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Dosage compensation of X-linked genes is a phenomenon of concerted, chromosome-wide regulation of gene expression underpinned by sustained and tightly regulated histone modifications and chromatin remodeling, coupled with constrains of nuclear architecture. This elaborate process allows the accomplishment of regulated expression of genes on the single male X chromosome to levels comparable to those expressed from the two X chromosomes in females. The ribonucleoprotein Male Specific Lethal (MSL) complex is enriched on the male X chromosome and is intricately involved in this process in Drosophila melanogaster. In this review we discuss the recent advances that highlight the complexity lying behind regulation of gene expression by just two-fold. 相似文献
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Genomic analyses of Drosophila species suggest that the X chromosome presents an
unfavourable environment for the expression of genes in the male germline. A previous
study in D. melanogaster used a reporter gene driven by a
testis-specific promoter to show that expression was greatly reduced when the gene was
inserted onto the X chromosome as compared with the autosomes. However, a limitation of
this study was that only the expression regulated by a single, autosomal-derived promoter
was investigated. To test for an increase in expression associated with
‘escaping'' the X chromosome, we analysed reporter gene expression driven by
the promoters of three X-linked, testis-expressed genes (CG10920,
CG12681 and CG1314) that were inserted randomly throughout the D.
melanogaster genome. In all cases, insertions on the autosomes showed significantly
higher expression than those on the X chromosome. Thus, even genes whose regulation has
adapted to the X-chromosomal environment show increased male germline expression when
relocated to an autosome. Our results provide direct experimental evidence for the
suppression of X-linked gene expression in the Drosophila male germline that is
independent of gene dose. 相似文献
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Maclean JA Chen MA Wayne CM Bruce SR Rao M Meistrich ML Macleod C Wilkinson MF 《Cell》2005,120(3):369-382
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J. Lawrence Marsh P. D. L. Gibbs Paula M. Timmons 《Molecular & general genetics : MGG》1985,198(3):393-403
Summary Seventeen new euchromatic integration sites of the dopa-decarboxylase gene (Ddc) have been generated using p-mediated transduction. The developmental expression of the integrated genes was examined by monitoring the embryonic induction of dopa decarboxylase enzyme activity (DDC) and by monitoring the developmental pattern of DDC activity from late third instar to eclosion. The majority of inserts are regulated correctly within about 30% of controls. Several cases of multiple insertion events were recovered and these show correspondingly elevated levels of activity and are regulated normally. The pattern of expression of one insert (15C) falls outside the normal range. Multiple copies of transduced Ddc genes are used to test for effects of elevated gene dose on levels of expression. One insert on the X chromosome shows little or no dosage compensation. Possible reasons for the differences between the regulation of transduced genes in Drosophila and the regulation of transformed genes in mammalian systems are discussed. 相似文献
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In most crosses between closely related species of Drosophila, the male hybrids are sterile and show postmeiotic abnormalities. A series of gene expression studies using genomic approaches have found significant down regulation of postmeiotic spermatogenesis genes in sterile male hybrids. These results have led some to suggest a direct relationship between down regulation in gene expression and hybrid sterility. An alternative explanation to a cause-and-effect relationship between misregulation of gene expression and male sterility is rapid divergence of male sex regulatory elements leading to incompatible interactions in an interspecies hybrid genome. To test the effect of regulatory divergence in spermatogenesis gene expression, we isolated 35 fertile D. simulans strains with D. mauritiana introgressions in either the X, second or third chromosome. We analyzed gene expression in these fertile hybrid strains for a subset of spermatogenesis genes previously reported as significantly under expressed in sterile hybrids relative to D. simulans. We found that fertile autosomal introgressions can cause levels of gene down regulation similar to that of sterile hybrids. We also found that X chromosome heterospecific introgressions cause significantly less gene down regulation than autosomal introgressions. Our results provide evidence that rapid male sex gene regulatory divergence can explain misexpression of spermatogenesis genes in hybrids. 相似文献
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Kobayashi S Isotani A Mise N Yamamoto M Fujihara Y Kaseda K Nakanishi T Ikawa M Hamada H Abe K Okabe M 《Current biology : CB》2006,16(2):166-172
Mammalian male preimplantation embryos develop more quickly than females . Using enhanced green fluorescent protein (EGFP)-tagged X chromosomes to identify the sex of the embryos, we compared gene expression patterns between male and female mouse blastocysts by DNA microarray. We detected nearly 600 genes with statistically significant sex-linked expression; most differed by 2-fold or less. Of 11 genes showing greater than 2.5-fold differences, four were expressed exclusively or nearly exclusively sex dependently. Two genes (Dby and Eif2s3y) were mapped to the Y chromosome and were expressed in male blastocysts. The remaining two (Rhox5/Pem and Xist) were mapped to the X chromosome and were predominantly expressed in female blastocysts. Moreover, Rhox5/Pem was expressed predominantly from the paternally inherited X chromosome, indicating sex differences in early epigenetic gene regulation. 相似文献
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Study of dosage compensation in Drosophila 总被引:1,自引:0,他引:1
