scholarly journals Bypass of a Meiotic Checkpoint by Overproduction of Meiotic Chromosomal Proteins

2000 ◽  
Vol 20 (13) ◽  
pp. 4838-4848 ◽  
Author(s):  
Julie M. Bailis ◽  
Albert V. Smith ◽  
G. Shirleen Roeder
Keyword(s):  
Meiotic Recombination ◽  
Meiotic Prophase ◽  
Homologous Chromosome ◽  
Strand Break ◽  
Chromosomal Protein ◽  
Chromosomal Proteins ◽  
Cycle Arrest ◽  
Homologous Chromosome Pairing ◽  
Synaptonemal Complex Formation ◽  
Break Formation

ABSTRACT The Saccharomyces cerevisiae zip1 mutant, which exhibits defects in synaptonemal complex formation and meiotic recombination, triggers a checkpoint that causes cells to arrest at the pachytene stage of meiotic prophase. Overproduction of either the meiotic chromosomal protein Red1 or the meiotic kinase Mek1 bypasses this checkpoint, allowing zip1 cells to sporulate. Red1 or Mek1 overproduction also promotes sporulation of other mutants (zip2, dmc1, hop2) that undergo checkpoint-mediated arrest at pachytene. In addition, Red1 overproduction antagonizes interhomolog interactions in thezip1 mutant, substantially decreasing double-strand break formation, meiotic recombination, and homologous chromosome pairing. Mek1 overproduction, in contrast, suppresses checkpoint-induced arrest without significantly decreasing meiotic recombination. Cooverproduction of Red1 and Mek1 fails to bypass the checkpoint; moreover, overproduction of the meiotic chromosomal protein Hop1 blocks the Red1 and Mek1 overproduction phenotypes. These results suggest that meiotic chromosomal proteins function in the signaling of meiotic prophase defects and that the correct stoichiometry of Red1, Mek1, and Hop1 is needed to achieve checkpoint-mediated cell cycle arrest at pachytene.

scholarly journals Regulating chromosomal movement by the cochaperone FKB-6 ensures timely pairing and synapsis

2017 ◽  
Vol 216 (2) ◽  
pp. 393-408 ◽  
Author(s):  
Benjamin Alleva ◽  
Nathan Balukoff ◽  
Amy Peiper ◽  
Sarit Smolikove
Keyword(s):  
Nuclear Envelope ◽  
Chromosome Pairing ◽  
Meiotic Prophase ◽  
Homologous Chromosome ◽  
Strand Break ◽  
Crossing Over ◽  
Chromosome Movement ◽  
Microtubule Network ◽  
Homologous Chromosome Pairing ◽  
Proper Movement

In meiotic prophase I, homologous chromosome pairing is promoted through chromosome movement mediated by nuclear envelope proteins, microtubules, and dynein. After proper homologue pairing has been established, the synaptonemal complex (SC) assembles along the paired homologues, stabilizing their interaction and allowing for crossing over to occur. Previous studies have shown that perturbing chromosome movement leads to pairing defects and SC polycomplex formation. We show that FKB-6 plays a role in SC assembly and is required for timely pairing and proper double-strand break repair kinetics. FKB-6 localizes outside the nucleus, and in its absence, the microtubule network is altered. FKB-6 is required for proper movement of dynein, increasing resting time between movements. Attenuating chromosomal movement in fkb-6 mutants partially restores the defects in synapsis, in agreement with FKB-6 acting by decreasing chromosomal movement. Therefore, we suggest that FKB-6 plays a role in regulating dynein movement by preventing excess chromosome movement, which is essential for proper SC assembly and homologous chromosome pairing.

scholarly journals Sex without crossing over in the yeastSaccharomycodes ludwigii

