Title

Maelstrom Represses Canonical Polymerase II Transcription within Bi-directional piRNA Clusters in Drosophila melanogaster

UMMS Affiliation

RNA Therapeutics Institute; Program in Bioinformatics and Integrative Biology; Department of Biochemistry and Molecular Pharmacology; Graduate School of Biomedical Sciences

Publication Date

2018-11-12

Document Type

Article

Disciplines

Amino Acids, Peptides, and Proteins | Biochemistry | Bioinformatics | Computational Biology | Genetics and Genomics | Molecular Biology | Nucleic Acids, Nucleotides, and Nucleosides

Abstract

In Drosophila, 23-30 nt long PIWI-interacting RNAs (piRNAs) direct the protein Piwi to silence germline transposon transcription. Most germline piRNAs derive from dual-strand piRNA clusters, heterochromatic transposon graveyards that are transcribed from both genomic strands. These piRNA sources are marked by the heterochromatin protein 1 homolog Rhino (Rhi), which facilitates their promoter-independent transcription, suppresses splicing, and inhibits transcriptional termination. Here, we report that the protein Maelstrom (Mael) represses canonical, promoter-dependent transcription in dual-strand clusters, allowing Rhi to initiate piRNA precursor transcription. Mael also represses promoter-dependent transcription at sites outside clusters. At some loci, Mael repression requires the piRNA pathway, while at others, piRNAs play no role. We propose that by repressing canonical transcription of individual transposon mRNAs, Mael helps Rhi drive non-canonical transcription of piRNA precursors without generating mRNAs encoding transposon proteins.

Keywords

Argonaute, Armitage, Maelstrom, PIWI-interacting RNA, Piwi, Rhino, piRNA, small silencing RNA, transcription, transposon

DOI of Published Version

10.1016/j.molcel.2018.10.038

Source

Mol Cell. 2018 Nov 12. pii: S1097-2765(18)30932-8. doi: 10.1016/j.molcel.2018.10.038. [Epub ahead of print]. Link to article on publisher's site

Journal/Book/Conference Title

Molecular cell

Related Resources

Link to Article in PubMed

PubMed ID

30527661

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