Mechanisms of intron gain and loss in Drosophila

BMC Evolutionary Biology

Research Article

Paul Yenerall¹  Bradlee Krupa²  Leming Zhou³ 

[1] Department of Biological Sciences, University of Pittsburgh, 15260, Pittsburgh, PA, USA;Department of Computer Science, University of Pittsburgh, 15260, Pittsburgh, PA, USA;Department of Health Information Management, University of Pittsburgh, 15260, Pittsburgh, PA, USA;Department of Bioengineering, University of Pittsburgh, 15260, Pittsburgh, PA, USA;

关键词: Direct Repeat;    Drosophila Species;    Double Strand Break Repair;    Genomic Deletion;    Intron Loss;   

DOI  :  10.1186/1471-2148-11-364

 received in 2011-09-07, accepted in 2011-12-19,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundIt is widely accepted that orthologous genes have lost or gained introns throughout evolution. However, the specific mechanisms that generate these changes have proved elusive. Introns are known to affect nearly every level of gene expression. Therefore, understanding their mechanism of evolution after their initial fixation in eukaryotes is pertinent to understanding the means by which organisms develop greater regulation and complexity.ResultsTo investigate possible mechanisms of intron gain and loss, we identified 189 intron gain and 297 intron loss events among 11 Drosophila species. We then investigated these events for signatures of previously proposed mechanisms of intron gain and loss. This work constitutes the first comprehensive study into the specific mechanisms that may generate intron gains and losses in Drosophila. We report evidence of intron gain via transposon insertion; the first intron loss that may have occurred via non-homologous end joining; intron gains via the repair of a double strand break; evidence of intron sliding; and evidence that internal or 5' introns may not frequently be deleted via the self-priming of reverse transcription during mRNA-mediated intron loss. Our data also suggest that the transcription process may promote or result in intron gain.ConclusionOur findings support the occurrence of intron gain via transposon insertion, repair of double strand breaks, as well as intron loss via non-homologous end joining. Furthermore, our data suggest that intron gain may be enabled by or due to transcription, and we shed further light on the exact mechanism of mRNA-mediated intron loss.

【 授权许可】

Unknown   
© Yenerall et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.