Imprinting of the Y Chromosome Influences Dosage Compensation in roX1 roX2 Drosophila melanogaster by ProQuest

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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. The RNA components of this complex, roX1 and roX2 (RNA on the X1, RNA on the X2), are functionally redundant. Males mutated for both roX genes have dramatically reduced survival. We show that reversal of sex chromosome inheritance suppresses lethality in roX1 roX2 males. Genetic tests indicate that the effect on male survival depends upon the presence and source of the Y chromosome, revealing a germ line imprint that influences dosage compensation. Conventional paternal transmission of the Y chromosome enhances roX1 roX2 lethality, while maternal transmission of the Y chromosome suppresses lethality. roX1 roX2 males with both maternal and paternal Y chromosomes have very low survival, indicating dominance of the paternal imprint. In an otherwise wild-type male, the Y chromosome does not appreciably affect dosage compensation. The influence of the Y chromosome, clearly apparent in roX1 roX2 mutants, thus requires a sensitized genetic background. We believe that the Y chromosome is likely to act through modulation of a process that is defective in roX1 roX2 mutants: X chromosome recognition or chromatin modification by the MSL complex. [PUBLICATION ABSTRACT]

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									Copyright Ó 2009 by the Genetics Society of America
DOI: 10.1534/genetics.109.107219



        Imprinting of the Y Chromosome Influences Dosage Compensation
                        in roX1 roX2 Drosophila melanogaster

                                        Debashish U. Menon and Victoria H. Meller1
                               Department of Biological Sciences, Wayne State University, Detroit, Michigan 48202
                                                         Manuscript received July 09, 2009
                                                      Accepted for publication August 14, 2009


                                                             ABSTRACT
                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. The RNA components of
             this complex, roX1 and roX2 (RNA on the X1, RNA on the X2), are functionally redundant. Males mutated for
             both roX genes have dramatically reduced survival. We show that reversal of sex chromosome inheritance
             suppresses lethality in roX1 roX2 males. Genetic tests indicate that the effect on male survival depends upon
             the presence and source of the Y chromosome, revealing a germ line imprint that influences dosage
             compensation. Conventional paternal transmission of the Y chromosome enhances roX1 roX2 lethality,
             while maternal transmission of the Y chromosome suppresses lethality. roX1 roX2 males with both maternal
             and paternal Y chromosomes have very low survival, indicating dominance of the paternal imprint. In an
             otherwise wild-type male, the Y chromosome does not appreciably affect dosage compensation. The
             influence of the Y chromosome, clearly apparent in roX1 roX2 mutants, thus requires a sensitized genetic
             background. We believe that the Y chromosome is likely to act through modulation of a process that is de-
             fective in roX1 roX2 mutants: X chromosome recognition or chromatin modification by the MSL complex.




M     ODIFICATION of genetic material in the parental
       germ line can affect the structure, segregation, or
expression of chromosomes in the zygote (reviewed by
                                                                            Golic 2002). Rearrangements of the X chromosome
                                                                            that move euchromatic genes into the vicinity of an
                                                                            imprinting center in proximal heterochromatin also
Lloyd 2000; de la Casa-Esperon and Sapienza 2003).                          display imprinted PEV (Anaka et al. 2009). A common
Parent-of-origin effects mediated by epigenetic marks                       theme in Drosophila imprinting is the central role of
on chromosomes are called germ line imprints. The                           heterochromatin. Imprinted marks reside in hetero-
importance of imprints for mammalian embryonic de-                          chromatin, and formation of heterochromatin in the
velopment is illustrated by the early lethality of uniparental              zygote is required for the maintenance of imprints
diploids (Surani et al. 1986). Unlike mammals, Drosoph-                     (Lloyd et al. 1999). Because PEV requires rearranged
ila uniparental diploids are viable and without apparent                    chromosomes or insertion of a transgene into hetero-
defect, suggesting that the role of imprinting in flies is                   chromatin, another recurring motif is that the affected
minor (Lindsley and Zimm 1992). In spite of this,                           chromosome is structurally abnormal, or a reporter has
imprinting does occur in Drosophila and is detected                         been moved into an abnormal chromatin environment.
through its effect on gene expression. Euchromatic                             Sex chromosomes are frequent targets of germ line
genes that are moved to heterochromatic environments                        imprints, perhaps because their fate is unusually pre-
by inversion or transposition are silenced (Wallrath                        dictable. Fathers always donate a Y to their sons (YP)
and Elgin 1995). Silencing, detected by variegated                          and an X (XP) to their daughters. Maternally derived
expression, is termed position effect variegation (PEV).                    X chromosomes (XM) are hemizygous when passed to a
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