Drosophila IRBP bZIP heterodimer binds P-element DNA and affects hybrid dysgenesis

  • Malik Joseph Francis
  • , Siobhan Roche
  • , Michael Jeffrey Cho
  • , Eileen Beall
  • , Bosun Min
  • , Ronaldo Paolo Panganiban
  • , Donald C. Rio

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

In Drosophila, P-element transposition causes mutagenesis and genome instability during hybrid dysgenesis. The P-element 31-bp terminal inverted repeats (TIRs) contain sequences essential for transposase cleavage and have been implicated in DNA repair via protein-DNA interactions with cellular proteins. The identity and function of these cellular proteins were unknown. Biochemical characterization of proteins that bind the TIRs identified a heterodimeric basic leucine zipper (bZIP) complex between an uncharacterized protein that we termed "Inverted Repeat Binding Protein (IRBP) 18" and its partner Xrp1. The reconstituted IRBP18/Xrp1 heterodimer binds sequence-specifically to its dsDNA-binding site within the P-element TIRs. Genetic analyses implicate both proteins as critical for repair of DNA breaks following transposase cleavage in vivo. These results identify a cellular protein complex that binds an active mobile element and plays amore general role in maintaining genome stability.

Original languageEnglish (US)
Pages (from-to)13003-13008
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume113
Issue number46
DOIs
StatePublished - Nov 15 2016

All Science Journal Classification (ASJC) codes

  • General

Fingerprint

Dive into the research topics of 'Drosophila IRBP bZIP heterodimer binds P-element DNA and affects hybrid dysgenesis'. Together they form a unique fingerprint.

Cite this