scholarly journals Noncanonical contributions of MutLγ to VDE-initiated crossovers during Saccharomyces cerevisiae meiosis

2019 ◽  
Author(s):  
Anura Shodhan ◽  
Darpan Medhi ◽  
Michael Lichten
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Meiotic Chromosome ◽  
Chromosome Size ◽  
Protein Enrichment ◽  
Poor Region ◽  
Primary Determinant ◽  
Recombination Pathway ◽  
Chromosome Axis ◽  
Dependent Processes

In Saccharomyces cerevisiae, the meiosis-specific axis proteins Hop1 and Red1 are present nonuniformly across the genome. In a previous study, the meiosis-specific VMAl-derived endonuclease (VDE) was used to examine Spo11-independent recombination in a recombination reporter inserted in a Hop1/Red1-enriched region (HIS4) and in a Hop1/Red1-poor region (URA3). VDE-initiated crossovers at HIS4 were mostly dependent on Mlh3, a component of the MutLγ meiotic recombination intermediate resolvase, while VDE-initiated crossovers at URA3 were mostly Mlh3-independent. These differences were abolished in the absence of the chromosome axis remodeler Pch2, and crossovers at both loci become partly Mlh3-dependent. To test the generality of these observations, we examined inserts at six additional loci that differed in terms of Hop1/Red1 enrichment, chromosome size, and distance from centromeres and telomeres. All six loci behaved similarly to URA3: the vast majority of VDE-initiated crossovers were Mlh3-independent. This indicates that, counter to previous suggestions, meiotic chromosome axis protein enrichment is not a primary determinant of which recombination pathway gives rise to crossovers during VDE-initiated meiotic recombination. In pch2Δ mutants, the fraction of VDE-induced crossovers that were Mlh3-dependent increased to levels previously observed for Spo11-initiated crossovers in pch2Δ, indicating that Pch2-dependent processes play an important role in controlling the distribution of factors necessary for MutLγ-dependent crossovers.

scholarly journals A conserved filamentous assembly underlies the structure of the meiotic chromosome axis

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Alan MV West ◽  
Scott C Rosenberg ◽  
Sarah N Ur ◽  
Madison K Lehmer ◽  
Qiaozhen Ye ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Budding Yeast ◽  
Meiotic Chromosome ◽  
Coiled Coil ◽  
Chromosome Organization ◽  
Molecular Architecture ◽  
Master Regulators ◽  
Core Proteins ◽  
Protein Components ◽  
Chromosome Axis

The meiotic chromosome axis plays key roles in meiotic chromosome organization and recombination, yet the underlying protein components of this structure are highly diverged. Here, we show that ‘axis core proteins’ from budding yeast (Red1), mammals (SYCP2/SYCP3), and plants (ASY3/ASY4) are evolutionarily related and play equivalent roles in chromosome axis assembly. We first identify ‘closure motifs’ in each complex that recruit meiotic HORMADs, the master regulators of meiotic recombination. We next find that axis core proteins form homotetrameric (Red1) or heterotetrameric (SYCP2:SYCP3 and ASY3:ASY4) coiled-coil assemblies that further oligomerize into micron-length filaments. Thus, the meiotic chromosome axis core in fungi, mammals, and plants shares a common molecular architecture, and likely also plays conserved roles in meiotic chromosome axis assembly and recombination control.

scholarly journals RAD10, an excision repair gene of Saccharomyces cerevisiae, is involved in the RAD1 pathway of mitotic recombination.

1990 ◽  
Vol 10 (6) ◽  
pp. 2485-2491 ◽  
Author(s):  
R H Schiestl ◽  
S Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
The Other ◽  
Gene Products ◽  
Repair Gene ◽  
Homologous Chromosomes ◽  
Intrachromosomal Recombination ◽  
Recombination Pathway

The RAD10 gene of Saccharomyces cerevisiae is required for the incision step of excision repair of UV-damaged DNA. We show that the RAD10 gene is also required for mitotic recombination. The rad10 delta mutation lowered the rate of intrachromosomal recombination of a his3 duplication in which one his3 allele has a deletion at the 3' end and the other his3 allele has a deletion at the 5' end (his3 delta 3' his3 delta 5'). The rate of formation of HIS3+ recombinants in the rad10 delta mutant was not affected by the rad1 delta mutation but decreased synergistically in the presence of the rad10 delta mutation in combination with the rad52 delta mutation. These observations indicate that the RAD1 and RAD10 genes function together in a mitotic recombination pathway that is distinct from the RAD52 recombination pathway. The rad10 delta mutation also lowered the efficiency of integration of linear DNA molecules and circular plasmids into homologous genomic sequences. We suggest that the RAD1 and RAD10 gene products act in recombination after the formation of the recombinogenic substrate. The rad1 delta and rad10 delta mutations did not affect meiotic intrachromosomal recombination of the his3 delta 3' his3 delta 5' duplication or mitotic and meiotic recombination of ade2 heteroalleles located on homologous chromosomes.

