The Replication Function of Rabies Virus P Protein Is Regulated by a Novel Phosphorylation Site in the N-Terminal N Protein-Binding Region

Viruses. 2025 Aug 1;17(8):1075. doi: 10.3390/v17081075.

Abstract

The rabies virus (RABV) phosphoprotein (P protein) has multiple functions, including acting as the essential non-catalytic cofactor of the viral polymerase (L protein) for genome replication and transcription; the principal viral antagonist of the interferon (IFN)-mediated innate immune response; and the chaperone for the viral nucleoprotein (N protein). Although P protein is known to undergo phosphorylation by cellular kinases, the location and functions of the phosphorylation sites remains poorly defined. Here, we report the identification by mass-spectrometry (MS) of residues of P protein that are modified by phosphorylation in mammalian cells, including several novel sites. Analysis of P protein with phospho-mimetic and phospho-inhibitory mutations of three novel residues/clusters that were commonly identified by MS (Ser48, Ser183/187, Ser217/219/220) indicate that phosphorylation at each of these sites does not have a major influence on nuclear trafficking or antagonistic functions toward IFN signalling pathways. However, phosphorylation of Ser48 in the N-terminus of P protein impaired function in transcription/replication and in the formation of replication structures that contain complexes of P and N proteins, suggestive of altered interactions of these proteins. The crystal structure of P protein containing the S48E phospho-mimetic mutation indicates that Ser48 phosphorylation facilitates the binding of residues 41-52 of P protein into the RNA-binding groove of non-RNA-bound N protein (N0), primarily through the formation of a salt bridge with Arg434 of N protein. These data indicate that Ser48 modification regulates the cycling of P-N0 chaperone complexes that deliver N protein to RNA to enable transcription/replication, such that enhanced interaction due to S48E phospho-mimetic mutation reduces N protein delivery to the RNA, inhibiting subsequent transcription/replication processes. These data are, to our knowledge, the first to implicate phosphorylation of RABV P protein in conserved replication functions of the P gene.

Keywords: N protein; P protein; mass spectrometry; nucleoprotein; phosphoprotein; phosphorylation; protein structure; rabies virus; viral replication.

MeSH terms

  • Animals
  • Binding Sites
  • Cell Line
  • Humans
  • Mass Spectrometry
  • Molecular Chaperones
  • Nucleocapsid Proteins* / chemistry
  • Nucleocapsid Proteins* / genetics
  • Nucleocapsid Proteins* / metabolism
  • Phosphoproteins* / chemistry
  • Phosphoproteins* / genetics
  • Phosphoproteins* / metabolism
  • Phosphorylation
  • Protein Binding
  • Rabies / virology
  • Rabies virus* / genetics
  • Rabies virus* / physiology
  • Viral Structural Proteins* / chemistry
  • Viral Structural Proteins* / genetics
  • Viral Structural Proteins* / metabolism
  • Virus Replication*

Substances

  • Phosphoproteins
  • P phosphoprotein, Rabies virus
  • Viral Structural Proteins
  • Nucleocapsid Proteins
  • nucleocapsid protein, Rabies virus
  • Molecular Chaperones