The Experts below are selected from a list of 156 Experts worldwide ranked by ideXlab platform
Justin P. Blumenstiel - One of the best experts on this subject based on the ideXlab platform.
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Hybrid Dysgenesis in drosophila virilis results in clusters of mitotic recombination and loss of heterozygosity but leaves meiotic recombination unaltered
Mobile Dna, 2020Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:Transposable elements (TEs) are endogenous mutagens and their harmful effects are especially evident in syndromes of Hybrid Dysgenesis. In Drosophila virilis, Hybrid Dysgenesis is a syndrome of incomplete gonadal atrophy that occurs when males with multiple active TE families fertilize females that lack active copies of the same families. This has been demonstrated to cause the transposition of paternally inherited TE families, with gonadal atrophy driven by the death of germline stem cells. Because there are abundant, active TEs in the male inducer genome, that are not present in the female reactive genome, the D. virilis syndrome serves as an excellent model for understanding the effects of Hybridization between individuals with asymmetric TE profiles. Using the D. virilis syndrome of Hybrid Dysgenesis as a model, we sought to determine how the landscape of germline recombination is affected by parental TE asymmetry. Using a genotyping-by-sequencing approach, we generated a high-resolution genetic map of D. virilis and show that recombination rate and TE density are negatively correlated in this species. We then contrast recombination events in the germline of dysgenic versus non-dysgenic F1 females to show that the landscape of meiotic recombination is hardly perturbed during Hybrid Dysgenesis. In contrast, Hybrid Dysgenesis in the female germline increases transmission of chromosomes with mitotic recombination. Using a de novo PacBio assembly of the D. virilis inducer genome we show that clusters of mitotic recombination events in dysgenic females are associated with genomic regions with transposons implicated in Hybrid Dysgenesis. Overall, we conclude that increased mitotic recombination is likely the result of early TE activation in dysgenic progeny, but a stable landscape of meiotic recombination indicates that either transposition is ameliorated in the adult female germline or that regulation of meiotic recombination is robust to ongoing transposition. These results indicate that the effects of parental TE asymmetry on recombination are likely sensitive to the timing of transposition.
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the meiotic recombination landscape of drosophila virilis is robust to mitotic damage during Hybrid Dysgenesis
bioRxiv, 2019Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:ABSTRACT Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of Hybrid Dysgenesis in Drosophila virilis. In this system, a cross between two strains of D. virilis with divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during Hybrid Dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that Hybrid Dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.
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the recombination landscape of drosophila virilis is robust to transposon activation in Hybrid Dysgenesis
bioRxiv, 2018Co-Authors: Lucas W Hemmer, Justin P. BlumenstielAbstract:DNA damage in the germline is a double-edged sword. Induced double-strand breaks establish the foundation for meiotic recombination and proper chromosome segregation but can also pose a significant challenge for genome stability. Within the germline, transposable elements are powerful agents of double-strand break formation. How different types of DNA damage are resolved within the germline is poorly understood. For example, little is known about the relationship between the frequency of double-stranded breaks, both endogenous and exogenous, and the decision to repair DNA through one of the many pathways, including crossing over and gene conversion. Here we use the Drosophila virilis Hybrid Dysgenesis model to determine how recombination landscapes change under transposable element activation. In this system, a cross between two strains of D. virilis with divergent transposable element profiles results in the Hybrid Dysgenesis phenotype, which includes the germline activation of diverse transposable elements, reduced fertility, and male recombination. However, only one direction of the cross results in Hybrid Dysgenesis. This allows the study of recombination in genetically identical F1 females; those with baseline levels of programmed DNA damage and those with an increased level of DNA damage resulting from transposable element proliferation. Using multiplexed shotgun genotyping to map crossover events, we compared the recombination landscapes of Hybrid dysgenic and non-Hybrid dysgenic individuals. The frequency and distribution of meiotic recombination appears to be robust during Hybrid Dysgenesis. However, Hybrid Dysgenesis is also associated with occasional clusters of recombination derived from single dysgenic F1 mothers. The clusters of recombination are hypothesized to be the result of mitotic crossovers during early germline development. Overall, these results show that meiotic recombination in D. virilis is robust to the damage caused by transposable elements during early development.
