A sequence motif enriched in regions bound by the Drosophila dosage compensation complex

Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Científicas (IBV-CSIC), Valencia, Spain.
BMC Genomics (Impact Factor: 4.04). 03/2010; 11:169. DOI: 10.1186/1471-2164-11-169
Source: PubMed

ABSTRACT In Drosophila melanogaster, dosage compensation is mediated by the action of the dosage compensation complex (DCC). How the DCC recognizes the fly X chromosome is still poorly understood. Characteristic sequence signatures at all DCC binding sites have not hitherto been found.
In this study, we compare the known binding sites of the DCC with oligonucleotide profiles that measure the specificity of the sequences of the D. melanogaster X chromosome. We show that the X chromosome regions bound by the DCC are enriched for a particular type of short, repetitive sequences. Their distribution suggests that these sequences contribute to chromosome recognition, the generation of DCC binding sites and/or the local spreading of the complex. Comparative data indicate that the same sequences may be involved in dosage compensation in other Drosophila species.
These results offer an explanation for the wild-type binding of the DCC along the Drosophila X chromosome, contribute to delineate the forces leading to the establishment of dosage compensation and suggest new experimental approaches to understand the precise biochemical features of the dosage compensation system.

Download full-text


Available from: Miguel Gallach, Jul 05, 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Repetitive DNA are DNA sequences that are repeated multiple times in the genome and normally considered non-functional. Several studies predict that the rapid evolution of chromosome-specific satellites led to hybrid incompatibilities and speciation. Interestingly, in Drosophila, the X and dot chromosomes share a unique and noteworthy property: they are identified by chromosome-specific binding proteins and they are particularly involved in genetic incompatibilities between closely related species. Here, I show that the X and dot chromosomes are overpopulated by certain repetitive elements that undergo recurrent turnover in Drosophila species. The portion of the X and dot chromosomes covered by such satellites is up to 52 times and 44 times higher than in other chromosomes, respectively. In addition, the newly evolved X chromosome in D. pseudoobscura (the chromosomal arm XR) has been invaded by the same satellite that colonized the ancestral X chromosome (chromosomal arm XL), while the autosomal homologs in other species remain mostly devoid of satellites. Contrarily, the Müller element F in D. ananassae, homolog to the dot chromosome in D. melanogaster, has no overrepresented DNA sequences compared to any other chromosome. The biology and evolutionary patterns of the characterized satellites suggest that they provide both chromosomes with some kind of structural identity and are exposed to natural selection. The rapid satellite turnover fits some speciation models and may explain why these two chromosomes are typically involved in hybrid incompatibilities.
    Genome Biology and Evolution 05/2014; DOI:10.1093/gbe/evu104
  • [Show abstract] [Hide abstract]
    ABSTRACT: Describes a set of metrics based on analytical methods which evaluate the efficiency of programmable logic architectures, whether programmable logic device (PLD), programmable logic array (PLA), field-programmable gate array (FPGA), or complex channeled PLD (CPLD). The metrics are easily derived and form an equable measure of architectural efficiency across any device. Further, the metrics provide a pragmatic approach to device selection by quantifying the demands of a circuit, and comparing this against the availability of resources within a programmable architecture. In addition, the author provides a tutorial on the use of the metrics while focusing on a quantitative approach to benchmarking.< >
    Compcon Spring '93, Digest of Papers.; 03/1993
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The Drosophila Male Specific Lethal (MSL) complex contains chromatin modifying enzymes and non-coding roX RNA. It paints the male X at hundreds of bands where it acetylates histone H4 at lysine 16. This epigenetic mark increases expression from the single male X chromosome approximately twofold above what gene-specific factors produce from each female X chromosome. This equalises X-linked gene expression between the sexes. Previous screens for components of dosage compensation relied on a distinctive male-specific lethal phenotype. Here, we report a new strategy relying upon an unusual male-specific mosaic eye pigmentation phenotype produced when the MSL complex acts upon autosomal roX1 transgenes. Screening the second chromosome identified at least five loci, two of which are previously described components of the MSL complex. We focused our analysis on the modifier alleles of MSL1 and MLE (for 'maleless'). The MSL1 lesions are not simple nulls, but rather alter the PEHE domain that recruits the MSL3 chromodomain and MOF ('males absent on first') histone acetyltransferase subunits to the complex. These mutants are compromised in their ability to recruit MSL3 and MOF, dosage compensate the X, and support long distance spreading from roX1 transgenes. Yet, paradoxically, they were isolated because they somehow increase MSL complex activity immediately around roX1 transgenes in combination with wild-type MSL1 subunits. We propose that these diverse phenotypes arise from perturbations in assembly of MSL subunits onto nascent roX transcripts. This strategy is a promising alternative route for identifying previously unknown components of the dosage compensation pathway and novel alleles of known MSL proteins.
    BMC Biology 06/2010; 8:80. DOI:10.1186/1741-7007-8-80