Changes in Chromosomal Localization of Heterochromatin-binding Proteins during the Cell Cycle in <i>Drosophila </i>

Platero, J. Suso; Csink, Amy K.; Quintanilla, Adrian; Henikoff, Steven

doi:10.1083/jcb.140.6.1297

Cited by 142 publications

(137 citation statements)

References 34 publications

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“…These data further suggest a mechanism for YRV that does not require the expression of Y-linked protein-coding genes. Cytological evidence from two chromatin-associated proteinsthe transcriptional activator trithorax-related (GAGA factor), which binds to AAGAG satellites, and the origin of replication complex protein 2 (ORC2), which binds to AT-rich repeatsindicates that they bind to simple sequence repeats in the Y chromosome (23,24). In view of autoregulatory feedback mechanisms in gene expression (25), we predicted that the expression of these two genes might vary across lines differing in the origin of the Y chromosome.…”

Section: Resultsmentioning

confidence: 99%

Epigenetic effects of polymorphic Y chromosomes modulate chromatin components, immune response, and sexual conflict

Lemos

Branco²,

Hartl³

2010

Proc. Natl. Acad. Sci. U.S.A.

174

190

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Genetic conflicts between sexes and generations provide a foundation for understanding the functional evolution of sex chromosomes and sexually dimorphic phenotypes. Y chromosomes of Drosophila contain multi-megabase stretches of satellite DNA repeats and a handful of protein-coding genes that are monomorphic within species. Nevertheless, polymorphic variation in heterochromatic Y chromosomes of Drosophila result in genome-wide gene expression variation. Here we show that such naturally occurring Y-linked regulatory variation (YRV) can be detected in somatic tissues and contributes to the epigenetic balance of heterochromatin/ euchromatin at three distinct loci showing position-effect variegation (PEV). Moreover, polymorphic Y chromosomes differentially affect the expression of thousands of genes in XXY female genotypes in which Y-linked protein-coding genes are not transcribed. The data show a disproportionate influence of YRV on the variable expression of genes whose protein products localize to the nucleus, have nucleic-acid binding activity, and are involved in transcription, chromosome organization, and chromatin assembly. These include key components such as HP1, Trithorax-like (GAGA factor), Su(var)3-9, Brahma, MCM2, ORC2, and inner centromere protein. Furthermore, mitochondria-related genes, immune response genes, and transposable elements are also disproportionally affected by Y chromosome polymorphism. These functional clusterings may arise as a consequence of the involvement of Y-linked heterochromatin in the origin and resolution of genetic conflicts between males and females. Taken together, our results indicate that Y chromosome heterochromatin serves as a major source of epigenetic variation in natural populations that interacts with chromatin components to modulate the expression of biologically relevant phenotypic variation.evolution | heterochromatin | position-effect variegation | regulatory

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Section: Resultsmentioning

confidence: 99%

Epigenetic effects of polymorphic Y chromosomes modulate chromatin components, immune response, and sexual conflict

Lemos

Branco²,

Hartl³

2010

Proc. Natl. Acad. Sci. U.S.A.

174

190

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“…Pericentric heterochromatin is involved in functions such as meiotic and mitotic chromosome segregation (Karpen et al 1996) and the transcriptional regulation of flanking sequences like rDNA loci (Hilliker and Appels 1982;Karpen et al 1988). However, the amount and composition of satellite DNA is highly variable among species (Lohe and Roberts 1988;Platero et al 1998). There is considerable variation in composition and quantity of satellite sequences between D. melanogaster and D. simulans (Lohe and Burtlag 1987;Ferree and Barbash 2009) as well as between the younger species of the D. simulans clade (Lohe and Roberts 1988;Platero et al 1998).…”

Section: Location Of Hhlmentioning

confidence: 99%

“…However, the amount and composition of satellite DNA is highly variable among species (Lohe and Roberts 1988;Platero et al 1998). There is considerable variation in composition and quantity of satellite sequences between D. melanogaster and D. simulans (Lohe and Burtlag 1987;Ferree and Barbash 2009) as well as between the younger species of the D. simulans clade (Lohe and Roberts 1988;Platero et al 1998). Given that the D. simulans clade species split from one another just 250,000 years ago (McDermott and Kliman 2008), the evolution of satellite DNAs occurs quickly.…”

Section: Location Of Hhlmentioning

confidence: 99%

Incompatibility Between X Chromosome Factor and Pericentric Heterochromatic Region Causes Lethality in Hybrids Between Drosophila melanogaster and Its Sibling Species

