Adaptation to P element transposon invasion in Drosophila melanogaster
Name:
Publisher version
View Source
Access full-text PDFOpen Access
View Source
Check access options
Check access options
Authors
Khurana, Jaspreet S.Wang, Jie
Xu, Jia
Koppetsch, Birgit S.
Thomson, Travis
Nowosielska, Anetta
Li, Chengjian
Zamore, Phillip D.
Weng, Zhiping
Theurkauf, William E.
UMass Chan Affiliations
Department of Biochemistry and Molecular PharmacologyProgram in Molecular Medicine
Program in Cell and Developmental Dynamics
Program in Bioinformatics and Integrative Biology
Document Type
Journal ArticlePublication Date
2011-12-23Keywords
Animals*DNA Transposable Elements
Drosophila melanogaster
*Evolution, Molecular
Female
Gene Silencing
Male
Ovary
RNA, Small Interfering
Bioinformatics
Computational Biology
Genetics and Genomics
Molecular Genetics
Metadata
Show full item recordAbstract
Transposons evolve rapidly and can mobilize and trigger genetic instability. Piwi-interacting RNAs (piRNAs) silence these genome pathogens, but it is unclear how the piRNA pathway adapts to invasion of new transposons. In Drosophila, piRNAs are encoded by heterochromatic clusters and maternally deposited in the embryo. Paternally inherited P element transposons thus escape silencing and trigger a hybrid sterility syndrome termed P-M hybrid dysgenesis. We show that P-M hybrid dysgenesis activates both P elements and resident transposons and disrupts the piRNA biogenesis machinery. As dysgenic hybrids age, however, fertility is restored, P elements are silenced, and P element piRNAs are produced de novo. In addition, the piRNA biogenesis machinery assembles, and resident elements are silenced. Significantly, resident transposons insert into piRNA clusters, and these new insertions are transmitted to progeny, produce novel piRNAs, and are associated with reduced transposition. P element invasion thus triggers heritable changes in genome structure that appear to enhance transposon silencing.Source
Cell. 2011 Dec 23;147(7):1551-63. doi: 10.1016/j.cell.2011.11.042. Link to article on publisher's site
DOI
10.1016/j.cell.2011.11.042Permanent Link to this Item
http://hdl.handle.net/20.500.14038/25876PubMed ID
22196730Related Resources
ae974a485f413a2113503eed53cd6c53
10.1016/j.cell.2011.11.042