Dataset Information

Non-random genomic integration - an intrinsic property of retrogenes in Drosophila?

ABSTRACT:

Background

The Drosophila X-chromosome shows a significant underrepresentation of genes with male-biased gene expression (demasculinization). This trend is matched by retrogenes, which typically have a male biased gene expression pattern and show a significant movement bias from X-chromosomes to autosomes. It is currently assumed that these patterns are best explained by selection, either mediated by male meiotic sex chromosome inactivation (MSCI) or sexually antagonistic forces. We scrutinized the evolutionary dynamics of retroposition by focusing on retrogenes for which the parental copy has degenerated.

Results

Consistent with a functional substitution of the degenerated gene by the retrogene, patterns of sequence evolution and gene expression were similar between retroposed and parental genes. Like previous studies, our set of retrogenes showed a significant movement off the X-chromosome. In contrast to data sets where retroposition caused gene duplication, the genes in our study showed primarily female-biased or unbiased gene expression.

Conclusions

Based on our results, the biased transposition pattern cannot be explained by MSCI and probably not by sexual antagonism. Rather, we propose that the movement away from the X-chromosome represents a general property of retroposition in Drosophila.

SUBMITTER: Metta M

PROVIDER: S-EPMC2879276 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature

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Publications

Non-random genomic integration - an intrinsic property of retrogenes in Drosophila?

Metta Muralidhar M Schlötterer Christian C

BMC evolutionary biology 20100428

<h4>Background</h4>The Drosophila X-chromosome shows a significant underrepresentation of genes with male-biased gene expression (demasculinization). This trend is matched by retrogenes, which typically have a male biased gene expression pattern and show a significant movement bias from X-chromosomes to autosomes. It is currently assumed that these patterns are best explained by selection, either mediated by male meiotic sex chromosome inactivation (MSCI) or sexually antagonistic forces. We scru ...[more]

PMID: 20426838

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Project description:BackgroundSeveral studies in Drosophila have shown excessive movement of retrogenes from the X chromosome to autosomes, and that these genes are frequently expressed in the testis. This phenomenon has led to several hypotheses invoking natural selection as the process driving male-biased genes to the autosomes. Metta and Schlötterer (BMC Evol Biol 2010, 10:114) analyzed a set of retrogenes where the parental gene has been subsequently lost. They assumed that this class of retrogenes replaced the ancestral functions of the parental gene, and reported that these retrogenes, although mostly originating from movement out of the X chromosome, showed female-biased or unbiased expression. These observations led the authors to suggest that selective forces (such as meiotic sex chromosome inactivation and sexual antagonism) were not responsible for the observed pattern of retrogene movement out of the X chromosome.ResultsWe reanalyzed the dataset published by Metta and Schlötterer and found several issues that led us to a different conclusion. In particular, Metta and Schlötterer used a dataset combined with expression data in which significant sex-biased expression is not detectable. First, the authors used a segmental dataset where the genes selected for analysis were less testis-biased in expression than those that were excluded from the study. Second, sex-biased expression was defined by comparing male and female whole-body data and not the expression of these genes in gonadal tissues. This approach significantly reduces the probability of detecting sex-biased expressed genes, which explains why the vast majority of the genes analyzed (parental and retrogenes) were equally expressed in both males and females. Third, the female-biased expression observed by Metta and Schlötterer is mostly found for parental genes located on the X chromosome, which is known to be enriched with genes with female-biased expression. Fourth, using additional gonad expression data, we found that autosomal genes analyzed by Metta and Schlötterer are less up regulated in ovaries and have higher chance to be expressed in meiotic cells of spermatogenesis when compared to X-linked genes.ConclusionsThe criteria used to select retrogenes and the sex-biased expression data based on whole adult flies generated a segmental dataset of female-biased and unbiased expressed genes that was unable to detect the higher propensity of autosomal retrogenes to be expressed in males. Thus, there is no support for the authors' view that the movement of new retrogenes, which originated from X-linked parental genes, was not driven by selection. Therefore, selection-based genetic models remain the most parsimonious explanations for the observed chromosomal distribution of retrogenes.

Project description:HPV DNA integration into the host genome is a characteristic but not an exclusive step during cervical carcinogenesis. It is still a matter of debate whether viral integration contributes to the transformation process beyond ensuring the constitutive expression of the viral oncogenes. There is mounting evidence for a non-random distribution of integration loci and the direct involvement of cellular cancer-related genes. In this study we addressed this topic by extending the existing data set by an additional 47 HPV16 and HPV18 positive cervical carcinoma. We provide supportive evidence for previously defined integration hotspots and have revealed another cluster of integration sites within the cytogenetic band 3q28. Moreover, in the vicinity of these hotspots numerous microRNAs (miRNAs) are located and may be influenced by the integrated HPV DNA. By compiling our data and published reports 9 genes could be identified which were affected by HPV integration at least twice in independent tumors. In some tumors the viral-cellular fusion transcripts were even identical with respect to the viral donor and cellular acceptor sites used. However, the exact integration sites are likely to differ since none of the integration sites analysed thus far have shown more than a few nucleotides of homology between viral and host sequences. Therefore, DNA recombination involving large stretches of homology at the integration site can be ruled out. It is however intriguing that by sequence alignment several regions of the HPV16 genome were found to have highly homologous stretches of up to 50 nucleotides to the aforementioned genes and the integration hotspots. One common region of homologies with cellular sequences is between the viral gene E5 and L2 (nucleotides positions 4100 to 4240). We speculate that this and other regions of homology are involved in the integration process. Our observations suggest that targeted disruption, possibly also of critical cellular genes, by HPV integration remains an issue to be fully resolved.

Dataset Information

Non-random genomic integration - an intrinsic property of retrogenes in Drosophila?

Background

Results

Conclusions

Publications

Non-random genomic integration - an intrinsic property of retrogenes in Drosophila?

Similar Datasets

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