Genetic control of meiotic recombination in Petunia hybrida: dosage effect of gene Rm1 on segments Hf1-Lg1 and An2-Rt; role of modifiers

Genome ◽  
1991 ◽  
Vol 34 (4) ◽  
pp. 515-523 ◽  
Author(s):  
N. Robert ◽  
E. Farcy ◽  
A. Cornu
Keyword(s):  
Genetic Control ◽  
Meiotic Recombination ◽  
Petunia Hybrida ◽  
Modifier Genes ◽  
Dosage Effect ◽  
Chromosome Segment ◽  
Marker Pair ◽  
Incomplete Dominance ◽  
Chromosome Segments

Populations segregating at locus Rm1 were used to measure recombination within two chromosome segments in Petunia hybrida. Gene Rm1 shows incomplete dominance and action that differs according to marker pair studied. It enhances recombination within the segment Hf1-Lg1 and restores it for the pair An2-Rt. Minor modifier genes exist, which act independent of or epistatic to Rm1 action. Like Rm1, they have effects that differ according to the chromosome segment analyzed, with the effects being more pronounced for strongly linked loci. Some of these genes are probably recessive.Key words: Petunia hybrida, gene Rm1, meiotic recombination, dosage effect.

scholarly journals Genetic Studies of mei-P26 Reveal a Link Between the Processes That Control Germ Cell Proliferation in Both Sexes and Those That Control Meiotic Exchange in Drosophila

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1757-1772 ◽  
Author(s):  
Scott L Page ◽  
Kim S McKim ◽  
Benjamin Deneen ◽  
Tajia L Van Hook ◽  
R Scott Hawley
Keyword(s):  
Meiotic Recombination ◽  
Double Mutant ◽  
P Element ◽  
Genetic Studies ◽  
Germline Differentiation ◽  
Males And Females ◽  
Bag Of Marbles ◽  
Differentiation And Proliferation

Abstract We present the cloning and characterization of mei-P26, a novel P-element-induced exchange-defective female meiotic mutant in Drosophila melanogaster. Meiotic exchange in females homozygous for mei-P261 is reduced in a polar fashion, such that distal chromosomal regions are the most severely affected. Additional alleles generated by duplication of the P element reveal that mei-P26 is also necessary for germline differentiation in both females and males. To further assess the role of mei-P26 in germline differentiation, we tested double mutant combinations of mei-P26 and bag-of-marbles (bam), a gene necessary for the control of germline differentiation and proliferation in both sexes. A null mutation at the bam locus was found to act as a dominant enhancer of mei-P26 in both males and females. Interestingly, meiotic exchange in mei-P261; bamΔ86/+ females is also severely decreased in comparison to mei-P261 homozygotes, indicating that bam affects the meiotic phenotype as well. These data suggest that the pathways controlling germline differentiation and meiotic exchange are related and that factors involved in the mitotic divisions of the germline may regulate meiotic recombination.

Saccharomyces cerevisiae Checkpoint Genes MEC1, RAD17 and RAD24 Are Required for Normal Meiotic Recombination Partner Choice

Genetics ◽  
1999 ◽  
Vol 153 (2) ◽  
pp. 607-620 ◽  
Author(s):  
Jeremy M Grushcow ◽  
Teresa M Holzen ◽  
Ken J Park ◽  
Ted Weinert ◽  
Michael Lichten ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Mitotic Checkpoint ◽  
Partner Choice ◽  
Wild Type ◽  
Spore Viability ◽  
Checkpoint Signaling ◽  
Ectopic Recombination ◽  
Meiotic Progression ◽  
Checkpoint Genes

Abstract Checkpoint gene function prevents meiotic progression when recombination is blocked by mutations in the recA homologue DMC1. Bypass of dmc1 arrest by mutation of the DNA damage checkpoint genes MEC1, RAD17, or RAD24 results in a dramatic loss of spore viability, suggesting that these genes play an important role in monitoring the progression of recombination. We show here that the role of mitotic checkpoint genes in meiosis is not limited to maintaining arrest in abnormal meioses; mec1-1, rad24, and rad17 single mutants have additional meiotic defects. All three mutants display Zip1 polycomplexes in two- to threefold more nuclei than observed in wild-type controls, suggesting that synapsis may be aberrant. Additionally, all three mutants exhibit elevated levels of ectopic recombination in a novel physical assay. rad17 mutants also alter the fraction of recombination events that are accompanied by an exchange of flanking markers. Crossovers are associated with up to 90% of recombination events for one pair of alleles in rad17, as compared with 65% in wild type. Meiotic progression is not required to allow ectopic recombination in rad17 mutants, as it still occurs at elevated levels in ndt80 mutants that arrest in prophase regardless of checkpoint signaling. These observations support the suggestion that MEC1, RAD17, and RAD24, in addition to their proposed monitoring function, act to promote normal meiotic recombination.

