Viral regulation of host cell biology by hijacking of the nucleolar DNA-damage response

Stephen M. Rawlinson, Tianyue Zhao, Ashley M. Rozario, Christina L. Rootes, Paul J. McMillan, Anthony W. Purcell, Amanda Woon, Glenn A. Marsh, Kim G. Lieu, Lin-Fa Wang, Hans J. Netter, Toby D. M. Bell, Cameron R. Stewart and Gregory W. Moseley ()
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Stephen M. Rawlinson: Biomedicine Discovery Institute, Monash University, Clayton
Tianyue Zhao: Biomedicine Discovery Institute, Monash University, Clayton
Ashley M. Rozario: School of Chemistry, Monash University, Clayton
Christina L. Rootes: Australian Animal Health Laboratory, Geelong
Paul J. McMillan: Bio21 Institute, The University of Melbourne, Melbourne
Anthony W. Purcell: Biomedicine Discovery Institute, Monash University, Clayton
Amanda Woon: Biomedicine Discovery Institute, Monash University, Clayton
Glenn A. Marsh: Australian Animal Health Laboratory, Geelong
Kim G. Lieu: Biomedicine Discovery Institute, Monash University, Clayton
Lin-Fa Wang: Programme in Emerging Infectious Diseases, Duke-NUS Medical School
Hans J. Netter: Melbourne Health, The Peter Doherty Institute
Toby D. M. Bell: School of Chemistry, Monash University, Clayton
Cameron R. Stewart: Australian Animal Health Laboratory, Geelong
Gregory W. Moseley: Biomedicine Discovery Institute, Monash University, Clayton

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Recent studies indicate that nucleoli play critical roles in the DNA-damage response (DDR) via interaction of DDR machinery including NBS1 with nucleolar Treacle protein, a key mediator of ribosomal RNA (rRNA) transcription and processing. Here, using proteomics, confocal and single molecule super-resolution imaging, and infection under biosafety level-4 containment, we show that this nucleolar DDR pathway is targeted by infectious pathogens. We find that the matrix proteins of Hendra virus and Nipah virus, highly pathogenic viruses of the Henipavirus genus in the order Mononegavirales, interact with Treacle and inhibit its function, thereby silencing rRNA biogenesis, consistent with mimicking NBS1–Treacle interaction during a DDR. Furthermore, inhibition of Treacle expression/function enhances henipavirus production. These data identify a mechanism for viral modulation of host cells by appropriating the nucleolar DDR and represent, to our knowledge, the first direct intranucleolar function for proteins of any mononegavirus.

Date: 2018
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DOI: 10.1038/s41467-018-05354-7

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