2021 ◽  
Author(s):  
Ioannis A. Papaioannou ◽  
Fabien Dutreux ◽  
France A. Peltier ◽  
Hiromi Maekawa ◽  
Nicolas Delhomme ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Strand Break ◽  
Crossing Over ◽  
Gene Repertoire ◽  
Evolutionary Trajectory ◽  
Dna Double Strand Break ◽  
Saccharomycodes Ludwigii ◽  
Fitness Benefits ◽  
Normal Meiosis ◽  
Break Formation

AbstractMeiotic recombination is a ubiquitous function of sexual reproduction throughout eukaryotes. Here we report that recombination is extremely suppressed during meiosis in the yeast speciesSaccharomycodes ludwigii. DNA double-strand break formation, processing and repair are required for normal meiosis but do not lead to crossing over. Although the species has retained an intact meiotic gene repertoire, genetic and population analyses suggest the exceptionally rare occurrence of meiotic crossovers. We propose thatSd. ludwigiihas followed a unique evolutionary trajectory that possibly derives fitness benefits from the combination of frequent fertilization within the meiotic tetrad with the absence of meiotic recombination.

scholarly journals Vilya, a component of the recombination nodule, is required for meiotic double-strand break formation in Drosophila

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Cathleen M Lake ◽  
Rachel J Nielsen ◽  
Fengli Guo ◽  
Jay R Unruh ◽  
Brian D Slaughter ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Crossing Over ◽  
Actual Process ◽  
Strand Breaks ◽  
Recombination Nodules ◽  
Immuno Electron Microscopy ◽  
Break Formation ◽  
Selection Of

Meiotic recombination begins with the induction of programmed double-strand breaks (DSBs). In most organisms only a fraction of DSBs become crossovers. Here we report a novel meiotic gene, vilya, which encodes a protein with homology to Zip3-like proteins shown to determine DSB fate in other organisms. Vilya is required for meiotic DSB formation, perhaps as a consequence of its interaction with the DSB accessory protein Mei-P22, and localizes to those DSB sites that will mature into crossovers. In early pachytene Vilya localizes along the central region of the synaptonemal complex and to discrete foci. The accumulation of Vilya at foci is dependent on DSB formation. Immuno-electron microscopy demonstrates that Vilya is a component of recombination nodules, which mark the sites of crossover formation. Thus Vilya links the mechanism of DSB formation to either the selection of those DSBs that will become crossovers or to the actual process of crossing over.

scholarly journals The Mnd1 Protein Forms a Complex with Hop2 To Promote Homologous Chromosome Pairing and Meiotic Double-Strand Break Repair

2002 ◽  
Vol 22 (9) ◽  
pp. 3078-3088 ◽  
Author(s):  
Hideo Tsubouchi ◽  
G. Shirleen Roeder
Keyword(s):  
Chromosome Pairing ◽  
Meiotic Prophase ◽  
Meiotic Chromosome ◽  
Strand Break ◽  
Rad51 Protein ◽  
Strand Breaks ◽  
Homolog Pairing ◽  
Cell Extracts ◽  
Homologous Chromosome Pairing ◽  
Multicopy Suppressors

ABSTRACT The hop2 mutant of Saccharomyces cerevisiae arrests in meiosis with extensive synaptonemal complex (SC) formation between nonhomologous chromosomes. A screen for multicopy suppressors of a hop2-ts allele identified the MND1 gene. The mnd1-null mutant arrests in meiotic prophase, with most double-strand breaks (DSBs) unrepaired. A low level of mature recombinants is produced, and the Rad51 protein accumulates at numerous foci along chromosomes. SC formation is incomplete, and homolog pairing is severely reduced. The Mnd1 protein localizes to chromatin throughout meiotic prophase, and this localization requires Hop2. Unlike recombination enzymes such as Rad51, Mnd1 localizes to chromosomes even in mutants that fail to initiate meiotic recombination. The Hop2 and Mnd1 proteins coimmunoprecipitate from meiotic cell extracts. These results suggest that Hop2 and Mnd1 work as a complex to promote meiotic chromosome pairing and DSB repair. The identification of Hop2 and Mnd1 homologs in other organisms suggests that the function of this complex is conserved among eukaryotes.

