High impact information on ObPVgp1

• Three (two frame-shift and one non-sense) mutants with an intact 130K but a defective 180K protein gene were not infectious, while two mutants with a one-amino-acid insertion in the 180K protein gene were infectious [1].
• Complete nucleotide sequencing of the TMV-R genomic RNA revealed amino acid changes in the 130K/ 180K replicase proteins, the 30K protein, and the coat protein and nucleotide changes in the 5' and 3' noncoding regions compared to TMV-U1 [2].
• Examination of the infection phenotypes of the 14 constructed chimeric viruses in BY showed that determinants defining the differential infection phenotype in BY reside in the 130K/180K replicase proteins and the 3' noncoding region [2].

Biological context of ObPVgp1

• The 130K (1,115 amino acids), 180K (1,615 amino acids), 30K (263 amino acids) and coat protein (158 amino acids) cistrons are located at residues 72-3442, 72-4922, 4906-5700, and 5703-6182 on the genome, respectively [3].
• Only three, which were in the common reading frame for both the 130K and 180K proteins, resulted in amino acid changes [4].
• The amino acid sequence homologies of the four encoded proteins (180K, 130K, 30K, coat protein) are from 95.9% to 98.0% compared with TMV-U1 [5].

Other interactions of ObPVgp1

• Remarkable differences between them were found in a part of the N-terminal portion of the 130K/180K protein and the C-terminal portion of the 30K protein [3].

References