Initiation and progression of homologous chromosome synapsis in Crepis capillaris: Variations on a theme

Genome ◽  
1999 ◽  
Vol 42 (5) ◽  
pp. 867-873 ◽  
Author(s):  
R. Banerjee ◽  
G.H. Jones
Keyword(s):  
Homologous Chromosome ◽  
Crepis Capillaris ◽  
Chromosome Synapsis ◽  
Variations On A Theme

Initiation and progression of homologous chromosome synapsis in Crepis capillaris: Variations on a theme

Genome ◽  
1999 ◽  
Vol 42 (5) ◽  
pp. 867-873 ◽  
Author(s):  
R Banerjee ◽  
G H Jones
Keyword(s):  
Synaptonemal Complex ◽  
Plant Species ◽  
Homologous Chromosome ◽  
Chromosome Length ◽  
Large Sample ◽  
Crepis Capillaris ◽  
Chromosome Synapsis ◽  
Meiotic Synapsis ◽  
Mother Cells ◽  
Variations On A Theme

The model cytogenetic plant species Crepis capillaris (2x = 6), in which all 3 chromosomes are readily distinguished, was used to analyse the initiation and progression of meiotic synapsis in a large sample of spread and silver-stained pollen mother cells. Particular emphasis was placed on detecting general patterns or trends of synaptic order, both among different bivalents and within (along) individual bivalents, and investigating the consistency or otherwise of these synaptic patterns. The order of synaptic progression and completion was partly related to chromosome length; as in other species, shorter bivalents tended to complete synapsis ahead of longer ones. Individual bivalents also showed distinct patterns of synapsis, with a tendency for subterminal regions to initiate synapsis early, followed by multiple synaptic initiations in internal bivalent regions. However, the analysis showed that these synaptic patterns are only general trends and significant variations in synaptic order and pattern, among and within bivalents, occur in individual cells.Key words: meiosis, synapsis, synaptonemal complex, Crepis.

scholarly journals Tex19.1 Regulates Meiotic DNA Double Strand Break Frequency in Mouse Spermatocytes

2017 ◽  
Author(s):  
James H. Crichton ◽  
Christopher J. Playfoot ◽  
Marie MacLennan ◽  
David Read ◽  
Howard J. Cooke ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
Meiotic Recombination ◽  
Homologous Chromosome ◽  
E3 Ubiquitin Ligase ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Genetic Pathway ◽  
Strand Breaks ◽  
Chromosome Synapsis ◽  
Meiotic Dsbs

AbstractMeiosis relies on the SPO11 endonuclease to generate the recombinogenic DNA double strand breaks (DSBs) required for homologous chromosome synapsis and segregation. The number of meiotic DSBs needs to be sufficient to allow chromosomes to search for and find their homologs, but not excessive to the point of causing genome instability. Here we report that meiotic DSB frequency in mouse spermatocytes is regulated by the mammal-specific gene Tex19.1. We show that the chromosome asynapsis previously reported in Tex19.1-/- spermatocytes is preceded by reduced numbers of recombination foci in leptotene and zygotene. Tex19.1 is required for the generation of normal levels of Spo11-dependent DNA damage during leptotene, but not for upstream events such as MEI4 foci formation or accumulation of H3K4me3 at recombination hotspots. Furthermore, we show that mice carrying mutations in the E3 ubiquitin ligase UBR2, a TEX19.1-interacting partner, phenocopy the Tex19.1-/- recombination defects. These data show that Tex19.1 and Ubr2 are required for mouse spermatocytes to generate sufficient meiotic DSBs to ensure that homology search is consistently successful, and reveal a hitherto unknown genetic pathway regulating meiotic DSB frequency in mammals.Author SummaryMeiosis is a specialised type of cell division that occurs during sperm and egg development to reduce chromosome number prior to fertilisation. Recombination is a key step in meiosis as it facilitates the pairing of homologous chromosomes prior to their reductional division, and generates new combinations of genetic alleles for transmission in the next generation. Regulating the amount of recombination is key for successful meiosis: too much will likely cause mutations, chromosomal re-arrangements and genetic instability, whereas too little causes defects in homologous chromosome pairing prior to the meiotic divisions. This study identifies a genetic pathway requiredto generate robust meiotic recombination in mouse spermatocytes. We show that male mice with mutations in Tex19.1 or Ubr2, which encodes an E3 ubiquitin ligase that interacts with TEX19.1, have defects in generating normal levels of meiotic recombination. We show that the defects in these mutants impact on the recombination process at the stage when programmed DNA double strand breaks are being made. This defect likely contributes to the chromosome synapsis and meiotic progression phenotypes previously described in these mutant mice. This study has implications for our understanding of how this fundamental aspect of genetics and inheritance is controlled.

