Nature Communications (Jun 2018)

Pervasive genetic interactions modulate neurodevelopmental defects of the autism-associated 16p11.2 deletion in Drosophila melanogaster

  • Janani Iyer,
  • Mayanglambam Dhruba Singh,
  • Matthew Jensen,
  • Payal Patel,
  • Lucilla Pizzo,
  • Emily Huber,
  • Haley Koerselman,
  • Alexis T. Weiner,
  • Paola Lepanto,
  • Komal Vadodaria,
  • Alexis Kubina,
  • Qingyu Wang,
  • Abigail Talbert,
  • Sneha Yennawar,
  • Jose Badano,
  • J. Robert Manak,
  • Melissa M. Rolls,
  • Arjun Krishnan,
  • Santhosh Girirajan

DOI
https://doi.org/10.1038/s41467-018-04882-6
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 19

Abstract

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The 16p11.2 deletion leads to a range of neurodevelopmental phenotypes, but to date, sequencing studies have not been able to pinpoint individual genes that are causative for the disease on their own. Here, using Drosophila homologs of 14 16p11.2 genes, the authors take a combinatorial approach to show that gene interactions contribute to a neurological phenotype.