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Whole genome sequencing in Drosophila virilis identifies Polyphemus, a recently activated Tc1-like transposon with a possible role in Hybrid Dysgenesis
Mobile DNA, 2014Co-Authors: Justin P. BlumenstielAbstract:Background: Hybrid dysgenic syndromes in Drosophila have been critical for characterizing host mechanisms of transposable element (TE) regulation. This is because a common feature of Hybrid Dysgenesis is germline TE mobilization that occurs when paternally inherited TEs are not matched with a maternal pool of silencing RNAs that maintain transgenerational TE control. In the face of this imbalance TEs become activated in the germline and can cause F1 sterility. The syndrome of Hybrid Dysgenesis in Drosophila virilis was the first to show that the mobilization of one dominant TE, the Penelope retrotransposon, may lead to the mobilization of other unrelated elements. However, it is not known how many different elements contribute and no exhaustive search has been performed to identify additional ones. To identify additional TEs that may contribute to Hybrid Dysgenesis in Drosophila virilis, I analyzed repeat content in genome sequences of inducer and non-inducer lines. Results: Here I describe Polyphemus, a novel Tc1-like DNA transposon, which is abundant in the inducer strain of D. virilis but highly degraded in the non-inducer strain. Polyphemus expression is also increased in the germline of progeny of the dysgenic cross relative to reciprocal progeny. Interestingly, like the Penelope element, it has experienced recent re-activation within the D. virilis lineage. Conclusions: Here I present the results of a comprehensive search to identify additional factors that may cause Hybrid Dysgenesis in D. virilis. Polyphemus, a novel Tc1-like DNA transposon, has recently become re-activated in Drosophila virilis and likely contributes to the Hybrid Dysgenesis syndrome. It has been previously shown that the Penelope element has also been re-activated in the inducer strain. This suggests that TE co-reactivation within species may synergistically contribute to syndromes of Hybrid Dysgenesis.
Lucas W Hemmer - One of the best experts on this subject based on the ideXlab platform.
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Hybrid Dysgenesis in drosophila virilis results in clusters of mitotic recombination and loss of heterozygosity but leaves meiotic recombination unaltered
Mobile Dna, 2020Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:Transposable elements (TEs) are endogenous mutagens and their harmful effects are especially evident in syndromes of Hybrid Dysgenesis. In Drosophila virilis, Hybrid Dysgenesis is a syndrome of incomplete gonadal atrophy that occurs when males with multiple active TE families fertilize females that lack active copies of the same families. This has been demonstrated to cause the transposition of paternally inherited TE families, with gonadal atrophy driven by the death of germline stem cells. Because there are abundant, active TEs in the male inducer genome, that are not present in the female reactive genome, the D. virilis syndrome serves as an excellent model for understanding the effects of Hybridization between individuals with asymmetric TE profiles. Using the D. virilis syndrome of Hybrid Dysgenesis as a model, we sought to determine how the landscape of germline recombination is affected by parental TE asymmetry. Using a genotyping-by-sequencing approach, we generated a high-resolution genetic map of D. virilis and show that recombination rate and TE density are negatively correlated in this species. We then contrast recombination events in the germline of dysgenic versus non-dysgenic F1 females to show that the landscape of meiotic recombination is hardly perturbed during Hybrid Dysgenesis. In contrast, Hybrid Dysgenesis in the female germline increases transmission of chromosomes with mitotic recombination. Using a de novo PacBio assembly of the D. virilis inducer genome we show that clusters of mitotic recombination events in dysgenic females are associated with genomic regions with transposons implicated in Hybrid Dysgenesis. Overall, we conclude that increased mitotic recombination is likely the result of early TE activation in dysgenic progeny, but a stable landscape of meiotic recombination indicates that either transposition is ameliorated in the adult female germline or that regulation of meiotic recombination is robust to ongoing transposition. These results indicate that the effects of parental TE asymmetry on recombination are likely sensitive to the timing of transposition.
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the meiotic recombination landscape of drosophila virilis is robust to mitotic damage during Hybrid Dysgenesis
bioRxiv, 2019Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:ABSTRACT Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of Hybrid Dysgenesis in Drosophila virilis. In this system, a cross between two strains of D. virilis with divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during Hybrid Dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that Hybrid Dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.
