cell in half to create gametes for sexual reproduction. A single round of chromosome duplication is followed by two rounds of chromosome segregation, Meiosis I (homologs segregate) and Meiosis II (sister chromatids segregate). Proper segregation at Meiosis I requires that homologs are connected by both crossovers and sister chromatid cohesion. Crossovers are formed by the repair of double strand breaks (DSBs) preferentially by the homolog. The choice of repair template is determined at the time of strand invasion, which is mediated by two recombinases, Rad51 and the meiosis-specific Dmc1. Rad51 is necessary for Dmc1 to function properly but its strand exchange activity is inhibited both by Dmc1 and Mek1, a meiosis-specific kinase, which is activated by DSBs. Mek1 suppresses interaction between Rad51 and its accessory factor Rad54 in two ways. First, phosphorylation of Rad54 lowers its affinity for Rad51. Second, phosphorylation stabilizes Hed1, a meiosis-specific protein that binds to Rad51 and excludes Rad54. Although RAD54 is not required for wild-type levels of interhomolog recombination, rad54Δ diploids exhibit decreased sporulation and spore viability, indicating the presence of unrepaired DSBs. My thesis tested the idea that Mek1 kinase activity is down-regulated after interhomolog recombination to allow Rad51-mediated repair of any remaining DSBs.

Meiotic recombination occurs in the context of a proteinaecous structure called the synaptonemal complex (SC). The SC is formed when sister chromatids condense along protein cores called axial elements (AEs) comprised of the meiosis-specific proteins, Hop1, Red1 and Rec8. AEs are brought together by interhomolog recombination, which creates stable connections and the gluing together of the AEs by the insertion of the transverse filament protein, Zip1, in a process called synapsis. Pachynema is the stage of meiotic prophase in which chromosomes are fully synapsed and where interhomolog recombination has proceeded to the double Holliday junction (dHJ) stage.

Meiotic progression requires transcription factor NDT80, a middle meiosis transcription factor required to express >200 genes, including the polo-like kinase, CDC5 (required for Holliday junction resolution and SC disassembly) and CLB1 (required for meiotic progression). Diploids deleted for NDT80 arrest in pachynema with unresolved dHJs. I used an inducible version of NDT80 (NDT80-IN ) to separate prophase into two phases: pre-NDT80, when interhomolog recombination occurs and post-NDT80, when it is proposed that inactivation of Mek1 allows intersister recombination to repair residual DSBs. RAD54 is sufficient to function after interhomolog recombination, as inducing both RAD54 and NDT80 simultaneously rescues the spore inviability defects observed in NDT80-IN rad54Δ diploids. Using an antibody specific for phosphorylated Hed1 as an indicator of Mek1 kinase activity, I showed that Mek1 is constitutively active in ndt80-arrested cells and that induction of NDT80 is sufficient to abolish Mek1 activity. Furthermore, inactivation of Mek1 by Ndt80 can occur in the absence of interhomolog strand invasion and synapsis. Mek1 inactivation correlates with the appearance of CDC5 and the degradation of Red1. My work demonstrates that the sole target of NDT80 responsible for inactivating Mek1 is CDC5.

Unrepaired DSBs trigger the meiotic recombination checkpoint resulting in prophase arrest, which requires Mek1 and works by sequestering Ndt80 in the cytoplasm. Mek1 also delays meiotic progression in wild-type cells, likely through inactivation of Ndt80. My work shows that Ndt80 in turn negatively regulates Mek1. Based on my observations, as well as published work showing that synapsis results in the removal of Mek1 from chromosomes, I propose that recombination and meiotic progression are coordinated by regulation of Mek1.

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Brockway, Heather Marie. "A role for the CSN/COP9 signalosome in synaptonemal complex assembly and meiotic progression." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1296.

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Defects in meiotic prophase I events, resulting in aneuploidy, are a leading cause of birth defects in humans; however, these are difficult to study in mammalian systems due to their occurrence very early in development. The nematode, Caenorhabditis elegans, is an excellent model for prophase I studies as its gonad is temporally and spatially organized around these meiotic events. Homolog pairing, synapsis, meiotic recombination and crossover formation are essential to the proper segregation of chromosomes into the respective gametes, either the egg or sperm. Disturbances in these events leads to missegregation of chromosomes in the gametes in the meiotic divisions. Synapsis is especially critical in meiosis as it precedes and is required for meiotic recombination in C. elegans. The formation of the synaptonemal complex (SC) is fundamental to chromosomal synapsis, yet the molecular mechanisms of synaptonemal complex morphogenesis are largely unknown. The investigations described in this thesis were undertaken to better understand the molecular contributions to synaptonemal complex morphogenesis. Chapter One reviews knowledge of morphogenesis and its relationship to the events of meiotic prophase I. Recent studies in our laboratory have implicated AKIRIN, a nuclear protein with multiple biological functions, as having a role in synaptonemal complex disassembly, specifically preventing the aggregation of synaptonemal proteins (Clemons et al., 2013). As a result of our efforts to discern the mechanism by which AKIRIN regulates disassembly, we found that the highly conserved CSN/COP9 signalosome has a role in SC assembly, leading to defects in prophase I events and in MAPK signaling , leading to the arrest of nuclei in the later stages of meiosis. While the CSN/COP9 signalosome has been implicated in general fertility in C. elegans (Pintard et al., 2003), no role had been defined in earlier meiotic stages until this study. Chapter Two describes an RNAi enhancer/suppressor screen undertaken in the akir-1 mutant background. Several RNAi clones were selected for future study based on a reduction in brood size; one of which, csn-5/, is the focus of the analysis presented in Chapter 3. Chapter Three describes the phenotypic characterization of two CSN/COP9 signalosome subunits, csn-2 and csn-5. Alleles of both genes display synaptonemal complex protein aggregation and defects in mitotic cell proliferation, homologous chromosome pairing, meiotic recombination and crossover formation, leading to an increase in apoptosis. Oocyte maturation is also disrupted by a lack of MAPK signaling, resulting in a lack of viable oocytes, which renders the csnmutant homozygotes sterile. These findings support a model suggesting the CSN/COP9 signalosome has an essential role in regulating meiotic prophase I events and oocyte maturation. Chapter 4 describes the methodology used in this study. Chapter 5 provides a summary of the thesis findings and examines the future directions to extend this work.
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Fraune, Johanna [Verfasser], Ricardo [Gutachter] Benavente, and Manfred [Gutachter] Schartl. "The evolutionary history of the mammalian synaptonemal complex / Johanna Fraune. Gutachter: Ricardo Benavente ; Manfred Schartl." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1110915446/34.

