Mitotic gene conversion tracts associated with repair of a defined double-strand break in<i>Saccharomyces cerevisiae</i>

Jinks-Robertson, Sue; Hum, Yee Fang

doi:10.1101/132167

Cited by 9 publications

(12 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These tracts, although numerous, are too short to seriously affect the total amount of shuffling [for example, the contribution from meiotic GCs in mammals will be of the order 10,000 times smaller than the contribution from COs (SI Appendix); in yeast, this figure is smaller-about 200 (SI Appendix)]; however, they may have important local effects (154,159). Mitotic GC tracts result from homologous chromosome repair, are typically much longer than meiotic GC tracts (often of order 10 kb) (160,161), and if they occur in germline cell divisions leading to meiocytes, can lead to shuffling of maternal and paternal DNA in gametes (which should especially affect males, who have more germline cell divisions). Too little is presently known about the global frequency of these events for us to give a reasonable quantitative estimate of how much shuffling they cause.…”

Section: Discussionmentioning

confidence: 99%

A rigorous measure of genome-wide genetic shuffling that takes into account crossover positions and Mendel’s second law

Veller

Kleckner

Nowak

2019

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Comparative studies in evolutionary genetics rely critically on evaluation of the total amount of genetic shuffling that occurs during gamete production. Such studies have been hampered by the absence of a direct measure of this quantity. Existing measures consider crossing-over by simply counting the average number of crossovers per meiosis. This is qualitatively inadequate, because the positions of crossovers along a chromosome are also critical: a crossover toward the middle of a chromosome causes more shuffling than a crossover toward the tip. Moreover, traditional measures fail to consider shuffling from independent assortment of homologous chromosomes (Mendel’s second law). Here, we present a rigorous measure of genome-wide shuffling that does not suffer from these limitations. We define the parameter r¯ as the probability that the alleles at two randomly chosen loci are shuffled during gamete production. This measure can be decomposed into separate contributions from crossover number and position and from independent assortment. Intrinsic implications of this metric include the fact that r¯ is larger when crossovers are more evenly spaced, which suggests a selective advantage of crossover interference. Utilization of r¯ is enabled by powerful emergent methods for determining crossover positions either cytologically or by DNA sequencing. Application of our analysis to such data from human male and female reveals that (i) r¯ in humans is close to its maximum possible value of 1/2 and that (ii) this high level of shuffling is due almost entirely to independent assortment, the contribution of which is ∼30 times greater than that of crossovers.

show abstract

Section: Discussionmentioning

confidence: 99%

A rigorous measure of genome-wide genetic shuffling that takes into account crossover positions and Mendel’s second law

Veller

Kleckner

Nowak

2019

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…They appear to occur at rates similar to those known in recombining genome portions of sexual species [66,67]. Mitotic gene conversion can also occur outside of palindromic regions, for example when double-stranded DNA breaks are repaired using the homologous chromosome as a template [68,69]. This can, in theory, contribute to the loss of heterozygosity under all forms of asexuality, but mitotic gene conversion rates have only rarely been studied in asexual species -or sexual ones for that matter.…”