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the recombination landscape of drosophila virilis is robust to transposon activation in Hybrid Dysgenesis
bioRxiv, 2018Co-Authors: Lucas W Hemmer, Justin P. BlumenstielAbstract:DNA damage in the germline is a double-edged sword. Induced double-strand breaks establish the foundation for meiotic recombination and proper chromosome segregation but can also pose a significant challenge for genome stability. Within the germline, transposable elements are powerful agents of double-strand break formation. How different types of DNA damage are resolved within the germline is poorly understood. For example, little is known about the relationship between the frequency of double-stranded breaks, both endogenous and exogenous, and the decision to repair DNA through one of the many pathways, including crossing over and gene conversion. Here we use the Drosophila virilis Hybrid Dysgenesis model to determine how recombination landscapes change under transposable element activation. In this system, a cross between two strains of D. virilis with divergent transposable element profiles results in the Hybrid Dysgenesis phenotype, which includes the germline activation of diverse transposable elements, reduced fertility, and male recombination. However, only one direction of the cross results in Hybrid Dysgenesis. This allows the study of recombination in genetically identical F1 females; those with baseline levels of programmed DNA damage and those with an increased level of DNA damage resulting from transposable element proliferation. Using multiplexed shotgun genotyping to map crossover events, we compared the recombination landscapes of Hybrid dysgenic and non-Hybrid dysgenic individuals. The frequency and distribution of meiotic recombination appears to be robust during Hybrid Dysgenesis. However, Hybrid Dysgenesis is also associated with occasional clusters of recombination derived from single dysgenic F1 mothers. The clusters of recombination are hypothesized to be the result of mitotic crossovers during early germline development. Overall, these results show that meiotic recombination in D. virilis is robust to the damage caused by transposable elements during early development.
Ashley Howard - One of the best experts on this subject based on the ideXlab platform.
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Hybrid Dysgenesis in drosophila virilis results in clusters of mitotic recombination and loss of heterozygosity but leaves meiotic recombination unaltered
Mobile Dna, 2020Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:Transposable elements (TEs) are endogenous mutagens and their harmful effects are especially evident in syndromes of Hybrid Dysgenesis. In Drosophila virilis, Hybrid Dysgenesis is a syndrome of incomplete gonadal atrophy that occurs when males with multiple active TE families fertilize females that lack active copies of the same families. This has been demonstrated to cause the transposition of paternally inherited TE families, with gonadal atrophy driven by the death of germline stem cells. Because there are abundant, active TEs in the male inducer genome, that are not present in the female reactive genome, the D. virilis syndrome serves as an excellent model for understanding the effects of Hybridization between individuals with asymmetric TE profiles. Using the D. virilis syndrome of Hybrid Dysgenesis as a model, we sought to determine how the landscape of germline recombination is affected by parental TE asymmetry. Using a genotyping-by-sequencing approach, we generated a high-resolution genetic map of D. virilis and show that recombination rate and TE density are negatively correlated in this species. We then contrast recombination events in the germline of dysgenic versus non-dysgenic F1 females to show that the landscape of meiotic recombination is hardly perturbed during Hybrid Dysgenesis. In contrast, Hybrid Dysgenesis in the female germline increases transmission of chromosomes with mitotic recombination. Using a de novo PacBio assembly of the D. virilis inducer genome we show that clusters of mitotic recombination events in dysgenic females are associated with genomic regions with transposons implicated in Hybrid Dysgenesis. Overall, we conclude that increased mitotic recombination is likely the result of early TE activation in dysgenic progeny, but a stable landscape of meiotic recombination indicates that either transposition is ameliorated in the adult female germline or that regulation of meiotic recombination is robust to ongoing transposition. These results indicate that the effects of parental TE asymmetry on recombination are likely sensitive to the timing of transposition.
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the meiotic recombination landscape of drosophila virilis is robust to mitotic damage during Hybrid Dysgenesis
bioRxiv, 2019Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:ABSTRACT Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of Hybrid Dysgenesis in Drosophila virilis. In this system, a cross between two strains of D. virilis with divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during Hybrid Dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that Hybrid Dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.
Casey M Bergman - One of the best experts on this subject based on the ideXlab platform.
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Hybrid Dysgenesis in drosophila virilis results in clusters of mitotic recombination and loss of heterozygosity but leaves meiotic recombination unaltered
Mobile Dna, 2020Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:Transposable elements (TEs) are endogenous mutagens and their harmful effects are especially evident in syndromes of Hybrid Dysgenesis. In Drosophila virilis, Hybrid Dysgenesis is a syndrome of incomplete gonadal atrophy that occurs when males with multiple active TE families fertilize females that lack active copies of the same families. This has been demonstrated to cause the transposition of paternally inherited TE families, with gonadal atrophy driven by the death of germline stem cells. Because there are abundant, active TEs in the male inducer genome, that are not present in the female reactive genome, the D. virilis syndrome serves as an excellent model for understanding the effects of Hybridization between individuals with asymmetric TE profiles. Using the D. virilis syndrome of Hybrid Dysgenesis as a model, we sought to determine how the landscape of germline recombination is affected by parental TE asymmetry. Using a genotyping-by-sequencing approach, we generated a high-resolution genetic map of D. virilis and show that recombination rate and TE density are negatively correlated in this species. We then contrast recombination events in the germline of dysgenic versus non-dysgenic F1 females to show that the landscape of meiotic recombination is hardly perturbed during Hybrid Dysgenesis. In contrast, Hybrid Dysgenesis in the female germline increases transmission of chromosomes with mitotic recombination. Using a de novo PacBio assembly of the D. virilis inducer genome we show that clusters of mitotic recombination events in dysgenic females are associated with genomic regions with transposons implicated in Hybrid Dysgenesis. Overall, we conclude that increased mitotic recombination is likely the result of early TE activation in dysgenic progeny, but a stable landscape of meiotic recombination indicates that either transposition is ameliorated in the adult female germline or that regulation of meiotic recombination is robust to ongoing transposition. These results indicate that the effects of parental TE asymmetry on recombination are likely sensitive to the timing of transposition.