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Tarsounas, Madalina Cecilia. "Synaptonemal complex proteins, post-translational modifications, protein-protein interactions and interaction with the rad51/dmc1 recombinases." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0007/NQ39313.pdf.

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Books on the topic "Synaptonemal Complex"

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Albini, Susan Margaret. Synaptonemal complex studies in Allium species. Birmingham: University of Birmingham, 1986.

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Ghosh, Ruby. Synaptonemal complex studies in higher plants. Birmingham: University of Birmingham, 1996.

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Zavala, Daniel A. F. Villagomez. Synaptonemal complex analysis of chromosome translocations in pigs and cattle. Uppsala: Sveriges Lantbruksuniversitet, 1993.

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Hernández-Hernández, Abrahan. Epigenetics of the Synaptonemal Complex. INTECH Open Access Publisher, 2012.

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Dookheran, Michelle Samantha. In situ hybridization on Lilium longiflorum whole mount chromosome synaptonemal complex spread preparations. 1996.

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Book chapters on the topic "Synaptonemal Complex"

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Haaf, T., A. Machens, and M. Schmid. "Human Autoantibodies to Synaptonemal Complex." In Molecular and Cell Biology of Autoantibodies and Autoimmunity. Abstracts, 23–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-46681-6_21.

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Spangenberg, Victor. "FISH—and the Characterization of Synaptonemal Complex." In Cytogenetics and Molecular Cytogenetics, 297–305. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003223658-25.

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Yang, F., and P. J. Wang. "The Mammalian Synaptonemal Complex: A Scaffold and Beyond." In Meiosis, 69–80. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000166620.

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Armstrong, Susan. "Analysis of the Synaptonemal Complex in Brassica Using TEM." In Methods in Molecular Biology, 159–66. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-333-6_16.

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Moses, M. J., P. A. Poorman, M. E. Dresser, G. K. DeWeese, and J. B. Gibson. "The Synaptonemal Complex in Meiosis: Significance of Induced Perturbations." In Aneuploidy, 337–52. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2127-9_23.

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Loidl, J. "The questionable role of the synaptonemal complex in meiotic chromosome pairing and recombination." In Chromosomes Today, 287–300. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1510-0_22.

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Stack, Stephen M., Lindsay A. Shearer, Leslie D. Lohmiller, and Lorinda K. Anderson. "Preparing Maize Synaptonemal Complex Spreads and Sequential Immunofluorescence and Fluorescence In Situ Hybridization." In Methods in Molecular Biology, 79–115. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9818-0_8.

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Cuñado, Nieves. "Surface Spreading Technique in Plant Meiocytes for Analysis of Synaptonemal Complex by Electron Microscopy." In Methods in Molecular Biology, 181–96. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9818-0_13.

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Darrier, Benoit, Mikel Arrieta, Sybille U. Mittmann, Pierre Sourdille, Luke Ramsay, Robbie Waugh, and Isabelle Colas. "Following the Formation of Synaptonemal Complex Formation in Wheat and Barley by High-Resolution Microscopy." In Methods in Molecular Biology, 207–15. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9818-0_15.

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Maguire, Marjorie P. "Techniques for Preparing Whole-Mount Spreads of Maize Pachytene Chromosome Complements for Electron-Microscopic Visualization of Synaptonemal Complex Structures." In The Maize Handbook, 442–46. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2694-9_67.

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Conference papers on the topic "Synaptonemal Complex"

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Kitano, Haruhisa, Joon-Yong Chung, Jun Hanaoka, Shuhei Inoue, Doki Yoshinori, Junya Fukuoka, and Stephen M. Hewitt. "Abstract 5184: Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5184.

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Atsayeva, Maret M., Zura I. Bisultanova, Petimat M. Dzhambetova, Nadezhda Yu Oyun, and Oksana L. Kolomiets. "The Study of the Transgeneration Genotoxic Effect of Drugs Based on the Analysis of Synaptonemal Complexes in Mouse Spermatocytes." In Proceedings of the International Symposium “Engineering and Earth Sciences: Applied and Fundamental Research” (ISEES 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/isees-18.2018.27.

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