scholarly journals Transcription dynamically patterns the meiotic chromosome-axis interface

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Xiaoji Sun ◽  
Lingzhi Huang ◽  
Tovah E Markowitz ◽  
Hannah G Blitzblau ◽  
Doris Chen ◽  
...  
Keyword(s):  
Protein Binding ◽  
Budding Yeast ◽  
Meiotic Chromosome ◽  
Cohesin Complex ◽  
Protein Enrichment ◽  
Meiotic Chromosomes ◽  
Convergent Transcription ◽  
Chromosome Axis ◽  
Ubiquitous Presence ◽  
Axial Element

Meiotic chromosomes are highly compacted yet remain transcriptionally active. To understand how chromosome folding accommodates transcription, we investigated the assembly of the axial element, the proteinaceous structure that compacts meiotic chromosomes and promotes recombination and fertility. We found that the axial element proteins of budding yeast are flexibly anchored to chromatin by the ring-like cohesin complex. The ubiquitous presence of cohesin at sites of convergent transcription provides well-dispersed points for axis attachment and thus chromosome compaction. Axis protein enrichment at these sites directly correlates with the propensity for recombination initiation nearby. A separate modulating mechanism that requires the conserved axial-element component Hop1 biases axis protein binding towards small chromosomes. Importantly, axis anchoring by cohesin is adjustable and readily displaced in the direction of transcription by the transcriptional machinery. We propose that such robust but flexible tethering allows the axial element to promote recombination while easily adapting to changes in chromosome activity.

A transcriptional cascade governs entry into meiosis in Saccharomyces cerevisiae

1989 ◽  
Vol 9 (5) ◽  
pp. 2142-2152
Author(s):  
H E Smith ◽  
A P Mitchell
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mating Type ◽  
Meiotic Recombination ◽  
Deletion Mutant ◽  
Type Locus ◽  
Mating Type Locus ◽  
Recombination Pathway

Two signals activate meiosis in yeast: starvation and expression of the a1 and alpha 2 products of the mating-type locus. Prior studies suggest that these signals stimulate expression of an activator of meiosis, the IME1 (inducer of meiosis) product. We have cloned a gene, IME2, with properties similar to those of IME1: both genes are required for meiosis, and both RNAs are induced in meiotic cells. Elevated dosage of IME1 or IME2 stimulates the meiotic recombination pathway without starvation; thus, the IME products may be part of the switch that activates meiosis. IME1 was found to be required for IME2 expression, and a multicopy IME2 plasmid permitted meiosis in an ime1 deletion mutant. Accordingly, we propose that the IME1 product stimulates meiosis mainly through activation of IME2 expression.

Analysis of Meiotic Recombination Pathways in the Yeast Saccharomyces cerevisiae

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 71-86 ◽  
Author(s):  
Yang Mao-Draayer ◽  
Anne M Galbraith ◽  
Douglas L Pittman ◽  
Marc Cool ◽  
Robert E Malone
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
The Other ◽  
Yeast Saccharomyces Cerevisiae ◽  
Recombination Hotspot ◽  
Early Genes ◽  
Intrachromosomal Recombination ◽  
Mutant Phenotypes ◽  
Recombination Pathway

Abstract In the yeast, Saccharomyces cerevisiae, several genes appear to act early in meiotic recombination. HOPl and REDl have been classified as such early genes. The data in this paper demonstrate that neither a redl nor a hopl mutation can rescue the inviable spores produced by a rad52 spol3 strain; this phenotype helps to distinguish these two genes from other early meiotic recombination genes such as SPOll, REC104, or A4EI4. In contrast, either a redl or a hopl mutation can rescue a rad50S spol3 strain; this phenotype is similar to that conferred by mutations in the other early recombination genes (e.g., REC104). These two different results can be explained because the data presented here indicate that a rad50S mutation does not diminish meiotic intrachromosomal recombination, similar to the mutant phenotypes conferred by redl or hopl. Of course, REDl and HOPl do act in the normal meiotic interchromosomal recombination pathway; they reduce interchromosomal recombination to ~10% of normal levels. We demonstrate that a mutation in a gene (REC104) required for initiation of exchange is completely epistatic to a mutation in REDl. Finally, mutations in either HOPl or RED1 reduce the number of doublestrand breaks observed at the HIS2 meiotic recombination hotspot.