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the meiotic recombination landscape of drosophila virilis is robust to mitotic damage during Hybrid Dysgenesis
bioRxiv, 2019Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:ABSTRACT Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of Hybrid Dysgenesis in Drosophila virilis. In this system, a cross between two strains of D. virilis with divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during Hybrid Dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that Hybrid Dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.
Kelley Van Vaerenberghe - One of the best experts on this subject based on the ideXlab platform.
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Hybrid Dysgenesis in drosophila virilis results in clusters of mitotic recombination and loss of heterozygosity but leaves meiotic recombination unaltered
Mobile Dna, 2020Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:Transposable elements (TEs) are endogenous mutagens and their harmful effects are especially evident in syndromes of Hybrid Dysgenesis. In Drosophila virilis, Hybrid Dysgenesis is a syndrome of incomplete gonadal atrophy that occurs when males with multiple active TE families fertilize females that lack active copies of the same families. This has been demonstrated to cause the transposition of paternally inherited TE families, with gonadal atrophy driven by the death of germline stem cells. Because there are abundant, active TEs in the male inducer genome, that are not present in the female reactive genome, the D. virilis syndrome serves as an excellent model for understanding the effects of Hybridization between individuals with asymmetric TE profiles. Using the D. virilis syndrome of Hybrid Dysgenesis as a model, we sought to determine how the landscape of germline recombination is affected by parental TE asymmetry. Using a genotyping-by-sequencing approach, we generated a high-resolution genetic map of D. virilis and show that recombination rate and TE density are negatively correlated in this species. We then contrast recombination events in the germline of dysgenic versus non-dysgenic F1 females to show that the landscape of meiotic recombination is hardly perturbed during Hybrid Dysgenesis. In contrast, Hybrid Dysgenesis in the female germline increases transmission of chromosomes with mitotic recombination. Using a de novo PacBio assembly of the D. virilis inducer genome we show that clusters of mitotic recombination events in dysgenic females are associated with genomic regions with transposons implicated in Hybrid Dysgenesis. Overall, we conclude that increased mitotic recombination is likely the result of early TE activation in dysgenic progeny, but a stable landscape of meiotic recombination indicates that either transposition is ameliorated in the adult female germline or that regulation of meiotic recombination is robust to ongoing transposition. These results indicate that the effects of parental TE asymmetry on recombination are likely sensitive to the timing of transposition.
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the meiotic recombination landscape of drosophila virilis is robust to mitotic damage during Hybrid Dysgenesis
bioRxiv, 2019Co-Authors: Lucas W Hemmer, Guilherme B Dias, Brittny R Smith, Kelley Van Vaerenberghe, Ashley Howard, Casey M Bergman, Justin P. BlumenstielAbstract:ABSTRACT Germline DNA damage is a double-edged sword. Programmed double-strand breaks establish the foundation for meiotic recombination and chromosome segregation. However, double-strand breaks also pose a significant challenge for genome stability. Because of this, meiotic double-strand break formation is tightly regulated. However, natural selection can favor selfish behavior in the germline and transposable elements can cause double-strand breaks independent of the carefully regulated meiotic process. To understand how the regulatory mechanisms of meiotic recombination accommodate unregulated transposition, we have characterized the female recombination landscape in a syndrome of Hybrid Dysgenesis in Drosophila virilis. In this system, a cross between two strains of D. virilis with divergent transposable element and piRNA profiles results in germline transposition of diverse transposable elements, reduced fertility, and male recombination. We sought to determine how increased transposition during Hybrid Dysgenesis might perturb the meiotic recombination landscape. Our results show that the overall frequency and distribution of meiotic recombination is extremely robust to germline transposable element activation. However, we also find that Hybrid Dysgenesis can result in mitotic recombination within the female germline. Overall, these results show that landscape of meiotic recombination may be insensitive to the DNA damage caused by transposition during early development.