Cattani

Presgraves

2012

Genetics

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The Dobzhansky-Muller model posits that postzygotic reproductive isolation results from the evolution of incompatible epistatic interactions between species: alleles that function in the genetic background of one species can cause sterility or lethality in the genetic background of another species. Progress in identifying and characterizing factors involved in postzygotic isolation in Drosophila has remained slow, mainly because Drosophila melanogaster, with all of its genetic tools, forms dead or sterile hybrids when crossed to its sister species, D. simulans, D. sechellia, and D. mauritiana. To circumvent this problem, we used chromosome deletions and duplications from D. melanogaster to map two hybrid incompatibility loci in F 1 hybrids with its sister species. We mapped a recessive factor to the pericentromeric heterochromatin of the X chromosome in D. simulans and D. mauritiana, which we call heterochromatin hybrid lethal (hhl), which causes lethality in F 1 hybrid females with D. melanogaster. As F 1 hybrid males hemizygous for a D. mauritiana (or D. simulans) X chromosome are viable, the lethality of deficiency hybrid females implies that a dominant incompatible partner locus exists on the D. melanogaster X. Using small segments of the D. melanogaster X chromosome duplicated onto the Y chromosome, we mapped a dominant factor that causes hybrid lethality to a small 24-gene region of the D. melanogaster X. We provide evidence suggesting that it interacts with hhl mau . The location of hhl is consistent with the emerging theme that hybrid incompatibilities in Drosophila involve heterochromatic regions and factors that interact with the heterochromatin. M ORE than 70 years ago, Dobzhansky (1937) and Muller (1942) proposed a simple two-locus model in which postzygotic isolation arises as a byproduct of divergence between effectively allopatric populations. Genes that function well in one species' genetic background might not be functional in a hybrid genetic background, rendering hybrids dead or sterile. Despite early acceptance of the Dobzhansky-Muller model, progress in identifying and characterizing factors involved in hybrid incompatibilities has remained slow. One of the reasons for the slow progress is that Drosophila melanogaster, with its many genetic tools, forms largely dead or sterile hybrids when crossed to its sister species D. simulans, D. sechellia, and D. mauritiana (Sturtevant 1920(Sturtevant , 1929Lachaise et al. 1986;Provine 1991;Barbash 2010).In general, three methods have been used to circumvent this problem. First, alleles that suppress postzygotic isolation, so-called hybrid rescue mutations, have been used to characterize hybrid inviability between D. melanogaster and its three sister species in the D. simulans complex. When D. melanogaster females are crossed to sibling species males, only hybrid females are produced while males die as larvae (Sturtevant 1920;Lachaise et al. 1986). These males are rescued by the D. melanogaster mutant allele of Hybrid male rescue (Hmr) (Hutter...

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“…These genes are clustered into functional classes related to mitochondria, immunity, as well as chromatin structure and maintenance (Lemos et al, 2008Paredes et al, 2011). Variable titration of nuclear proteins by the Y chromosome might cause imbalances in the nucleus and consequently the modulation of gene expression (Platero et al, 1998;Janssen et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Natural variation of the Y chromosome suppresses sex ratio distortion and modulates testis-specific gene expression in Drosophila simulans

Branco¹,

Tao

Hartl

et al. 2013

Heredity

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X-linked sex-ratio distorters that disrupt spermatogenesis can cause a deficiency in functional Y-bearing sperm and a femalebiased sex ratio. Y-linked modifiers that restore a normal sex ratio might be abundant and favored when a X-linked distorter is present. Here we investigated natural variation of Y-linked suppressors of sex-ratio in the Winters systems and the ability of these chromosomes to modulate gene expression in Drosophila simulans. Seventy-eight Y chromosomes of worldwide origin were assayed for their resistance to the X-linked sex-ratio distorter gene Dox. Y chromosome diversity caused males to sire B63% to B98% female progeny. Genome-wide gene expression analysis revealed hundreds of genes differentially expressed between isogenic males with sensitive (high sex ratio) and resistant (low sex ratio) Y chromosomes from the same population. Although the expression of about 75% of all testis-specific genes remained unchanged across Y chromosomes, a subset of post-meiotic genes was upregulated by resistant Y chromosomes. Conversely, a set of accessory gland-specific genes and mitochondrial genes were downregulated in males with resistant Y chromosomes. The D. simulans Y chromosome also modulated gene expression in XXY females in which the Y-linked protein-coding genes are not transcribed. The data suggest that the Y chromosome might exert its regulatory functions through epigenetic mechanisms that do not require the expression of protein-coding genes. The gene network that modulates sex ratio distortion by the Y chromosome is poorly understood, other than that it might include interactions with mitochondria and enriched for genes expressed in post-meiotic stages of spermatogenesis.

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Changes in Chromosomal Localization of Heterochromatin-binding Proteins during the Cell Cycle in Drosophila

Cited by 142 publications

References 34 publications

Epigenetic effects of polymorphic Y chromosomes modulate chromatin components, immune response, and sexual conflict

Epigenetic effects of polymorphic Y chromosomes modulate chromatin components, immune response, and sexual conflict

Incompatibility Between X Chromosome Factor and Pericentric Heterochromatic Region Causes Lethality in Hybrids Between Drosophila melanogaster and Its Sibling Species

Natural variation of the Y chromosome suppresses sex ratio distortion and modulates testis-specific gene expression in Drosophila simulans

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