SRA

Isolation of copy number variations and chromosomal duplications at high frequency in Caenorhabditis elegans suggested that this organism tolerates dosage problems. Here we addressed if this tolerance is due to a genome-wide compensation mechanism acting at the level of mRNA expression. We characterized several chromosomal duplication strains using DNA-seq and analyzed gene expression in two duplication and a fosmid integration strain using mRNA-seq. Our results show that on average, increased gene dosage leads to increased mRNA expression, pointing to a lack of genome-wide dosage compensation. Different genes within the same duplicated region show variable changes in mRNA expression, suggesting feedback regulation of individual genes. Transcriptional repression by somatic dosage compensation and germline silencing contribute to the level of mRNA increase from a large X chromosomal duplication. In sum, our results show a lack of genome-wide dosage compensation mechanism acting at the mRNA level in C. elegans and highlight the role of epigenetic and individual gene regulation contributing to the varied consequences of increased gene dosage. Overall design: DNA-seq and RNA-seq in large duplication strains to look at copy number variation and effect of DCC recruitment on the transcriptional output of duplicated segments in CNV. Comparison between strains that recruit DCC and those that do not.