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Gupta, Vaijayanti; Parisi, Michael; Sturgill, David; Nuttall, Rachel; Doctolero, Michael H.; Dudko, Olga K.; Malley, James D.; Eastman, Peter; Oliver, Brian

doi:10.1186/jbiol30

Cited by 285 publications

(207 citation statements)

References 68 publications

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“…Log2-normalized intensities from all experiments were zero centered (Gene Expression Omnibus platform GPL-20) to create an adjusted intensity for the heat diagram, as shown by different colors (24).…”

Section: Methodsmentioning

confidence: 99%

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Characterization of mitochondrial ferritin in Drosophila

Missirlis

Holmberg

Georgieva

et al. 2006

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

109

110

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Mitochondrial function depends on iron-containing enzymes and proteins, whose maturation requires available iron for biosynthesis of iron-sulfur clusters and heme. Little is known about how mitochondrial iron homeostasis is maintained, although the recent discovery of a mitochondrial ferritin in mammals and plants has uncovered a potential key player in the process. Here, we show that Drosophila melanogaster expresses mitochondrial ferritin from an intron-containing gene. It has high similarity to the mouse and human mitochondrial ferritin sequences and, as in mammals, is expressed mainly in testis. This ferritin contains a putative mitochondrial targeting sequence and an epitope-tagged version localizes to mitochondria in transfected cells. Overexpression of mitochondrial ferritin fails to alter both total-body iron levels and iron that is bound to secretory ferritins. However, the viability of iron-deficient flies is compromised by overexpression of mitochondrial ferritin, suggesting that it may sequester iron at the expense of other important cellular functions. The conservation of mitochondrial ferritin in an insect species underscores the importance of this iron-storage molecule.iron ͉ metabolism ͉ mitochondria ͉ paraquat ͉ testis

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Section: Methodsmentioning

confidence: 99%

“…To confirm that Fer3HCH expression was testis-specific, we also analyzed multiple microarray gene-expression experiments comparing global gene-expression levels in testis, ovary, and soma of both sexes (24). Normalized, color-coded expression data for Fer3HCH from these experiments are shown in Fig.…”

Section: Fer3hch Is Preferentially Expressed In Testismentioning

confidence: 99%

Characterization of mitochondrial ferritin in Drosophila

Missirlis

Holmberg

Georgieva

et al. 2006

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

109

110

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show abstract

“…Recent evidence suggests that these strategies operate at two levels. A primary mechanism is to increase gene expression of the single X chromosome by 2-fold in the heterogametic sex, a strategy that appears to be universally conserved in animals (3,4). However, different animal lineages have adopted diverse, secondary strategies to equilibrate gene expression in the two sexes (5).…”

mentioning

confidence: 99%

Species-specific positive selection of the male-specific lethal complex that participates in dosage compensation in Drosophila

Rodríguez

Vermaak

Bayes

et al. 2007

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

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In many taxa, males and females have unequal ratios of sex chromosomes to autosomes, which has resulted in the invention of diverse mechanisms to equilibrate gene expression between the sexes (dosage compensation). Failure to compensate for sex chromosome dosage results in male lethality in Drosophila. In Drosophila, a male-specific lethal (MSL) complex of proteins and noncoding RNAs binds to hundreds of sites on the single male X chromosome and up-regulates gene expression. Here we use population genetics of two closely related Drosophila species to show that adaptive evolution has occurred in all five proteincoding genes of the MSL complex. This positive selection is asymmetric between closely related species, with a very strong signature apparent in Drosophila melanogaster but not in Drosophila simulans. In particular, the MSL1 and MSL2 proteins have undergone dramatic positive selection in D. melanogaster, in domains previously shown to be responsible for their specific targeting to the X chromosome. This signature of positive selection at an essential protein-DNA interface of the complex is unexpected and suggests that X chromosomal MSL-binding DNA segments may themselves be changing rapidly. This highly asymmetric, rapid evolution of the MSL genes further suggests that misregulated dosage compensation may represent one of the underlying causes of male hybrid inviability in Drosophila, wherein the fate of hybrid males depends on which species' X chromosome is inherited.hromosomal aneuploidy is highly deleterious; deletions larger than 3% of the genome and duplications larger than 10% are not tolerated in Drosophila (1), presumably because an imbalance of expression levels of many genes is hard to accommodate in stoichiometric complexes involving many different proteins (2). In organisms with highly diverged sex chromosomes, there is frequently a difference in number of sex chromosomes versus autosomes in the heterogametic sex (XY or ZW). This difference requires ''dosage compensation'' strategies to equilibrate expression levels in both sexes. Recent evidence suggests that these strategies operate at two levels. A primary mechanism is to increase gene expression of the single X chromosome by 2-fold in the heterogametic sex, a strategy that appears to be universally conserved in animals (3, 4). However, different animal lineages have adopted diverse, secondary strategies to equilibrate gene expression in the two sexes (5). In mammals, this secondary modification involves the inactivation of one of the two female X chromosomes, whereas in Caenorhabditis elegans, it is achieved by 2-fold lower transcriptional output from both X chromosomes in hermaphrodites. Flies adopt a different strategy; they double the transcriptional output of the single male X chromosome in somatic cells (6, 7), which requires the targeting of a male-specific lethal complex (MSL) to the X chromosome but not to autosomes in Drosophila males (5).In Drosophila melanogaster, the MSL complex consists of proteins encoded by five genes: male-s...

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“…Additionally, addressing the X organization in males can provide insights into the yet unexplored mechanisms of the suggested male X chromosome upregulation. [21][22][23] Here, we discuss a new model of DC in worms based on the latest findings. We describe an X specific organization in C. elegans and the possible links between tridimensional folding of the chromosome inside the nucleus and its transcriptional regulation.…”

Section: A Nuclear Organizationmentioning

confidence: 99%

“…Animals deficient for set-4, the methyltransferase carrying di-and trimethylation of H4K20, in which the entire genome is marked with H4K20 monomethyl have no dosage compensation related phenotypes. Finally, X-linked genes appear transcriptionally overexpressed compared to autosomal genes in males and dosage compensation deficient animals, [21][22][23] suggesting an X-specific transcription activation mechanism.…”

Section: Introductionmentioning

confidence: 99%

Linking dosage compensation and X chromosome nuclear organization inC. elegans

Sharma

Meister

2015

Nucleus

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A nimal sex is determined by the number of X chromosomes in many species, creating unequal gene dosage (aneuploidy) between sexes. Dosage Compensation mechanisms equalize this dosage difference by regulating X-linked gene expression. In the nematode C. elegans the current model suggests that DC is achieved by a 2-fold transcriptional downregulation in hermaphrodites mediated by the Dosage Compensation Complex (DCC), which restricts access to RNA Polymerase II by an unknown mechanism. Taking a nuclear organization point of view, we showed that the male X chromosome resides in the pore proximal subnuclear compartment whereas the DCC bound to the X, inhibits this spatial organization in the hermaphrodites. Here we discuss our results and propose a model that reassigns the role of DCC from repression of genes to inhibition of activation.

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Cited by 285 publications

References 68 publications

Characterization of mitochondrial ferritin in Drosophila

Characterization of mitochondrial ferritin in Drosophila

Species-specific positive selection of the male-specific lethal complex that participates in dosage compensation in Drosophila

Linking dosage compensation and X chromosome nuclear organization inC. elegans

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