Project description:We measured gene expression in two isogenic Drosophila lines heterozygous for long deletions. We find that a majority of genes are at least partially compensated at transcription for ½-fold dosage. The degree of compensation does not vary among functional classes of genes. Compensation for deletions is stronger for highly expressed genes than for genes with low expression level. In contrast, the degree of compensation for duplications observed in Gupta et al, 2006, (J. of Biology 5, 3) data for heterozygotes for a duplication is stronger for weakly expressed genes. Thus, transcriptional compensation appears to be based on general regulatory mechanisms that insure high levels of transcription some genes and low transcription levels of other genes, instead of precise maintenance of a particular homeostatic expression level. Given the ubiquity of transcriptional compensation, dominance of wild-type alleles may be at least partially caused by of the regulation at transcription level. Keywords: Genome-wise dosage compensation study
Project description:We measured gene expression in two isogenic Drosophila lines heterozygous for long deletions. We find that a majority of genes are at least partially compensated at transcription for ½-fold dosage. The degree of compensation does not vary among functional classes of genes. Compensation for deletions is stronger for highly expressed genes than for genes with low expression level. In contrast, the degree of compensation for duplications observed in Gupta et al, 2006, (J. of Biology 5, 3) data for heterozygotes for a duplication is stronger for weakly expressed genes. Thus, transcriptional compensation appears to be based on general regulatory mechanisms that insure high levels of transcription some genes and low transcription levels of other genes, instead of precise maintenance of a particular homeostatic expression level. Given the ubiquity of transcriptional compensation, dominance of wild-type alleles may be at least partially caused by of the regulation at transcription level. Keywords: Genome-wise dosage compensation study Two DrosDel [34] Drosophila melanogaster isogenic lines, Df(3L)ED4475 and Df(3L)ED4543, heterozygous for long deletions on 3L chromosomal branch both maintained against the TM6C balancer were used for microarray experiment. Twenty five adult flies 2-5 days after eclosion were frozen in liquid nitrogen and used for RNA extraction by Trizol method (Invitrogen ®, Carlsbad, CA) in twelve replicates from each line. The two deletion lines served as controls to each other.
Project description:This experiment was designed to investigate the epigenetic basis of sex chromosome dosage compensation. Such mechanisms often operate through epigenetic modifications, including histone modifications, which alter chromatin structure and gene expression. In Drosophila melanogaster, dosage compensation is achieved by upregulating the single X chromosome in males through acetylation of histone H4 at lysine 16 (H4K16ac). We therefore used D. melanogaster as a positive control to validate our approach. In contrast, the mechanism of dosage compensation in Bacillus grandii remains unknown. By profiling H4K16ac in this species, we aim to test whether this histone modification may have been convergently recruited to mediate dosage compensation.
Project description:Drosophila X chromosomes are subject to dosage compensation in males and are known to have a specialized chromatin structure in the male soma. We are interested in how specific chromatin structure change contributes to X chromosome hyperactivity and dosage compensation. We have conducted a global analysis of localize two dosage compensation complex dependent histone marks H4AcK16 and H3PS10 and one dosage compensation complex independent histone mark H3diMeK4 in the genome, especially on X chromosome by ChIP-chip approach in both male and female adult flies. We also probed general genomewide chromatin structure by deep DNA sequencing of sheared ChIP input DNA from male and female adult flies.