Rotaviral nonstructural protein 4 triggers dynamin-related protein 1-dependent mitochondrial fragmentation during infection

• DOI: 10.1111/cmi.12831
• Publication Date: 2018-02-14T21:48:34Z
• Authors: Arpita Mukherjee; Upayan Patra; Rahul Bhowmick; Mamta Chawla-Sarkar
• Keywords: DNAJA3; MFN2; PINK1; DNM1L; MFN1; FIS1; Mitochondrial apoptosis-induced channel

Dynamic equilibrium between mitochondrial fission and fusion serves as an important quality control system within cells ensuring cellular vitality homeostasis. Viruses often target dynamics a part of their obligatory reprogramming. The present study was undertaken to assess the status regulation during rotavirus infection. Distinct fragmentation syncytia observed late hours RV (SA11, Wa, A5-13) nonstructural protein 4 (NSP4) identified viral trigger for disrupted morphology. Severance interconnections found be dynamin-related 1 (Drp1)-dependent process resulting synergistically from augmented attenuated fusion. Cyclin-dependent kinase subsequently responsible fission-active Ser616 phosphorylation Drp1. In addition its positive role in fission, Drp1 also resulted translocation E3-ubiquitin ligase Parkin leading degradation Mitofusin 1. Interestingly, RV-NSP4 interact with involved recruiting pool Serine 616 phosphoDrp1 (Ser616 pDrp1) mitochondria independent accessory adaptors Mitochondrial factor Fission (Fis1). Inhibition either or pDrp1 significant decrease RV-NSP4-induced intrinsic apoptotic pathway. Overall, this underscores efficient strategy utilised by couple apoptosis facilitating dissemination progeny.