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. 2002 Aug;76(15):7747–7759. doi: 10.1128/JVI.76.15.7747-7759.2002

TABLE 6.

Characteristics of mutant viruses

Mutant virus Repression in pustule formation Infectivitya Genome organizationb
cDNA ClampR
Δp40a No 3/3 (P, P, P) Dicistronic Monocistronic
Δp40b No 3/3 (S, S, S) Monocistronic Monocistronic
Δp29 Yes 3/3 (S, S, S) Dicistronic Dicistronic
p69aΔ25-253 Yes 3/3 (S, S, S) Dicistronic Dicistronic
p69aΔ25-271 Yes 3/3 (S, S, S) Dicistronic Dicistronic
p69aΔ25-287 Yes 3/3 (S, S, S) Dicistronic Dicistronic
p69aΔ25-299 Noc 3/3 (S, S, S) Dicistronic Dicistronic
p69aΔ25-312 No 1/3 (P) Dicistronic Monocistronic
p69aΔ25-325 No 1/3 (P) Dicistronic Monocistronic
p69aΔ25-360 No 3/3 (S, S, S) Dicistronic Mono/dicistronicd
p69aΔ25-384 No 3/3 (S, S, P) Dicistronic Mono/dicistronic
p69aΔ25-545 No 1/3 (P) Dicistronic Monocistronic
Δp69a No 3/3 (S, S, S) Dicistronic Dicistronic
Δp69b No 3/3 (S, S, S) Monocistronic Monocistronic
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.