Project description:Transposons evolve rapidly and can mobilize and trigger genetic instability. piRNAs silence these genome pathogens, but it is unclear how the piRNA pathway adapts to new transposons. In Drosophila piRNAs, encoded by heterochromatic clusters are maternally deposited in the embryo. Paternally inherited P-element transposons thus escape silencing and trigger a genetic instability and sterility. We show that this syndrome, termed P-M hybrid dysgenesis, also disrupts the piRNA biogenesis machinery and activates resident transposons. As dysgenic hybrids age, however, fertility is restored, P-elements are silenced, and P-element piRNAs are produced de novo. In addition, the piRNA biogenesis machinery is restored and resident elements are silenced. Significantly, new resident transposons insertions accumulate in piRNA clusters, and these new insertions are transmitted to progeny with high fidelity, produce novel piRNAs, and are associated with reduced transposition. P-M hybrid dysgenesis thus leads to heritable changes in chromosome structure that appear to enhance transposon silencing.
Project description:Recent studies have revealed key roles of non-coding RNAs in sex-related pathways, but little is known about the evolutionary forces acting on these non-coding RNAs. We used whole-genome tiling arrays to profile the transcriptome of Drosophila melanogaster tissues and found that 15% of male-biased transcribed fragments (transfrags) are intergenic non-coding RNAs (incRNAs), suggesting a potentially important role for incRNAs in sex-related biological processes. Statistical analysis revealed a paucity of male-biased incRNAs and coding genes on the X chromosome, suggesting that similar evolutionary forces could be affecting the genomic organization of both coding and non-coding genes. Expression profiling across germline and somatic tissues further suggests that both male meiotic sex chromosome inactivation (MSCI) and sexual antagonism contribute to the chromosomal distribution of male-biased incRNAs. Comparative sequence analysis shows that the evolutionary age of male-biased incRNAs is a significant predictor of their chromosomal locations. In addition to identifying abundant sex-biased incRNAs in fly genome, our work unveils a global picture of the complex interplay between non-coding RNAs and sexual chromosome evolution.
Project description:Transposons evolve rapidly and can mobilize and trigger genetic instability. piRNAs silence these genome pathogens, but it is unclear how the piRNA pathway adapts to new transposons. In Drosophila piRNAs, encoded by heterochromatic clusters are maternally deposited in the embryo. Paternally inherited P-element transposons thus escape silencing and trigger a genetic instability and sterility. We show that this syndrome, termed P-M hybrid dysgenesis, also disrupts the piRNA biogenesis machinery and activates resident transposons. As dysgenic hybrids age, however, fertility is restored, P-elements are silenced, and P-element piRNAs are produced de novo. In addition, the piRNA biogenesis machinery is restored and resident elements are silenced. Significantly, new resident transposons insertions accumulate in piRNA clusters, and these new insertions are transmitted to progeny with high fidelity, produce novel piRNAs, and are associated with reduced transposition. P-M hybrid dysgenesis thus leads to heritable changes in chromosome structure that appear to enhance transposon silencing. 3 replicates of each sample (Har 2-4 days, w1 x Har 2-4 days, w1 x Har 21 days), total RNA samples hybridized to tiling array.
Project description:Recent studies have revealed key roles of non-coding RNAs in sex-related pathways, but little is known about the evolutionary forces acting on these non-coding RNAs. We used whole-genome tiling arrays to profile the transcriptome of Drosophila melanogaster tissues and found that 15% of male-biased transcribed fragments (transfrags) are intergenic non-coding RNAs (incRNAs), suggesting a potentially important role for incRNAs in sex-related biological processes. Statistical analysis revealed a paucity of male-biased incRNAs and coding genes on the X chromosome, suggesting that similar evolutionary forces could be affecting the genomic organization of both coding and non-coding genes. Expression profiling across germline and somatic tissues further suggests that both male meiotic sex chromosome inactivation (MSCI) and sexual antagonism contribute to the chromosomal distribution of male-biased incRNAs. Comparative sequence analysis shows that the evolutionary age of male-biased incRNAs is a significant predictor of their chromosomal locations. In addition to identifying abundant sex-biased incRNAs in fly genome, our work unveils a global picture of the complex interplay between non-coding RNAs and sexual chromosome evolution. We used whole-genome tiling arrays to assess sex-biased transcription in D. melanogaster adult whole bodies, and testis, ovary, and accessory gland samples. Gut and thorax, tissues expected to exhibit little or no sex-biased expression, were included as controls. Expression was measured in 2-4 replicates for each tissue.
Project description:Curration of small RNAs from four melanogaster-subgroup species (Drosophila simulans, Drosophila sechellia, Drosophila erecta, and Drosophila yakuba) for the purpose of non-coding RNA annotation and comparative genomics assessment.