TABLE 6.

Characteristics of mutant viruses

Mutant virusRepression in pustule formationInfectivityaGenome organizationb
cDNAClampR
Δp40aNo3/3 (P, P, P)DicistronicMonocistronic
Δp40bNo3/3 (S, S, S)MonocistronicMonocistronic
Δp29Yes3/3 (S, S, S)DicistronicDicistronic
p69aΔ25-253Yes3/3 (S, S, S)DicistronicDicistronic
p69aΔ25-271Yes3/3 (S, S, S)DicistronicDicistronic
p69aΔ25-287Yes3/3 (S, S, S)DicistronicDicistronic
p69aΔ25-299Noc3/3 (S, S, S)DicistronicDicistronic
p69aΔ25-312No1/3 (P)DicistronicMonocistronic
p69aΔ25-325No1/3 (P)DicistronicMonocistronic
p69aΔ25-360No3/3 (S, S, S)DicistronicMono/dicistronicd
p69aΔ25-384No3/3 (S, S, P)DicistronicMono/dicistronic
p69aΔ25-545No1/3 (P)DicistronicMonocistronic
Δp69aNo3/3 (S, S, S)DicistronicDicistronic
Δp69bNo3/3 (S, S, S)MonocistronicMonocistronic
  • a Infectivity is shown as the ratio of infected plates (colonies) to total plates (colonies) regenerated from transfected spheroplasts and by the letters P and S, indicating partial and systemic infection.

  • b Genome organization of mutant viruses is based on sequences of cDNA originally designed for in vitro transcription and sequences of ClampR fragments that were amplified on dsRNA recovered from transfected fungal colonies.

  • c Although only the center of an infected colony produced stromal pustules, the surrounding area was suppressed in pustule production.

  • d Both monocistronic and dicistronic genomes were detected in the progeny virus population.