Using a sensitive RT-QPCR assay, we analyzed the regulatory effects of sex and different dosage compensation mutations in Drosophila. To validate the assay, we showed that regulation for several genes indeed varied with the number of functional copies of that gene. We then confirmed that dosage compensation occurred for most genes we examined in male and female flies. Finally, we examined the effects on regulation of several genes in the MSL pathway, presumed to be involved in sex-dependent determination of regulation. Rather than seeing global alterations of either X chromosomal or autosomal genes, regulation of genes on either the X chromosome or the autosomes could be elevated, depressed, or unaltered between sexes in unpredictable ways for the various MSL mutations. Relative dosage for a given gene between the sexes could vary at different developmental times. Autosomal genes often showed deranged regulatory levels, indicating they were in pathways perturbed by X chromosomal changes. As exemplified by the BR-C locus and its dependent Sgs genes, multiple genes in a given pathway could exhibit coordinate regulatory modulation. The variegated pattern shown for expression of both X chromosomal and autosomal loci underscores the complexity of gene expression so that the phenotype of MSL mutations does not reflect only simple perturbations of genes on the X chromosome. 相似文献
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Battle of the Xs 总被引:4,自引:0,他引:4
Oliver B Parisi M 《BioEssays : news and reviews in molecular, cellular and developmental biology》2004,26(5):543-548
Females and males often exhibit conspicuous morphological, physiological and behavioral differences. Similarly, gene expression profiles indicate that a large portion of the genome is sex‐differentially deployed, particularly in the germ line. Because males and females are so fundamentally different, each sex is likely to have a different optimal gene expression profile that is never fully achieved in either sex because of antagonistic selection in females versus males. Males are hemizygous for the X chromosome, which means that recessive male‐favorable de novo mutations on the X chromosome are subject to immediate selection. In females, a recessive female‐favorable mutation on one of two X chromosomes is not available for selection until it becomes frequent enough in the local population to result in homozygous individuals. Given that most mutations are recessive, one would expect that genes or alleles favoring males should accumulate on the X chromosome. Recent microarray work in Drosophila and C. elegans clearly shows the opposite. Why is the X chromosome a highly disfavored location for genes with male‐biased expression in these animals? BioEssays 26:543–548, 2004. Published 2004 Wiley Periodicals, Inc. 相似文献
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Dosage compensation refers to the equal expression between the sexes despite the fact that the dosage of the X chromosome
is different in males and females. In Drosophila there is a twofold upregulation of the single male X. In triple X metafemales, there is also dosage compensation, which occurs
by a two-thirds downregulation. There is a concomitant reduction in expression of many autosomal genes in metafemales. The
male specific lethal (MSL) complex is present on the male X chromosome. Evidence is discussed showing that the MSL complex
sequesters a histone acetyltransferase to the X chromosome to mute an otherwise increased expression by diminishing the histone
acetylation on the autosomes. Several lines of evidence indicate that a constraining activity occurs from the MSL complex
to prevent overcompensation on the X that might otherwise occur from the high level of acetylation present. Together, the
evidence suggests that dosage compensation is a modification of a regulatory inverse dosage effect that is a reflection of
intrinsic gene regulatory mechanisms and that the MSL complex has evolved in reaction in order to equalize the expression
on both the X and autosomes of males and females. 相似文献
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X Chromosome Inactivation during Drosophila Spermatogenesis 总被引:1,自引:1,他引:0
Genes with male- and testis-enriched expression are under-represented on the Drosophila melanogaster X chromosome. There is also an excess of retrotransposed genes, many of which are expressed in testis, that have “escaped” the X chromosome and moved to the autosomes. It has been proposed that inactivation of the X chromosome during spermatogenesis contributes to these patterns: genes with a beneficial function late in spermatogenesis should be selectively favored to be autosomal in order to avoid inactivation. However, conclusive evidence for X inactivation in the male germline has been lacking. To test for such inactivation, we used a transgenic construct in which expression of a lacZ reporter gene was driven by the promoter sequence of the autosomal, testis-specific ocnus gene. Autosomal insertions of this transgene showed the expected pattern of male- and testis-specific expression. X-linked insertions, in contrast, showed only very low levels of reporter gene expression. Thus, we find that X linkage inhibits the activity of a testis-specific promoter. We obtained the same result using a vector in which the transgene was flanked by chromosomal insulator sequences. These results are consistent with global inactivation of the X chromosome in the male germline and support a selective explanation for X chromosome avoidance of genes with beneficial effects late in spermatogenesis. 相似文献
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Chess A 《Nature reviews. Genetics》2012,13(6):421-428
Although random monoallelic expression has been known for decades to affect genes on the X chromosome in female placental mammals, until a few years ago it was thought that there were few autosomal genes that were regulated in this manner. New tools for assaying gene expression genome-wide are now revealing that there are perhaps more genes that are subject to random monoallelic expression on mammalian autosomes than there are on the X chromosome and that these expression properties are achieved by diverse molecular mechanisms. This mode of expression has the potential to have an impact on natural selection and on the evolution of gene families. 相似文献