The Experts below are selected from a list of 132 Experts worldwide ranked by ideXlab platform
Victoria H. Meller - One of the best experts on this subject based on the ideXlab platform.
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Satellite Repeats Identify X Chromatin for Dosage Compensation in Drosophila melanogaster Males
Current biology : CB, 2017Co-Authors: Sonal S. Joshi, Victoria H. MellerAbstract:A common feature of seX chromosomes is coordinated regulation of X-linked genes in one seX. Drosophila melanogaster males have one X chromosome, whereas females have two. The resulting imbalance in gene dosage is corrected by increased eXpression from the single X chromosome of males, a process known as dosage compensation. In flies, compensation involves recruitment of the male-specific lethal (MSL) compleX to X-linked genes and modification of Chromatin to increase eXpression. The eXtraordinary selectivity of the MSL compleX for the X chromosome has never been eXplained. We previously demonstrated that the small interfering RNA (siRNA) pathway and siRNA from a family of X-linked satellite repeats (1.688X repeats) promote X recognition. Now, we test the ability of 1.688X DNA to attract compensation to genes nearby and report that autosomal integration of 1.688X repeats increases MSL recruitment and gene eXpression in surrounding regions. Placement of 1.688X repeats opposite a lethal autosomal deletion achieves partial rescue of males, demonstrating functional compensation of autosomal Chromatin. Females block formation of the MSL compleX and are not rescued. The 1.688X repeats are therefore cis-acting elements that guide dosage compensation. Furthermore, 1.688X siRNA enhances rescue of males with a lethal deletion but only when repeat DNA is present on the intact homolog. We propose that the siRNA pathway promotes X recognition by enhancing the ability of 1.688X DNA to attract compensation in cis. The dense and near-eXclusive distribution of 1.688X sequences along the X chromosome suggests that they play a primary role in determining X identity during dosage compensation.
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siRNAs from an X-linked satellite repeat promote X-chromosome recognition in Drosophila melanogaster
Proceedings of the National Academy of Sciences of the United States of America, 2014Co-Authors: Debashish U. Menon, Cristian Coarfa, Weimin Xiao, Preethi H. Gunaratne, Victoria H. MellerAbstract:Highly differentiated seX chromosomes create a lethal imbalance in gene eXpression in one seX. To accommodate hemizygosity of the X chromosome in male fruit flies, eXpression of X-linked genes increases twofold. This is achieved by the male- specific lethal (MSL) compleX, which modifies Chromatin to increase eXpression. Mutations that disrupt the X localization of this compleX decrease the eXpression of X-linked genes and reduce male survival. The mechanism that restricts the MSL compleX to X Chromatin is not understood. We recently reported that the siRNA pathway contributes to localization of the MSL compleX, raising questions about the source of the siRNAs involved. The X-linked 1.688 g/cm3 satellite related repeats (1.688X repeats) are restricted to the X chromosome and produce small RNA, making them an attractive candidate. We tested RNA from these repeats for a role in dosage compensation and found that ectopic eXpression of single-stranded RNAs from 1.688X repeats enhanced the male lethality of mutants with defective X recognition. In contrast, eXpression of double-stranded hairpin RNA from a 1.688X repeat generated abundant siRNA and dramatically increased male survival. Consistent with improved survival, X localization of the MSL compleX was largely restored in these males. The striking distribution of 1.688X repeats, which are nearly eXclusive to the X chromosome, suggests that these are cis-acting elements contributing to identification of X Chromatin.
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A role for siRNA in X-chromosome dosage compensation in Drosophila melanogaster.
Genetics, 2012Co-Authors: Debashish U. Menon, Victoria H. MellerAbstract:SeX-chromosome dosage compensation requires selective identification of X Chromatin. How this occurs is not fully understood. We show that small interfering RNA (siRNA) mutations enhance the lethality of Drosophila males deficient in X recognition and partially rescue females that inappropriately dosage-compensate. Our findings are consistent with a role for siRNA in selective recognition of X Chromatin.
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roX RNAs and Genome Regulation in Drosophila Melanogaster.
Progress in molecular and subcellular biology, 2010Co-Authors: S. Kiran Koya, Victoria H. MellerAbstract:Organisms with dimorphic seX chromosomes suffer a potentially lethal imbalance in gene eXpression in one seX. Addressing this fundamental problem can be considered the first, and most essential, aspect of seXual differentiation. In the model organisms Drosophila, Caenorhabditis elegans, and mouse, eXpression from X-linked genes is modulated by selective recruitment of Chromatin-modifying compleXes to X Chromatin. In both flies and mammals, large noncoding RNAs have a central role in recruitment and activity of these compleXes. This review will summarize current knowledge of the function of the noncoding roX genes in this process in Drosophila. Identification of an autosomal function for the roX RNAs raises intriguing questions about the origin of the modern dosage compensation system in flies.
Debashish U. Menon - One of the best experts on this subject based on the ideXlab platform.
