A Conserved Checkpoint Monitors Meiotic Chromosome Synapsis in Caenorhabditis elegans

Science ◽  
2005 ◽  
Vol 310 (5754) ◽  
pp. 1683-1686 ◽  
Author(s):  
N. Bhalla
Keyword(s):  
Caenorhabditis Elegans ◽  
Meiotic Chromosome ◽  
Chromosome Synapsis

ATM and RPA in meiotic chromosome synapsis and recombination

1997 ◽  
Vol 17 (4) ◽  
pp. 457-461 ◽  
Author(s):  
Annemieke W. Plug ◽  
Antoine H.F.M Peters ◽  
Yang Xu ◽  
Kathleen S. Keegan ◽  
Merl F. Hoekstra ◽  
...  
Keyword(s):  
Meiotic Chromosome ◽  
Chromosome Synapsis

scholarly journals X Chromosome Control of Meiotic Chromosome Synapsis in Mouse Inter-Subspecific Hybrids

PLoS Genetics ◽  
2014 ◽  
Vol 10 (2) ◽  
pp. e1004088 ◽  
Author(s):  
Tanmoy Bhattacharyya ◽  
Radka Reifova ◽  
Sona Gregorova ◽  
Petr Simecek ◽  
Vaclav Gergelits ◽  
...  
Keyword(s):  
X Chromosome ◽  
Meiotic Chromosome ◽  
Chromosome Synapsis

scholarly journals A pseudo-meiotic centrosomal function of TEX12 in cancer

2019 ◽  
Author(s):  
S Sandhu ◽  
LJ Salmon ◽  
JE Hunter ◽  
CL Wilson ◽  
ND Perkins ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Meiotic Chromosome ◽  
Cancer Therapeutics ◽  
Structural Protein ◽  
Multiple Cancer ◽  
Aberrant Expression ◽  
Homologous Chromosomes ◽  
Chromosome Synapsis ◽  
Cancer Models ◽  
The Many

AbstractCell division by meiosis involves an extraordinary chromosome choreography including pairing, synapsis and crossing over between homologous chromosomes1, 2. The many meiosis-specific genes involved in these processes also constitute a latent toolbox of chromosome remodelling and recombination factors that may be exploited through aberrant expression in cancer3, 4. Here, we report that TEX12, a structural protein involved in meiotic chromosome synapsis5–7, is aberrantly expressed in human cancers, with high TEX12 levels correlating with poor prognosis. We find that TEX12 knock-down causes proliferative failure in multiple cancer cell lines, and confirm its role in the early stages of oncogenesis through murine cancer models. Remarkably, somatically expressed TEX12 localises to centrosomes, leading to altered centrosome number and structure, features associated with cancer development. Further, we identify TEX12 in meiotic centrin-rich bodies, likely precursors of the mitotic centrosome, suggesting that this may represent an additional cellular function of TEX12 in meiosis that has been previously overlooked. Thus, we propose that an otherwise meiotic function of TEX12 in centrosome duplication is responsible for promoting oncogenesis and cellular proliferation in cancer, which may be targeted for novel cancer therapeutics and diagnostics.

Meiotic chromosome synapsis in a haploid yeast

Chromosoma ◽  
1991 ◽  
Vol 100 (4) ◽  
pp. 221-228 ◽  
Author(s):  
Josef Loidl ◽  
Knud Nairz ◽  
Franz Klein
Keyword(s):  
Meiotic Chromosome ◽  
Chromosome Synapsis

scholarly journals The AtRAD51C Gene Is Required for Normal Meiotic Chromosome Synapsis and Double-Stranded Break Repair in Arabidopsis

2005 ◽  
Vol 138 (2) ◽  
pp. 965-976 ◽  
Author(s):  
Wuxing Li ◽  
Xiaohui Yang ◽  
Zhenguo Lin ◽  
Ljudmilla Timofejeva ◽  
Rong Xiao ◽  
...  
Keyword(s):  
Meiotic Chromosome ◽  
Chromosome Synapsis ◽  
Break Repair

scholarly journals Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Sona Gregorova ◽  
Vaclav Gergelits ◽  
Irena Chvatalova ◽  
Tanmoy Bhattacharyya ◽  
Barbora Valiskova ◽  
...  
Keyword(s):  
Meiotic Chromosome ◽  
Hybrid Sterility ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Recombination Hotspots ◽  
Chromosome Synapsis ◽  
Reproductive Isolation Mechanisms ◽  
Meiotic Recombination Hotspots ◽  
Isolation Mechanisms

Hybrid sterility is one of the reproductive isolation mechanisms leading to speciation. Prdm9, the only known vertebrate hybrid-sterility gene, causes failure of meiotic chromosome synapsis and infertility in male hybrids that are the offspring of two mouse subspecies. Within species, Prdm9 determines the sites of programmed DNA double-strand breaks (DSBs) and meiotic recombination hotspots. To investigate the relation between Prdm9-controlled meiotic arrest and asynapsis, we inserted random stretches of consubspecific homology on several autosomal pairs in sterile hybrids, and analyzed their ability to form synaptonemal complexes and to rescue male fertility. Twenty-seven or more megabases of consubspecific (belonging to the same subspecies) homology fully restored synapsis in a given autosomal pair, and we predicted that two or more DSBs within symmetric hotspots per chromosome are necessary for successful meiosis. We hypothesize that impaired recombination between evolutionarily diverged chromosomes could function as one of the mechanisms of hybrid sterility occurring in various sexually reproducing species.

scholarly journals Crossing over is coupled to late meiotic prophase bivalent differentiation through asymmetric disassembly of the SC

2005 ◽  
Vol 168 (5) ◽  
pp. 683-689 ◽  
Author(s):  
Kentaro Nabeshima ◽  
Anne M. Villeneuve ◽  
Monica P. Colaiácovo
Keyword(s):  
Caenorhabditis Elegans ◽  
Symmetry Breaking ◽  
Synaptonemal Complex ◽  
Central Region ◽  
Meiotic Prophase ◽  
Homologous Chromosome ◽  
Meiotic Chromosome ◽  
Crossing Over ◽  
Γ Irradiation ◽  
Irradiation Treatment

Homologous chromosome pairs (bivalents) undergo restructuring during meiotic prophase to convert a configuration that promotes crossover recombination into one that promotes bipolar spindle attachment and localized cohesion loss. We have imaged remodeling of meiotic chromosome structures after pachytene exit in Caenorhabditis elegans. Chromosome shortening during diplonema is accompanied by coiling of chromosome axes and highly asymmetric departure of synaptonemal complex (SC) central region proteins SYP-1 and SYP-2, which diminish over most of the length of each desynapsing bivalent while becoming concentrated on axis segments distal to the single emerging chiasma. This and other manifestations of asymmetry along chromosomes are lost in synapsis-proficient crossover-defective mutants, which often retain SYP-1,2 along the full lengths of coiled diplotene axes. Moreover, a γ-irradiation treatment that restores crossovers in the spo-11 mutant also restores asymmetry of SYP-1 localization. We propose that crossovers or crossover precursors serve as symmetry-breaking events that promote differentiation of subregions of the bivalent by triggering asymmetric disassembly of the SC.

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