[A point mutation in the coat protein gene affects long distance transport of the tobacco mosaic virus].
A mutation resulting in substitution of positively charged Lys53 with negatively charged Glu in the coat protein was introduced in the infectious cDNA copy of the genome of wild-type tobacco mosaic virus strain U1. Kinetic analysis of long-distance virus transport in plants showed that systemic distribution of the mutant virus was delayed by 5-6 days as compared with the wild-type one. On evidence of RNA sequencing in the mutant progeny, Glu50 of the coat protein was substituted with Lys after passage I to compensate for the loss of the positive charge at position 53. Electron microscopy revealed atypical inclusions (rodlike structures, multiple electron-dense globular particles) in the nuclear interchromatin space of leaf mesophyll cells infected with the mutant but not with the wild-type virus.
Koshkina
T E
TE
Institute of Agricultural Biotechnology, Russian Academy of Agricultural Sciences, Moscow, 127550 Russia.
Baranova
E N
EN
Zavriev
S K
SK
D000595:Amino Acid Sequence; D001692:Biological Transport; D018698:Glutamic Acid / Q000235:genetics; D007700:Kinetics; D008239:Lysine / Q000235:genetics; D008854:Microscopy, Electron; D008969:Molecular Sequence Data; D018515:Plant Leaves / Q000648:ultrastructure / Q000821:virology; D017354:Point Mutation; D014026:Nicotiana / Q000821:virology; D014027:Tobacco Mosaic Virus / Q000235:genetics* / Q000472:pathogenicity; D014764:Viral Proteins / Q000235:genetics* / Q000378:metabolism
D014764:Viral Proteins; D018698:Glutamic Acid; D008239:Lysine