RECOMBINATION BETWEEN GENES LOCATED ON NONHOMOLOGOUS CHROMOSOMES IN <i>SACCHAROMYCES CEREVISIAE</i>

Mikus, Margaret Dubay; Petes, Thomas D.

doi:10.1093/genetics/101.3-4.369

Cited by 65 publications

(2 citation statements)

References 15 publications

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“…Another possibility is the following: Recombination between insertions at different sites would lead to chromosome rearrangements that are generally dominant lethal, or so deleterious that their probability of transmission a n d / o r survival in subsequent generations is substantially reduced when compared with that of a simple insertional mutation. There is good evidence from bacteria, yeast, and mammals for such events (Mikus & Petes, 1982;Roeder, 1983;Maeda & Smithies, in press). In Drosophila, there is also some evidence suggesting their occurrence (Goldberg et al 1983;Davis, Shen & Judd, in press).…”

Section: (I) Distribution Of Elements On the X Vs The Autosomesmentioning

confidence: 99%

A test for the role of natural selection in the stabilization of transposable element copy number in a population ofDrosophila melanogaster

1987

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SummaryThe numbers of members of three families of copia-like elements were counted on twenty X, 2nd and 3rd chromosomes collected from a natural population of Drosophila melanogaster. Theoretical predictions were computed for two models of copy number stabilization: (1) element frequencies are regulated by a simple genetic process such as copy number dependent transposition or excision, independent of chromosomal location; (2) elements are eliminated by natural selection against mutational effects of their insertion into the chromosome. Since insertions into the X can be expected to suffer more selection than autosomal insertions, due to expression of mutant phenotypes in the hemizygous state, hypothesis 2, called the disproportional model, predicts that the proportion of elements on the X will be smaller than the proportion of the genome contributed by the X, while hypothesis 1, called the equiproportional model, predicts that this proportionality will be unaffected. Two of the elements, 297 and roo, showed no evidence for deficiency of X-linked elements, but the data for a third element, 412, were consistent with the prediction based on the selective model.These results indicate that simple selection against mutational effects of insertions of transposable elements is not generally adequate to account for their distribution within populations. We argue that a mechanism such as recombination between elements at different chromosomal sites, leading to rearrangements with highly deleterious, dominant effects could play a role in stabilizing copy number. This process would lead to a higher abundance of elements in genomic regions with restricted crossing over. We present some data indicating such an effect, and discuss possible interpretations.

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Section: (I) Distribution Of Elements On the X Vs The Autosomesmentioning

confidence: 99%

A test for the role of natural selection in the stabilization of transposable element copy number in a population ofDrosophila melanogaster

1987

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“…Recombination between non-homologous chromosomes and non-allelic positions through misalignment occurs frequently in eukaryotic organisms. For example, Mikus and Petes reported recombination between genes on different chromosomes in Saccharomyces cerevisiae, resulting in both non-reciprocal and reciprocal translocations [5]. This recombination mechanism is critical in the evolution of these organisms and is widely recognized for recurrent, high-frequency rearrangements often driven by highly-identical segmental duplications through non-allelic homologous recombination [6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Interchromosomal segmental duplication drives translocation and loss ofP. falciparumhistidine-rich protein 3

