Adaptive Evolution Targets a piRNA Precursor Transcription Network
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UMass Chan AffiliationsGraduate School of Biomedical Sciences
Program in Bioinformatics and Integrative Biology
Program in Molecular Medicine
Document TypeJournal Article
piRNA cluster transcriptional regulation
Ecology and Evolutionary Biology
Nucleic Acids, Nucleotides, and Nucleosides
MetadataShow full item record
AbstractIn Drosophila, transposon-silencing piRNAs are derived from heterochromatic clusters and a subset of euchromatic transposon insertions, which are bound by the Rhino-Deadlock-Cutoff complex. The HP1 homolog Rhino binds to Deadlock, which recruits TRF2 to promote non-canonical transcription from both genomic strands. Cuff function is less well understood, but this Rai1 homolog shows hallmarks of adaptive evolution, which can remodel functional interactions within host defense systems. Supporting this hypothesis, Drosophila simulans Cutoff is a dominant-negative allele when expressed in Drosophila melanogaster, in which it traps Deadlock, TRF2, and the conserved transcriptional co-repressor CtBP in stable complexes. Cutoff functions with Rhino and Deadlock to drive non-canonical transcription. In contrast, CtBP suppresses canonical transcription of transposons and promoters flanking the major germline clusters, and canonical transcription interferes with downstream non-canonical transcription and piRNA production. Adaptive evolution thus targets interactions among Cutoff, TRF2, and CtBP that balance canonical and non-canonical piRNA precursor transcription.
Parhad SS, Yu T, Zhang G, Rice NP, Weng Z, Theurkauf WE. Adaptive Evolution Targets a piRNA Precursor Transcription Network. Cell Rep. 2020 Feb 25;30(8):2672-2685.e5. doi: 10.1016/j.celrep.2020.01.109. PMID: 32101744; PMCID: PMC7061269. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/41371
RightsCopyright 2020 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Except where otherwise noted, this item's license is described as Copyright 2020 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).