Section: Palindromes and Gene Conversionmentioning

confidence: 98%

Genomic features of parthenogenetic animals

Jaroň

Bast²,

Nowell

et al. 2018

Preprint

View full text Add to dashboard Cite

Evolution under asexuality is predicted to impact genomes in numerous ways, but empirical evidence remains unclear. Case studies of individual asexual animals have reported peculiar genomic features which were suggested to be caused by asexuality, including high heterozygosity, a high abundance of horizontally acquired genes, a low transposable element load, or the presence of palindromes. We systematically characterized these genomic features in published genomes of 26 asexual animals representing at least 18 independent transitions to asexuality. Surprisingly, not a single feature is systematically replicated across a majority of these transitions, suggesting that no genomic feature is characteristic of asexuality and that previously reported patterns were lineage specific rather than caused by asexuality. We found that only asexuals of hybrid origin were characterized by high heterozygosity levels. Asexuals that were not of hybrid origin appeared to be largely homozygous, independently of the cellular mechanism underlying asexuality. Overall, despite the importance of recombination rate variation for the evolution of sexual animal genomes, the genome-wide absence of recombination does not appear to have had the dramatic effects which are expected from classical theoretical models. The reasons for this are probably a combination of lineage-specific patterns, impact of the origin of asexuality, and a survivorship bias of asexual lineages. Box 1: Transitions to asexualityMeiotic sex and recombination evolved once in the common ancestor of eukaryotes [41].Asexual animals therefore derive from a sexual ancestor, but how transitions from sexual to asexual reproduction occur can vary and have different expected consequences for the genome [13]. Hybrid origin:Hybridization between sexual species can generate hybrid females that reproduce asexually [13,42]. Asexuality caused by hybridization can generate a highly heterozygous genome, depending on the divergence between the parental sexual species prior to hybridization. Hybridization can also result in a burst of transposable element activity [12]. Intraspecific origins: Endosymbiont infection. Infection with intracellular endosymbionts (such asWolbachia, Cardinium or Rickettsia) can cause asexuality, a pattern that is frequent in species with haplodiploid sex determination [43]. This type of transition often (but not always) results in fully homozygous lineages because induction of asexuality frequently occurs via gamete duplication (see Box 2). Spontaneous mutations/Contagious asexuality. Spontaneous mutations can alsounderlie transitions from sexual to asexual reproduction. In addition, asexual females of some species produce males that mate with females of sexual lineages, and thereby generate new asexual strains (contagious asexuality). In both cases, the genomes of incipient asexual lineages are expected to be very similar to those of their sexual relatives and subsequent changes should be largely driven by the cellular mechanism underlying asexuality (Box 2). an...

show abstract

“…These tracts, though numerous, are too short to seriously affect the total amount of shuffling [for example, the contribution from meiotic GCs in mammals will be of order 10,000 times smaller than the contribution from crossovers (SI Appendix); in yeast, this figure is smaller-about 200 (SI Appendix)-owing to their longer GC tracts and smaller genomes], though they may have important local effects [154,159]. Mitotic GC tracts result from homologous chromosome repair, are typically much longer than meiotic GC tracts (often of order 10kb; e.g., [160,161]), and, if they occur in germline cell divisions leading to meiocytes, can lead to shuffling of maternal and paternal DNA in gametes (which should especially affect males, who have more germline cell divisions).…”

Section: Taking Gene Conversion Into Accountmentioning

confidence: 99%

A rigorous measure of genome-wide genetic shuffling that takes into account crossover positions and Mendel’s second law

Veller

Kleckner

Nowak

2017

Preprint

View full text Add to dashboard Cite

Comparisons of genetic recombination, whether across species, the sexes, individuals, or different chromosomes, require a measure of total recombination. Traditional measures, such as map length, crossover frequency, and the recombination index, are not influenced by the positions of crossovers along chromosomes. Intuitively, though, a crossover in the middle of a chromosome causes more recombination than a crossover at the tip. Similarly, two crossovers very close to each other cause less recombination than if they were evenly spaced. Here, we study a measure of total recombination that does account for crossover position: average r, the probability that a random pair of loci recombines in the production of a gamete. Consistent with intuition, average r is larger when crossovers are more evenly spaced. We show that average r can be decomposed into distinct components deriving from intra-chromosomal recombination (crossing over) and inter-chromosomal recombination (independent assortment of chromosomes), allowing separate analysis of these components. Average r can be calculated given knowledge of crossover positions either at meiosis I or in gametes/offspring. Technological advances in cytology and sequencing over the past two decades make calculation of average r possible, and we demonstrate its calculation for male and female humans using both kinds of data.

show abstract

Mitotic gene conversion tracts associated with repair of a defined double-strand break inSaccharomyces cerevisiae

Cited by 9 publications

References 23 publications

A rigorous measure of genome-wide genetic shuffling that takes into account crossover positions and Mendel’s second law

A rigorous measure of genome-wide genetic shuffling that takes into account crossover positions and Mendel’s second law

Genomic features of parthenogenetic animals

A rigorous measure of genome-wide genetic shuffling that takes into account crossover positions and Mendel’s second law

Contact Info

Product

Resources

About