Unknown,Transcriptomics,Genomics,Proteomics

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Evolutionary shift of X aneuploid targets from X chromosome to Autosomeand their dose dependent expression are mitigated by maleless gene.

ABSTRACT: During sexual dimorphism, the loss of one entire X chromosome in Drosophila males is achieved largely via a broad genome-wide aneuploid effect. Exploring how MSL proteins and two large non coding RNAs (roX1 and roX2) modulate trans-acting aneuploid effect for equality to females, we employ a system biology approach (microarray) to investigate the global aneuploid effect of maleless(mle) mutation by disrupting MSL binding. A large number of the genes (144) that encode a broad spectrum of cellular transport proteins and transcription factors are located in the autosomes of Drosophila melanogaster. We find these autosomal targets are sensitive to the aneuploid effect and are poorly conserved in primitive Drosophila species and Anopheles gambiae autosomes. It is expected that during evolutionary process, they shifted gradually from their X chromosomal position in primitive Drosophila to autosomes in melanogaster, suggesting that MSL favors inverse counteraction of these autosomal targets along with X-linked genes. These findings suggest a remarkable and previously unsuspected level of complexity among aneuploid-sensitive genes, that creates a functional shift of the aneuploid effect from X to autosomes during evolution, which is resolved by the binding of MSL complex on the X chromosome.. Drosophila larvae were selected based on genotypes particularly with Tb phenotypes. Total cellular RNA were extracted from each genotypes and hebridized with affymetrix Drosophila Microarray chip. Gene Expression profiling of fly base to understand the role of maleless mutation in aneuploid targets.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Utpal Bhadra

PROVIDER: E-GEOD-78227 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Drosophila males double transcription of their single X chromosome to equalize X-linked gene expression with females, which carry two X chromosomes. Increased transcription requires the Male-Specific Lethal (MSL) complex. One of the primary functions of the MSL complex is thought to be enrichment of H4Ac16 on the male X chromosome, a modification linked to elevated transcription. The roX1 and roX2 RNAs are essential but redundant components of the MSL complex. Simultaneous removal of both roX RNAs reduces MSL X-localization and leads to ectopic binding of these proteins at autosomal sites and to the chromocenter. Some H4Ac16 accumulates at these ectopic sites in roX1- roX2- males, suggesting the possibility of increased expression. The global effect of roX mutations on gene expression was measured by microarray analysis. We found that expression of the X chromosome was decreased by 26% in roX1- roX2- male larvae, supporting the involvement of roX RNAs in the up-regulation of X-linked genes. This finding is broadly comparable to reports of reduced X chromosome expression following msl2 RNAi knockdown in S2 cells. In spite of strong MSL binding and H4Ac16 accumulation at autosomal sites in roX1- roX2- males, enhanced gene expression could not be detected at these sites by microarray analysis or reverse northern blotting. Thus, failure to compensate X-linked genes, rather than inappropriate up-regulation of autosomal genes at ectopic sites of MSL binding, appears to cause male lethality upon loss of roX RNAs. Experiment Overall Design: Total RNA was prepared from groups of 50 third instar larvae by TRIzol (Invitrogen) extraction and purified using the RNeasy kit (Qiagen). Three independent RNA preparations for each genotype served as templates for probe synthesis. Affymetrix Drosophila Genome 2.0 chips were hybridized to these probes (Santa Clara, CA). The affymertrix Drosophila annotation of December 2004 was used to map genes to their cytological locations. Genes were filtered for present/absent calls by a PM-MM (Perfect match- Mismatch) comparison. Autosomal transcripts were normalized on a chip-by-chip basis to bring their median values to 100. The identical degree of adjustment was used to normalize X-linked transcripts. Changes in gene expression were determined by comparing the mean signal intensities of genes on arrays hybridized with roX1SMC17A roX2- probes to those hybridized with roX1+ roX2- probes.

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Evolutionary shift of X aneuploid targets from X chromosome to Autosomeand their dose dependent expression are mitigated by maleless gene.

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