scholarly journals Cyclin B3 is dispensable for mouse spermatogenesis

2019 ◽  
Author(s):  
Mehmet E. Karasu ◽  
Scott Keeney
Keyword(s):  
Homologous Chromosome ◽  
Histological Analysis ◽  
Seminiferous Tubules ◽  
Specific Expression ◽  
Cyclin Dependent Kinases ◽  
Meiotic Progression ◽  
Chromosome Synapsis ◽  
Cyclin E2 ◽  
Sexual Production ◽  
Cyclin B3

AbstractCyclins, as regulatory partners of cyclin-dependent kinases (CDKs), control the switch-like cell cycle transitions that orchestrate orderly duplication and segregation of genomes. Compared to mitosis, relatively little is known about how cyclin-CDK complexes control meiosis, the specialized cell division that generates gametes for sexual production. Mouse cyclin B3 was previously shown to have expression restricted to the beginning of meiosis, making it a candidate to regulate meiotic events. Indeed, female mice lacking cyclin B3 are sterile because oocytes arrest at the metaphase-to-anaphase transition of meiosis I. However, whether cyclin B3 functions during spermatogenesis was untested. Here, we found that males lacking cyclin B3 are fertile and show no detectable defects in spermatogenesis based on histological analysis of seminiferous tubules. Cytological analysis further showed no detectable defects in homologous chromosome synapsis or meiotic progression, and suggested that recombination is initiated and completed efficiently. Moreover, absence of cyclin B3 did not exacerbate previously described meiotic defects in mutants deficient for cyclin E2, suggesting a lack of redundancy between these cyclins. Thus, unlike in females, cyclin B3 is not essential for meiosis in males despite its prominent meiosis-specific expression.

scholarly journals The Mouse RecA -like Gene Dmc1 Is Required for Homologous Chromosome Synapsis during Meiosis

1998 ◽  
Vol 1 (5) ◽  
pp. 707-718 ◽  
Author(s):  
Kayo Yoshida ◽  
Gen Kondoh ◽  
Yoichi Matsuda ◽  
Toshiyuki Habu ◽  
Yoshitake Nishimune ◽  
...  
Keyword(s):  
Homologous Chromosome ◽  
Chromosome Synapsis

scholarly journals The role of OsCOM1 in homologous chromosome synapsis and recombination in rice meiosis

2012 ◽  
Vol 72 (1) ◽  
pp. 18-30 ◽  
Author(s):  
Jianhui Ji ◽  
Ding Tang ◽  
Kejian Wang ◽  
Mo Wang ◽  
Lixiao Che ◽  
...  
Keyword(s):  
Homologous Chromosome ◽  
Chromosome Synapsis

scholarly journals The dual role of HOP2 in mammalian meiotic homologous recombination

2013 ◽  
Vol 42 (4) ◽  
pp. 2346-2357 ◽  
Author(s):  
Roberto J. Pezza ◽  
Oleg N. Voloshin ◽  
Alexander A. Volodin ◽  
Kingsley A. Boateng ◽  
Marina A. Bellani ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Homologous Chromosome ◽  
Strand Break ◽  
Dsb Repair ◽  
Chromosome Synapsis ◽  
Homologous Chromosome Pairing ◽  
Strand Invasion ◽  
High Level

Abstract Deletion of Hop2 in mice eliminates homologous chromosome synapsis and disrupts double-strand break (DSB) repair through homologous recombination. HOP2 in vitro shows two distinctive activities: when it is incorporated into a HOP2–MND1 complex it stimulates DMC1 and RAD51 recombination activities and the purified HOP2 alone is proficient in promoting strand invasion. We observed that a fraction of Mnd1−/− spermatocytes, which express HOP2 but apparently have inactive DMC1 and RAD51 due to lack of the HOP2–MND1 complex, exhibits a high level of chromosome synapsis and that most DSBs in these spermatocytes are repaired. This suggests that DSB repair catalyzed solely by HOP2 supports homologous chromosome pairing and synapsis. In addition, we show that in vitro HOP2 promotes the co-aggregation of ssDNA with duplex DNA, binds to ssDNA leading to unstacking of the bases, and promotes the formation of a three-strand synaptic intermediate. However, HOP2 shows distinctive mechanistic signatures as a recombinase. Namely, HOP2-mediated strand exchange does not require ATP and, in contrast to DMC1, joint molecules formed by HOP2 are more sensitive to mismatches and are efficiently dissociated by RAD54. We propose that HOP2 may act as a recombinase with specific functions in meiosis.

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