scholarly journals Suppressor Analysis of the Saccharomyces cerevisiae Gene REC104 Reveals a Genetic Interaction With REC102

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1261-1272 ◽  
Author(s):  
Laura Salem ◽  
Natalie Walter ◽  
Robert Malone
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Null Allele ◽  
Genetic Interaction ◽  
In Vitro Mutagenesis ◽  
Conditional Mutations ◽  
Suppressor Analysis

Abstract REC104 is a gene required for the initiation of meiotic recombination in Saccharomyces cerevisiae. To better understand the role of REC104 in meiosis, we used an in vitro mutagenesis technique to create a set of temperature-conditional mutations in REC104 and used one ts allele (rec104-8) in a screen for highcopy suppressors. An increased dosage of the early exchange gene REC102 was found to suppress the conditional recombinational reduction in rec104-8 as well as in several other conditional rec104 alleles. However, no suppression was observed for a null allele of REC104, indicating that the suppression by REC102 is not “bypass” suppression. Overexpression of the early meiotic genes REC114, RAD50, HOP1, and RED1 fails to suppress any of the rec104 conditional alleles, indicating that the suppression might be specific to REC102.

The use of linkage disequilibrium to map quantitative trait loci

2005 ◽  
Vol 45 (8) ◽  
pp. 837 ◽  
Author(s):  
M. E. Goddard ◽  
T. H. E. Meuwissen
Keyword(s):  
Linkage Disequilibrium ◽  
Quantitative Trait Loci ◽  
Statistical Model ◽  
Quantitative Trait ◽  
Linear Models ◽  
Chromosome Segment ◽  
Identical By Descent ◽  
Trait Loci ◽  
Linkage Disequilibrium Information ◽  
Chromosome Segments

This paper reviews the causes of linkage disequilibrium and its use in mapping quantitative trait loci. The many causes of linkage disequilibrium can be understood as due to similarity in the coalescence tree of different loci. Consideration of the way this comes about allows us to divide linkage disequilibrium into 2 types: linkage disequilibrium between any 2 loci, even if they are unlinked, caused by variation in the relatedness of pairs of animals; and linkage disequilibrium due to the inheritance of chromosome segments that are identical by descent from a common ancestor. The extent of linkage disequilibrium due to the latter cause can be logically measured by the chromosome segment homozygosity which is the probability that chromosome segments taken at random from the population are identical by descent. This latter cause of linkage disequilibrium allows us to map quantitative trait loci to chromosome regions. The former cause of linkage disequilibrium can cause artefactual quantitative trait loci at any position in the genome. These artefacts can be avoided by fitting the relatedness of animals in the statistical model used to map quantitative trait loci. In the future it may be convenient to estimate this degree of relatedness between individuals from markers covering the whole genome. The statistical model for mapping quantitative trait loci also requires us to estimate the probability that 2 animals share quantitative trait loci alleles at a particular position because they have inherited a chromosome segment containing the quantitative trait loci identical by descent. Current methods to do this all involve approximations. Methods based on concepts of coalescence and chromosome segment homozygosity are useful, but improvements are needed for practical analysis of large datasets. Once these probabilities are estimated they can be used in flexible linear models that conveniently combine linkage and linkage disequilibrium information.

scholarly journals RAD54 is essential for RAD51-mediated repair of meiotic DSB in Arabidopsis

PLoS Genetics ◽  
2021 ◽  
Vol 17 (5) ◽  
pp. e1008919
Author(s):  
Miguel Hernandez Sanchez-Rebato ◽  
Alida M. Bouatta ◽  
Maria E. Gallego ◽  
Charles I. White ◽  
Olivier Da Ines
Keyword(s):  
Homologous Recombination ◽  
Meiotic Recombination ◽  
Dna Supercoiling ◽  
Homology Search ◽  
Detectable Effect ◽  
Damage Repair ◽  
Meiotic Dsbs ◽  
Dna Translocase