Hathaway

Kim

Young

et al. 2022

Preprint

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Background: Significant progress has been made in the fight against P. falciparum malaria due in part to the widespread adoption of rapid diagnostic tests (RDTs) that detect histidine-rich protein 2 (PfHRP2) and its paralog PfHRP3 encoded by the pfhrp2 and pfhrp3 genes, respectively. Parasites without pfhrp2 and pfhrp3 genes are not detected by these RDTs. Pfhrp3 loss appears to be more common in some geographical regions and has been observed in vitro. We sought to gain insight into geographic patterns of pfhrp3 deletion and define the mechanism of gene loss. Methods: Over 9,830 publicly available, whole-genome sequenced (WGS) P. falciparum field samples were analyzed for genotypes and coverage using PathWeaver for local assembly . DNA from two cultured isolates with pfhrp3 deletion, HB3 and SD01, were sequenced with Oxford Nanopore Technologies (ONT) long-read sequencing, assembled with Canu and Flye, and genes annotated with Companion. Results: Two distinct pfhrp3 deletion patterns were detected: 1) segmental deletion of chromosome 13 just centromeric to pfhrp3 extending to the end of the chromosome, with co-occurring segmental duplication of the chromosome 11 subtelomeric region, and 2) segmental deletion of chromosome 13 starting at various locations centromeric to pfhrp3 without chromosome 11 duplication. Pattern 1 was almost exclusively found in samples from Africa and South America, while pattern 2 was observed predominantly in Southeast Asia. The pattern 1 boundary fell within a 15kb nearly identical duplication on both chromosomes containing ribosomal genes. ONT assembly of HB3 and SD01 parasite lines revealed hybrid chromosomes and long-reads spanning the ribosomal duplication, consistent with recombination between non-homologous chromosomes. Conclusion: Our findings demonstrate duplication-mediated non-homologous recombination creating a hybrid 13-11 chromosome that replaces pfhrp3 and telomeric chromosome 13 with a translocated telomeric chromosome 11 sequence--essentially yielding a deletion of chromosome 13 sequence and interchromosomal duplication of chromosome 11 sequence. Given that existing ribosomal duplications likely predispose to the frequent occurrence of this translocation during meiosis, it suggests that subsequent selective forces are driving its presence or absence in different geographical regions. This mechanism appears to explain pfhrp3 deletion in South America and Africa and may explain why pfhrp3 deletions are more prevalent than pfhrp2 deletions in many localities. However, the forces driving emergence of pfhrp3- parasites may be complex and encompass other genes affected by the recombination event. Further studies of the origins of pfhrp2- and pfhrp3-deleted strains and the selective pressures suppressing their occurrence or driving their expansion are needed.

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A family of laboratory strains ofSaccharomyces cerevisiae carry rearrangements involving chromosomes I and III

Casarégola

Nguyen

Lépingle

et al. 1998

Yeast

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In order to study meiotic segregation of chromosome length polymorphism in yeast, we analysed the progeny of a cross involving two laboratory strains FL100trp and YNN295. Analysis of the parental strains led us to detect an important length polymorphism of chromosomes I and III in FL100trp. A reciprocal translocation involving 80 kb of the left arm of chromosome III and 45 kb of the right arm of chromosome I was shown to be the cause for the observed polymorphism in this strain. The characterization of the translocation breakpoints revealed the existence of a transposition hot‐spot on chromosome I: the sequence of the translocation joints on chromosomes I and III suggests that the mechanism very likely involved homologous recombination between Ty2 transposable elements on each chromosome. Analysis of FL100, FL200 and FL100trp ura, which are related to FL100trp, shows that this reciprocal translocation is present in some of the strains of the FL series, whereas the parental strain FL100 does not carry the same rearrangement. We evidenced instead the duplication of 80 kb of chromosome III on chromosome I and a deletion of 45 kb of the right arm of chromosome I in this strain, indicating that secondary events might have taken place and that the strain currently named FL100 is not the common ancestor of the FL series. © 1998 John Wiley & Sons, Ltd.

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RECOMBINATION BETWEEN GENES LOCATED ON NONHOMOLOGOUS CHROMOSOMES IN SACCHAROMYCES CEREVISIAE

Cited by 65 publications

References 15 publications

A test for the role of natural selection in the stabilization of transposable element copy number in a population ofDrosophila melanogaster

A test for the role of natural selection in the stabilization of transposable element copy number in a population ofDrosophila melanogaster

Interchromosomal segmental duplication drives translocation and loss ofP. falciparumhistidine-rich protein 3

A family of laboratory strains ofSaccharomyces cerevisiae carry rearrangements involving chromosomes I and III

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