Promoter contribution to the testis-specific expression of Stellate gene family in Drosophila melanogaster

Olenkina, Oxana M.; Egorova, Ksenia S.; Kibanov, Mikhail V.; Gervaziev, Yuri V.; Гвоздев, В. А.; Olenina, Ludmila V.

doi:10.1016/j.gene.2012.03.023

Cited by 14 publications

(7 citation statements)

References 46 publications

(70 reference statements)

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“…In general, there is little data on the regulation of CK2 gene expression, and presumably both genetic and epigenetic mechanism may be involved. A number of studies show that regulation of CK2 transcription happens at the promoter level for CK2α and CK2β [43] , [44] , [45] . However, there is no data on whether CK2 genes themselves are controlled by epigenetic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Mining CK2 in Cancer

2014

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Cancer is a leading cause of death worldwide. Cancer cells proliferate uncontrollably and, many cases, spread to other parts of the body. A protein historically involved in cancer is protein kinase CK2. CK2 is a serine-threonine kinase that has been involved in cell growth, cell proliferation and cell apoptosis. CK2 functions as an oncogene when overexpressed in mouse tissues, and can synergize with known oncogenes, such as ras, to induce cell transformation in cells in culture. CK2, typically the CK2α protein, is found elevated in a number of human tumors. However, we have little information on CK2α' and CK2β proteins, and scarce information on CK2 gene transcript expression. Here, we explore the expression of CK2 transcripts in primary tumor tissues using the database Oncomine in the six cancers with the highest mortality in the U.S.A. In addition, we studied the correlation between CK2 expression and overall survival using the Kaplan-Meier Plotter database in breast, ovarian, and lung cancers. We found widespread upregulation in the expression of CK2 genes in primary tumor tissues. However, we found underexpression of CK2α' transcripts in some tumors, increased CK2β transcripts in some invasive tumors, and deregulation of CK2 transcripts in some tumor precursors. There was also correlation between CK2 expression levels and patient survival. These data provides additional evidence for CK2 as a biomarker for cancer studies and as a target for cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Mining CK2 in Cancer

2014

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“…Alternatively, the effects of MSCI could be too subtle to detect via our whole testis dissections [ 49 ]. We note, however, that whole testis dissections are easily sufficient to detect X suppression (and escape from X suppression) using transgenes and transpositions (Tables 1 and 2 ; [ 40 , 51 , 53 , 57 ]).…”

Section: Resultsmentioning

confidence: 99%

Sex Chromosome-wide Transcriptional Suppression and Compensatory Cis-Regulatory Evolution Mediate Gene Expression in the Drosophila Male Germline

et al. 2016

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The evolution of heteromorphic sex chromosomes has repeatedly resulted in the evolution of sex chromosome-specific forms of regulation, including sex chromosome dosage compensation in the soma and meiotic sex chromosome inactivation in the germline. In the male germline of Drosophila melanogaster, a novel but poorly understood form of sex chromosome-specific transcriptional regulation occurs that is distinct from canonical sex chromosome dosage compensation or meiotic inactivation. Previous work shows that expression of reporter genes driven by testis-specific promoters is considerably lower—approximately 3-fold or more—for transgenes inserted into X chromosome versus autosome locations. Here we characterize this transcriptional suppression of X-linked genes in the male germline and its evolutionary consequences. Using transgenes and transpositions, we show that most endogenous X-linked genes, not just testis-specific ones, are transcriptionally suppressed several-fold specifically in the Drosophila male germline. In wild-type testes, this sex chromosome-wide transcriptional suppression is generally undetectable, being effectively compensated by the gene-by-gene evolutionary recruitment of strong promoters on the X chromosome. We identify and experimentally validate a promoter element sequence motif that is enriched upstream of the transcription start sites of hundreds of testis-expressed genes; evolutionarily conserved across species; associated with strong gene expression levels in testes; and overrepresented on the X chromosome. These findings show that the expression of X-linked genes in the Drosophila testes reflects a balance between chromosome-wide epigenetic transcriptional suppression and long-term compensatory adaptation by sex-linked genes. Our results have broad implications for the evolution of gene expression in the Drosophila male germline and for genome evolution.

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“…A cluster of Stellate sequences on the D. melanogaster X chromosome codes for a homolog of the β subunit of protein kinase CK2 and its overexpression causes male sterility. RNA interference mediated by Y-linked Su (Ste) repeats prevents Stellate overexpression [84,85], demonstrating that male fertility strongly depends on the interaction between the X and Y chromosomes. A similar model of fertility regulation utilizes the Odysseus-site homeobox protein (OdsH), which is encoded by an X-chromosomal locus in species of the melanogaster group.…”

Section: Discussionmentioning

confidence: 99%

The effects of the sex chromosomes on the inheritance of species-specific traits of the copulatory organ shape in Drosophila virilis and Drosophila lummei

et al. 2020

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The shape of the male genitalia in many taxa is the most rapidly evolving morphological structure, often driving reproductive isolation, and is therefore widely used in systematics as a key character to distinguish between sibling species. However, only a few studies have used the genital arch of the male copulatory organ as a model to study the genetic basis of species-specific differences in the Drosophila copulatory system. Moreover, almost nothing is known about the effects of the sex chromosomes on the shape of the male mating organ. In our study, we used a set of crosses between D. virilis and D. lummei and applied the methods of quantitative genetics to assess the variability of the shape of the male copulatory organ and the effects of the sex chromosomes and autosomes on its variance. Our results showed that the male genital shape depends on the species composition of the sex chromosomes and autosomes. Epistatic interactions of the sex chromosomes with autosomes and the species origin of the Y-chromosome in a male in interspecific crosses also influenced the expression of species-specific traits in the shape of the male copulatory system. Overall, the effects of sex chromosomes were comparable to the effects of autosomes despite the great differences in gene numbers between them. It may be reasonably considered that sexual selection for specific genes associated with the shape of the male mating organ prevents the demasculinization of the X chromosome.

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Promoter contribution to the testis-specific expression of Stellate gene family in Drosophila melanogaster

Cited by 14 publications

References 46 publications

Mining CK2 in Cancer

Mining CK2 in Cancer

Sex Chromosome-wide Transcriptional Suppression and Compensatory Cis-Regulatory Evolution Mediate Gene Expression in the Drosophila Male Germline

The effects of the sex chromosomes on the inheritance of species-specific traits of the copulatory organ shape in Drosophila virilis and Drosophila lummei

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