PID-1 is a novel factor that operates during 21U-RNA biogenesis in Caenorhabditis elegans

• Published in: Genes & development Vol. 28; no. 7; pp. 683 - 688
• Main Authors: de Albuquerque, Bruno F M, Luteijn, Maartje J, Cordeiro Rodrigues, Ricardo J, van Bergeijk, Petra, Waaijers, Selma, Kaaij, Lucas J T, Klein, Holger, Boxem, Mike, Ketting, René F
• Format: Journal Article
• Language: English
• Published: United States Cold Spring Harbor Laboratory Press 01.04.2014
• Subjects: Animals; Argonaute Proteins - genetics; Argonaute Proteins - metabolism; Caenorhabditis elegans; Caenorhabditis elegans - genetics; Caenorhabditis elegans - metabolism; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Methylation; Mutation; Protein Precursors - metabolism; Research Communication; RNA Interference - physiology; RNA, Small Interfering - biosynthesis; Transgenes - genetics; C. elegans; pid-1; 21U; 22G; piRNA; biogenesis; Piwi
• ISSN: 0890-9369; 1549-5477
• DOI: 10.1101/gad.238220.114

The Piwi-piRNA pathway represents a small RNA-based mechanism responsible for the recognition and silencing of invading DNA. Biogenesis of piRNAs (21U-RNAs) is poorly understood. In Caenorhabditis elegans, the piRNA-binding Argonaute protein PRG-1 is the only known player acting downstream from precursor transcription. From a screen aimed at the isolation of piRNA-induced silencing-defective (Pid) mutations, we identified, among known Piwi pathway components, PID-1 as a novel player. PID-1 is a mostly cytoplasmic, germline-specific factor essential for 21U-RNA biogenesis, affecting an early step in the processing or transport of 21U precursor transcripts. We also show that maternal 21U-RNAs are essential to initiate silencing.