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: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.
Project description:In Drosophila, two chromosome-wide compensatory systems have been characterized; the dosage compensation system acting on the male X-chromosome and the chromosome specific regulation of genes located on the heterochromatic 4th chromosome. Dosage compensation in Drosophila is accomplished by hypertranscription of the single male X-chromosome mediated by the MSL-complex. The mechanism for this compensation is suggested to be an MSL-complex mediated enhanced transcriptional elongation while the mechanism for the compensation mediated by Painting of fourth (POF) on the 4th chromosome has remained elusive. Here we show that POF binds to nascent RNA and this binding is associated with an increase in amount of chromosome 4 transcripts. Furthermore, genes located on the 4th chromosome are enriched in binding of the nucleoplasmic nucleporin component NUP98 and this enrichment correlates to increased POF binding. We also show that genes located in heterochromatic regions have a shorter transition time from site of transcription and to the nuclear envelope. Our current work broadens the understanding about how genes in heterochromatic regions can overcome the repressive influence of their hostile environment.