An essential component of the homologous recombination machinery in eukaryotes, the RAD54 protein is a member of the SWI2/SNF2 family of helicases with dsDNA-dependent ATPase, DNA translocase, DNA supercoiling and chromatin remodelling activities. It is a motor protein that translocates along dsDNA and performs multiple functions in homologous recombination. In particular, RAD54 is an essential cofactor for regulating RAD51 activity. It stabilizes the RAD51 nucleofilament, remodels nucleosomes, and stimulates homology search and strand invasion activity of RAD51. Accordingly, deletion of RAD54 has dramatic consequences on DNA damage repair in mitotic cells. In contrast, its role in meiotic recombination is less clear. RAD54 is essential for meiotic recombination in Drosophila and C. elegans, but plays minor roles in yeast and mammals. We present here characterization of the roles of RAD54 in meiotic recombination in the model plant Arabidopsis thaliana. Absence of RAD54 has no detectable effect on meiotic recombination in otherwise wild-type plants but RAD54 becomes essential for meiotic DSB repair in absence of DMC1. In Arabidopsis, dmc1 mutants have an achiasmate meiosis, in which RAD51 repairs meiotic DSBs. Lack of RAD54 leads to meiotic chromosomal fragmentation in absence of DMC1. The action of RAD54 in meiotic RAD51 activity is thus mainly downstream of the role of RAD51 in supporting the activity of DMC1. Equivalent analyses show no effect on meiosis of combining dmc1 with the mutants of the RAD51-mediators RAD51B, RAD51D and XRCC2. RAD54 is thus required for repair of meiotic DSBs by RAD51 and the absence of meiotic phenotype in rad54 plants is a consequence of RAD51 playing a RAD54-independent supporting role to DMC1 in meiotic recombination.

scholarly journals Molecular basis of the dual role of the Mlh1-Mlh3 endonuclease in MMR and in meiotic crossover formation

2021 ◽  
Vol 118 (23) ◽  
pp. e2022704118
Author(s):  
Jingqi Dai ◽  
Aurore Sanchez ◽  
Céline Adam ◽  
Lepakshi Ranjha ◽  
Giordano Reginato ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Molecular Basis ◽  
Crystal Packing ◽  
Critical Role ◽  
Holliday Junctions ◽  
Dual Roles ◽  
Terminal Domain ◽  
C Terminus ◽  
Meiotic Crossover

In budding yeast, the MutL homolog heterodimer Mlh1-Mlh3 (MutLγ) plays a central role in the formation of meiotic crossovers. It is also involved in the repair of a subset of mismatches besides the main mismatch repair (MMR) endonuclease Mlh1-Pms1 (MutLα). The heterodimer interface and endonuclease sites of MutLγ and MutLα are located in their C-terminal domain (CTD). The molecular basis of MutLγ’s dual roles in MMR and meiosis is not known. To better understand the specificity of MutLγ, we characterized the crystal structure of Saccharomyces cerevisiae MutLγ(CTD). Although MutLγ(CTD) presents overall similarities with MutLα(CTD), it harbors some rearrangement of the surface surrounding the active site, which indicates altered substrate preference. The last amino acids of Mlh1 participate in the Mlh3 endonuclease site as previously reported for Pms1. We characterized mlh1 alleles and showed a critical role of this Mlh1 extreme C terminus both in MMR and in meiotic recombination. We showed that the MutLγ(CTD) preferentially binds Holliday junctions, contrary to MutLα(CTD). We characterized Mlh3 positions on the N-terminal domain (NTD) and CTD that could contribute to the positioning of the NTD close to the CTD in the context of the full-length MutLγ. Finally, crystal packing revealed an assembly of MutLγ(CTD) molecules in filament structures. Mutation at the corresponding interfaces reduced crossover formation, suggesting that these superstructures may contribute to the oligomer formation proposed for MutLγ. This study defines clear divergent features between the MutL homologs and identifies, at the molecular level, their specialization toward MMR or meiotic recombination functions.

New insights into the role of DNA synthesis in meiotic recombination

2016 ◽  
Vol 61 (16) ◽  
pp. 1260-1269 ◽  
Author(s):  
Jiyue Huang ◽  
Gregory P. Copenhaver ◽  
Hong Ma ◽  
Yingxiang Wang
Keyword(s):  
Dna Synthesis ◽  
Meiotic Recombination
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