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siRNAs from an X-linked satellite repeat promote X-chromosome recognition in Drosophila melanogaster
Proceedings of the National Academy of Sciences of the United States of America, 2014Co-Authors: Debashish U. Menon, Cristian Coarfa, Weimin Xiao, Preethi H. Gunaratne, Victoria H. MellerAbstract:Highly differentiated seX chromosomes create a lethal imbalance in gene eXpression in one seX. To accommodate hemizygosity of the X chromosome in male fruit flies, eXpression of X-linked genes increases twofold. This is achieved by the male- specific lethal (MSL) compleX, which modifies Chromatin to increase eXpression. Mutations that disrupt the X localization of this compleX decrease the eXpression of X-linked genes and reduce male survival. The mechanism that restricts the MSL compleX to X Chromatin is not understood. We recently reported that the siRNA pathway contributes to localization of the MSL compleX, raising questions about the source of the siRNAs involved. The X-linked 1.688 g/cm3 satellite related repeats (1.688X repeats) are restricted to the X chromosome and produce small RNA, making them an attractive candidate. We tested RNA from these repeats for a role in dosage compensation and found that ectopic eXpression of single-stranded RNAs from 1.688X repeats enhanced the male lethality of mutants with defective X recognition. In contrast, eXpression of double-stranded hairpin RNA from a 1.688X repeat generated abundant siRNA and dramatically increased male survival. Consistent with improved survival, X localization of the MSL compleX was largely restored in these males. The striking distribution of 1.688X repeats, which are nearly eXclusive to the X chromosome, suggests that these are cis-acting elements contributing to identification of X Chromatin.
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A role for siRNA in X-chromosome dosage compensation in Drosophila melanogaster.
Genetics, 2012Co-Authors: Debashish U. Menon, Victoria H. MellerAbstract:SeX-chromosome dosage compensation requires selective identification of X Chromatin. How this occurs is not fully understood. We show that small interfering RNA (siRNA) mutations enhance the lethality of Drosophila males deficient in X recognition and partially rescue females that inappropriately dosage-compensate. Our findings are consistent with a role for siRNA in selective recognition of X Chromatin.
Brian Oliver - One of the best experts on this subject based on the ideXlab platform.
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An evolutionary consequence of dosage compensation on Drosophila melanogaster female X-Chromatin structure?
BMC Genomics, 2010Co-Authors: Yu Zhang, Brian OliverAbstract:Background X chromosomes are subject to dosage compensation in Drosophila males. Dosage compensation requires cis sequence features of the X chromosome that are present in both seXes by definition and trans acting factors that target Chromatin modifying machinery to the X specifically in males. The evolution of this system could result in neutral X Chromatin changes that will be apparent in females. Results We find that the general Chromatin structure of female X chromosomes is distinct from autosomes. Additionally, specific histone marks associated with dosage compensation and active Chromatin marks on the male X chromosome are also enriched on the X chromosomes of females, albeit to a lesser degree. Conclusions Our data indicate that X Chromatin structure is fundamentally different from autosome structure in both seXes. We suggest that the differences between the X chromosomes and autosomes in females are a consequence of mechanisms that have evolved to ensure sufficient X chromosome eXpression in the soma of males.
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An evolutionary consequence of dosage compensation on Drosophila melanogaster female X-Chromatin structure?
BMC genomics, 2010Co-Authors: Yu Zhang, Brian OliverAbstract:Background X chromosomes are subject to dosage compensation in Drosophila males. Dosage compensation requires cis sequence features of the X chromosome that are present in both seXes by definition and trans acting factors that target Chromatin modifying machinery to the X specifically in males. The evolution of this system could result in neutral X Chromatin changes that will be apparent in females.
Sonal S. Joshi - One of the best experts on this subject based on the ideXlab platform.
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Satellite Repeats Identify X Chromatin for Dosage Compensation in Drosophila melanogaster Males
Current biology : CB, 2017Co-Authors: Sonal S. Joshi, Victoria H. MellerAbstract:A common feature of seX chromosomes is coordinated regulation of X-linked genes in one seX. Drosophila melanogaster males have one X chromosome, whereas females have two. The resulting imbalance in gene dosage is corrected by increased eXpression from the single X chromosome of males, a process known as dosage compensation. In flies, compensation involves recruitment of the male-specific lethal (MSL) compleX to X-linked genes and modification of Chromatin to increase eXpression. The eXtraordinary selectivity of the MSL compleX for the X chromosome has never been eXplained. We previously demonstrated that the small interfering RNA (siRNA) pathway and siRNA from a family of X-linked satellite repeats (1.688X repeats) promote X recognition. Now, we test the ability of 1.688X DNA to attract compensation to genes nearby and report that autosomal integration of 1.688X repeats increases MSL recruitment and gene eXpression in surrounding regions. Placement of 1.688X repeats opposite a lethal autosomal deletion achieves partial rescue of males, demonstrating functional compensation of autosomal Chromatin. Females block formation of the MSL compleX and are not rescued. The 1.688X repeats are therefore cis-acting elements that guide dosage compensation. Furthermore, 1.688X siRNA enhances rescue of males with a lethal deletion but only when repeat DNA is present on the intact homolog. We propose that the siRNA pathway promotes X recognition by enhancing the ability of 1.688X DNA to attract compensation in cis. The dense and near-eXclusive distribution of 1.688X sequences along the X chromosome suggests that they play a primary role in determining X identity during dosage compensation.
J. Del Mazo - One of the best experts on this subject based on the ideXlab platform.
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A case of trisomy 8 mosaicism 47, XX + 8/46, XX.
Clinical genetics, 2008Co-Authors: V. Aller, J. A. Abrisqueta, A. Perez, M. A. Martin, Clara Goday, J. Del MazoAbstract:The cytogenetic study is reported of a female infant affected with several malformations and presenting a mosaicism of the type 47,XX, + 8/46,XX in her karyotype. G-band analysis and the distribution curves of these bands were studied in order to obtain a more objective identification of trisomy 8. Results of Q-banding, X-Chromatin and der-matoglyphic studies are given and compared with previous reports.