scholarly journals Topoisomerases modulate the timing of meiotic DNA breakage and chromosome morphogenesis in Saccharomyces cerevisiae

2019 ◽  
Author(s):  
Jonna Heldrich ◽  
Xiaoji Sun ◽  
Luis A. Vale-Silva ◽  
Tovah E. Markowitz ◽  
Andreas Hochwagen
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Meiotic Prophase ◽  
Meiotic Chromosome ◽  
Strand Break ◽  
Temperature Sensitive ◽  
Chromosomal Dna ◽  
Meiotic Chromosomes ◽  
Chromosome Synapsis ◽  
Intergenic Regions

AbstractDuring meiotic prophase, concurrent transcription, recombination, and chromosome synapsis, place substantial topological strain on chromosomal DNA, but the role of topoisomerases in this context remains poorly defined. Here, we analyzed the roles topoisomerases I and II (Top1 and Top2) during meiotic prophase in Saccharomyces cerevisiae. We show that both topoisomerases accumulate primarily in promoter-containing intergenic regions of actively transcribing genes. Enrichment partially overlaps meiotic double-strand break (DSB) hotspots, but disruption of either topoisomerase has different effects during meiotic recombination. TOP1 disruption delays DSB induction and shortens the window of DSB accumulation by an unknown mechanism. By contrast, temperature-sensitive top2-1 mutants accumulate DSBs on synapsed chromosomes and exhibit a marked delay in meiotic chromosome remodeling. This defect results from a delay in recruiting the meiotic chromosome remodeler Pch2/TRIP13 but, unexpectedly, is not due to a loss of Top2 catalytic activity. Instead, mutant Top2-1 protein has reduced contact with chromatin but remains associated with meiotic chromosomes, and we provide evidence that this altered binding is responsible for the delay in chromosome remodeling. Our results imply independent roles for topoisomerases I and II in modulating meiotic recombination.

scholarly journals Mutations in Saccharomyces cerevisiae That Block Meiotic Prophase Chromosome Metabolism and Confer Cell Cycle Arrest at Pachytene Identify Two New Meiosis-Specific Genes SAE1 and SAE3

Genetics ◽  
1997 ◽  
Vol 146 (3) ◽  
pp. 817-834 ◽  
Author(s):  
Andrew H Z McKee ◽  
Nancy Kleckner
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Meiotic Recombination ◽  
Meiotic Prophase ◽  
Double Strand Breaks ◽  
Wild Type ◽  
Reading Frame ◽  
Strand Breaks ◽  
Cycle Arrest ◽  
Short Open Reading Frame

Two new meiosis-specific genes, SAE1 and SAE3, have been identified in a screen for mutations that confer an intermediate block in meiotic prophase. Such mutations confer a block to spore formation that is circumvented by addition of a mutation that eliminates meiotic recombination initiation and other aspects of chromosome metabolism, i.e., spo11. We show that sae1-1 and sae3-1 mutations each confer a distinct defect in meiotic recombination. sae1-1 produces recombinants but very slowly and ultimately to less than half the wild-type level; sae3-1 makes persistent hyper-resected meiotic double-strand breaks and has a severe defect in formation of recombinants. Both mutants arrest at the pachytene stage of meiotic prophase, sae1-1 temporarily and sae3-1 permanently. The phenotypes conferred by sae3-1 are similar to those conferred by mutation of the yeast RecA homologue DMC1, suggesting that SAE3 and DMC1 act at the same step(s) of chromosome metabolism. These results provide further evidence that intermediate blocks to prophase chromosome metabolism cause cell-cycle arrest. SAE1 encodes a 208-residue protein homologous to vertebrate mRNA cap-binding protein 20. SAE3 corresponds to a meiosis-specific RNA encoding an unusually short open reading frame of 50 codons.

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