siRNA that participates in Drosophila dosage compensation is produced by many 1.688X and 359 bp repeats.

Organisms with differentiated sex chromosomes must accommodate unequal gene dosage in males and females. Male fruit flies increase X-linked gene expression to compensate for hemizygosity of their single X chromosome. Full compensation requires localization of the Male-Specific Lethal (MSL) complex to active genes on the male X, where it modulates chromatin to elevate expression.

Identification of X chromatin is modulated by complementary pathways in Drosophila melanogaster.

Drosophila melanogaster males have one X chromosome while females have two. This creates an imbalance in X:A gene dosage between the sexes. This imbalance is corrected by increasing transcription from male X-linked genes approximately 2-fold.

When Down Is Up: Heterochromatin, Nuclear Organization and X Upregulation.

Organisms with highly differentiated sex chromosomes face an imbalance in X-linked gene dosage. Male solve this problem by increasing expression from virtually every gene on their single X chromosome, a process known as dosage compensation. This involves a ribonucleoprotein complex that is recruited to active, X-linked genes to remodel chromatin and increase expression.

Chromatin That Guides Dosage Compensation Is Modulated by the siRNA Pathway in .

Many heterogametic organisms adjust sex chromosome expression to accommodate differences in gene dosage. This requires selective recruitment of regulatory factors to the modulated chromosome. How these factors are localized to a chromosome with requisite accuracy is poorly understood.

Satellite Repeats Identify X Chromatin for Dosage Compensation in Drosophila melanogaster Males.

A common feature of sex chromosomes is coordinated regulation of X-linked genes in one sex. Drosophila melanogaster males have one X chromosome, whereas females have two. The resulting imbalance in gene dosage is corrected by increased expression from the single X chromosome of males, a process known as dosage compensation.

Host-Symbiont Interactions: Male-Killers Exposed.

Male-killing is one strategy used by maternally transmitted bacterial symbionts to boost transmission and spread in populations. In Drosophila melanogaster, Spiroplasma target males by hijacking an essential, male-limited epigenetic process. A new study reveals clues to the mode of killing.

Modulation of Chromatin by Noncoding RNA.

Noncoding RNAs (ncRNAs) are remarkably powerful, flexible, and pervasive cellular regulators. The involvement of these molecules in virtually all aspects of eukaryotic chromatin function is notable. Long and short ncRNAs play broadly complementary roles in these processes.

Modulation of Heterochromatin by Male Specific Lethal Proteins and roX RNA in Drosophila melanogaster Males.

The ribonucleoprotein Male Specific Lethal (MSL) complex is required for X chromosome dosage compensation in Drosophila melanogaster males. Beginning at 3 h of development the MSL complex binds transcribed X-linked genes and modifies chromatin. A subset of MSL complex proteins, including MSL1 and MSL3, is also necessary for full expression of autosomal heterochromatic genes in males, but not females.

Identification of the Drosophila X chromosome: The long and short of it.

The different dose of X chromosomes in males and females produces a potentially fatal imbalance in X-linked gene products. This imbalance is addressed by dosage compensation, a process that modulates expression from an entire X chromosome in one sex. Dosage compensation acts on thousands of genes with disparate expression patterns.

Sex Differences in Drosophila melanogaster Heterochromatin Are Regulated by Non-Sex Specific Factors.

The eukaryotic genome is assembled into distinct types of chromatin. Gene-rich euchromatin has active chromatin marks, while heterochromatin is gene-poor and enriched for silencing marks. In spite of this, genes native to heterochromatic regions are dependent on their normal environment for full expression.

Sex chromosome evolution: life, death and repetitive DNA.

Dimorphic sex chromosomes create problems. Males of many species, including Drosophila, are heterogametic, with dissimilar X and Y chromosomes. The essential process of dosage compensation modulates the expression of X-linked genes in one sex to maintain a constant ratio of X to autosomal expression.

siRNAs from an X-linked satellite repeat promote X-chromosome recognition in Drosophila melanogaster.

Highly differentiated sex chromosomes create a lethal imbalance in gene expression in one sex. To accommodate hemizygosity of the X chromosome in male fruit flies, expression of X-linked genes increases twofold. This is achieved by the male- specific lethal (MSL) complex, which modifies chromatin to increase expression.

A strategy for generation and balancing of autosome: Y chromosome translocations.

We describe a method for generation and maintenance of translocations that move large autosomal segments onto the Y chromosome. Using this strategy we produced ( 2;Y) translocations that relocate between 1.5 and 4.

Generation of a useful roX1 allele by targeted gene conversion.

Methods for altering the sequence of endogenous Drosophila melanogaster genes remain labor-intensive. We have tested a relatively simple strategy that enables the introduction of engineered mutations in the vicinity of existing P-elements. This method was used to generate useful alleles of the roX1 gene, which produces a noncoding RNA involved in dosage compensation.

Homologue pairing in flies and mammals: gene regulation when two are involved.

Chromosome pairing is usually discussed in the context of meiosis. Association of homologues in germ cells enables chromosome segregation and is necessary for fertility. A few organisms, such as flies, also pair their entire genomes in somatic cells.

A role for siRNA in X-chromosome dosage compensation in Drosophila melanogaster.

Sex-chromosome dosage compensation requires selective identification of X chromatin. How this occurs is not fully understood. We show that small interfering RNA (siRNA) mutations enhance the lethality of Drosophila males deficient in X recognition and partially rescue females that inappropriately dosage-compensate.

roX RNAs and Genome Regulation in Drosophila Melanogaster.

Organisms with dimorphic sex chromosomes suffer a potentially lethal imbalance in gene expression in one sex. Addressing this fundamental problem can be considered the first, and most essential, aspect of sexual differentiation. In the model organisms Drosophila, Caenorhabditis elegans, and mouse, expression from X-linked genes is modulated by selective recruitment of chromatin-modifying complexes to X chromatin.

The Drosophila homolog of the mammalian imprint regulator, CTCF, maintains the maternal genomic imprint in Drosophila melanogaster.

Background: CTCF is a versatile zinc finger DNA-binding protein that functions as a highly conserved epigenetic transcriptional regulator. CTCF is known to act as a chromosomal insulator, bind promoter regions, and facilitate long-range chromatin interactions. In mammals, CTCF is active in the regulatory regions of some genes that exhibit genomic imprinting, acting as insulator on only one parental allele to facilitate parent-specific expression.

Germ line imprinting in Drosophila: Epigenetics in search of function.

Germ line imprinting produces parent-specific differences in the behavior of chromosomes or expression of genes. Epigenetic marks, placed on chromosomes in the parental germ line, govern classical imprinted effects such as chromosomal inactivation, chromosome elimination and mono-allelic expression. Germ line imprinting occurs in insects, plants and mammals.

Imprinting of the Y chromosome influences dosage compensation in roX1 roX2 Drosophila melanogaster.

Drosophila melanogaster males have a well-characterized regulatory system that increases X-linked gene expression. This essential process restores the balance between X-linked and autosomal gene products in males. A complex composed of the male-specific lethal (MSL) proteins and RNA is recruited to the body of transcribed X-linked genes where it modifies chromatin to increase expression.

Coordinated regulation of heterochromatic genes in Drosophila melanogaster males.

Dosage compensation modifies the chromatin of X-linked genes to assure equivalent expression in sexes with unequal X chromosome dosage. In Drosophila dosage compensation is achieved by increasing expression from the male X chromosome. The ribonucleoprotein dosage compensation complex (DCC) binds hundreds of sites along the X chromosome and modifies chromatin to facilitate transcription.