RAD10, an excision repair gene of Saccharomyces cerevisiae, is involved in the RAD1 pathway of mitotic recombination

1990 ◽  
Vol 10 (6) ◽  
pp. 2485-2491
Author(s):  
R H Schiestl ◽  
S Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
The Other ◽  
Gene Products ◽  
Repair Gene ◽  
Homologous Chromosomes ◽  
Intrachromosomal Recombination ◽  
Recombination Pathway

The RAD10 gene of Saccharomyces cerevisiae is required for the incision step of excision repair of UV-damaged DNA. We show that the RAD10 gene is also required for mitotic recombination. The rad10 delta mutation lowered the rate of intrachromosomal recombination of a his3 duplication in which one his3 allele has a deletion at the 3' end and the other his3 allele has a deletion at the 5' end (his3 delta 3' his3 delta 5'). The rate of formation of HIS3+ recombinants in the rad10 delta mutant was not affected by the rad1 delta mutation but decreased synergistically in the presence of the rad10 delta mutation in combination with the rad52 delta mutation. These observations indicate that the RAD1 and RAD10 genes function together in a mitotic recombination pathway that is distinct from the RAD52 recombination pathway. The rad10 delta mutation also lowered the efficiency of integration of linear DNA molecules and circular plasmids into homologous genomic sequences. We suggest that the RAD1 and RAD10 gene products act in recombination after the formation of the recombinogenic substrate. The rad1 delta and rad10 delta mutations did not affect meiotic intrachromosomal recombination of the his3 delta 3' his3 delta 5' duplication or mitotic and meiotic recombination of ade2 heteroalleles located on homologous chromosomes.

scholarly journals Heteroduplex DNA formation and homolog pairing in yeast meiotic mutants.

Genetics ◽  
1995 ◽  
Vol 141 (1) ◽  
pp. 75-86
Author(s):  
D K Nag ◽  
H Scherthan ◽  
B Rockmill ◽  
J Bhargava ◽  
G S Roeder
Keyword(s):  
In Situ Hybridization ◽  
Chromosome Pairing ◽  
Meiotic Recombination ◽  
Meiotic Chromosome ◽  
Wild Type ◽  
Heteroduplex Dna ◽  
Homolog Pairing ◽  
Meiotic Chromosome Pairing ◽  
Recombination Pathway

Abstract Previous studies of Saccharomyces cerevisiae have identified several meiosis-specific genes whose products are required for wild-type levels of meiotic recombination and for normal synaptonemal complex (SC) formation. Several of these mutants were examined in a physical assay designed to detect heteroduplex DNA (hDNA) intermediates in meiotic recombination. hDNA was not detected in the rec102, mei4 and hop1 mutants; it was observed at reduced levels in red1, mek1 and mer1 strains and at greater than the wild-type level in zip1. These results indicate that the REC102, MEI4, HOP1, RED1, MEK1 and MER1 gene products act before hDNA formation in the meiotic recombination pathway, whereas ZIP1 acts later. The same mutants assayed for hDNA formation were monitored for meiotic chromosome pairing by in situ hybridization of chromosome-specific DNA probes to spread meiotic nuclei. Homolog pairing occurs at wild-type levels in the zip1 and mek1 mutants, but is substantially reduced in mei4, rec102, hop1, red1 and mer1 strains. Even mutants that fail to recombine or to make any SC or SC precursors undergo a significant amount of meiotic chromosome pairing. The in situ hybridization procedure revealed defects in meiotic chromatin condensation in mer1, red1 and hop1 strains.

scholarly journals Reduced dosage of the chromosome axis factor Red1 selectively disrupts the meiotic recombination checkpoint in Saccharomyces cerevisiae

PLoS Genetics ◽  
2017 ◽  
Vol 13 (7) ◽  
pp. e1006928 ◽  
Author(s):  
Tovah E. Markowitz ◽  
Daniel Suarez ◽  
Hannah G. Blitzblau ◽  
Neem J. Patel ◽  
Andrew L. Markhard ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Recombination Checkpoint ◽  
Chromosome Axis

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 The rec102 mutant of yeast is defective in meiotic recombination and chromosome synapsis.

Genetics ◽  
1992 ◽  
Vol 130 (1) ◽  
pp. 59-69
Author(s):  
J Bhargava ◽  
J Engebrecht ◽  
G S Roeder
Keyword(s):  
Synaptonemal Complex ◽  
Chromosome Segregation ◽  
Meiotic Recombination ◽  
Meiotic Chromosome ◽  
Crossing Over ◽  
Homologous Chromosomes ◽  
Chromosome Synapsis ◽  
Recombination Pathway ◽  
Yeast Mutants ◽  
Meiosis I

Abstract A mutation at the REC102 locus was identified in a screen for yeast mutants that produce inviable spores. rec102 spore lethality is rescued by a spo13 mutation, which causes cells to bypass the meiosis I division. The rec102 mutation completely eliminates meiotically induced gene conversion and crossing over but has no effect on mitotic recombination frequencies. Cytological studies indicate that the rec102 mutant makes axial elements (precursors to the synaptonemal complex), but homologous chromosomes fail to synapse. In addition, meiotic chromosome segregation is significantly delayed in rec102 strains. Studies of double and triple mutants indicate that the REC102 protein acts before the RAD52 gene product in the meiotic recombination pathway. The REC102 gene was cloned based on complementation of the mutant defect and the gene was mapped to chromosome XII between CDC25 and STE11.

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