Sex without crossing over in the yeastSaccharomycodes ludwigii

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.

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mus309 mutation, defective in DNA double-strand break repair, affects intergenic but not intragenic meiotic recombination in Drosophila melanogaster

Genetics Research ◽

10.1017/s0016672305007883 ◽

2005 ◽

Vol 86 (3) ◽

pp. 185-191 ◽

Cited By ~ 10

Author(s):

PETTER PORTIN

Keyword(s):

X Chromosome ◽

Meiotic Recombination ◽

Strand Break ◽

Double Strand Break ◽

Double Strand Break Repair ◽

Crossing Over ◽

Dna Double Strand Break ◽

D Loop ◽

Break Repair ◽

Strand Annealing

The effect was investigated of the hypomorphic DNA double-strand break repair, notably synthesis-dependent strand annealing, deficient mutation mus309 on the third chromosome of Drosophila melanogaster on intergenic and intragenic meiotic recombination in the X chromosome. The results showed that the mutation significantly increases the frequency of intergenic crossing over in two of three gene intervals of the X chromosome studied. Interestingly the increase was most prevalent in the tip of the X chromosome where crossovers normally are least frequent per physical map unit length. In particular crossing over interference was also affected, indicating that the effect of the mus309 mutation involves preconditions of crossing over but not the event of crossing over itself. On the other hand, the results also show that most probably the mutation does not have any effect on intragenic recombination, i.e. gene conversion. These results are fully consistent with the present molecular models of meiotic crossing over initiated by double-strand breaks of DNA followed by formation of a single-end-invasion intermediate, or D-loop, which is subsequently processed to generate either crossover or non-crossover products involving formation of a double Holliday junction. In particular the results suggest that the mus309 gene is involved in resolution of the D-loop, thereby affecting the choice between double-strand-break repair (DSBR) and synthesis-dependent strand annealing (SDSA) pathways of meiotic recombination.

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

eLife ◽

10.7554/elife.08287 ◽

2015 ◽

Vol 4 ◽

Cited By ~ 23

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.

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CXXC1 is not essential for normal DNA double-strand break formation and meiotic recombination in mouse

PLoS Genetics ◽

10.1371/journal.pgen.1007657 ◽

2018 ◽

Vol 14 (10) ◽

pp. e1007657 ◽

Cited By ~ 9

Author(s):

Hui Tian ◽

Timothy Billings ◽

Petko M. Petkov

Keyword(s):

Meiotic Recombination ◽

Strand Break ◽

Double Strand Break ◽

Dna Double Strand Break ◽

Break Formation

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CXXC1 is redundant for normal DNA double-strand break formation and meiotic recombination in mouse

10.1101/305508 ◽

2018 ◽

Cited By ~ 1

Author(s):

Hui Tian ◽

Timothy Billings ◽

Petko M. Petkov

Keyword(s):

Dna Sequences ◽

Meiotic Recombination ◽

Strand Break ◽

Double Strand Break ◽

Conditional Knockout ◽

Strand Breaks ◽

Conditional Knockout Mouse ◽

Dna Double Strand Break ◽

Chromosome Axis ◽

Break Formation

AbstractIn most mammals, including mice and humans, meiotic recombination is determined by the meiosis specific histone methytransferase PRDM9, which binds to specific DNA sequences and trimethylates histone 3 at lysine-4 and lysine-36 at the adjacent nucleosomes. These actions ensure successful DNA double strand break initiation and repair that occur on the proteinaceous structure forming the chromosome axis. The process of hotspot association with the axis after their activation by PRDM9 is poorly understood. Previously, we and others have identified CXXC1, an ortholog of S. cerevisiae Spp1 in mammals, as a PRDM9 interactor. In yeast, Spp1 is a histone methyl reader that links H3K4me3 sites with the recombination machinery, promoting DSB formation. Here we investigated whether CXXC1 has a similar function in mouse meiosis. We found that CXXC1 is co-expressed and interacts with PRDM9 in mouse spermatocytes. To investigate the meiotic function of CXXC1, we created a Cxxc1 conditional knockout mouse to deplete CXXC1 before the onset of meiosis. Surprisingly, knockout mice were fertile, and the loss of CXXC1 in spermatocytes had no effect on hotspot trimethylation activity, double-strand break formation or repair. Our results demonstrate that CXXC1 is not an essential link between recombination hotspot sites and DSB machinery and that the hotspot recognition pathway in mouse is independent of CXXC1.Author SummaryMeiotic recombination increases genetic diversity by ensuring novel combination of alleles passing onto the next generation correctly. In most mammals, the meiotic recombination sites are determined by histone methyltransferase PRDM9. These sites subsequently become associated with the chromosome axis with the participation of additional proteins and undergo double strand breaks, which are repaired by homologous recombination. In Saccharomyces cerevisiae, Spp1 (ortholog of CXXC1) binds to methylated H3K4 and connects these sites with chromosome axis promoting DSB formation. However, our data suggest that even though CXXC1 interacts with PRDM9 in male germ cells, it does not play a crucial role in mouse meiotic recombination. These results indicate that, unlike in S. cerevisiae, a recombination initiation pathway that includes CXXC1 could only serve as a non-essential pathway in mouse meiotic recombination.

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