Hou-Jong M H, Larsen S H, Roman A
J Virol. 1987 Mar;61(3):937-9. doi: 10.1128/JVI.61.3.937-939.1987.
Analysis of two agnogene mutants, dl2304 deleted over the entire agnogene and in2379 carrying a 2-base insert, indicated that the mutant phenotype of small plaque formation must be the result of a defect late in the maturation pathway. Both mutants were removed from the pool of molecules available for replication with wild-type kinetics. Whereas dl2304 was somewhat reduced in its rate of progression from chromatin to previrions-virions, in2379, which produced even smaller plaques than dl2304 did, progressed with wild-type kinetics. Therefore, the agnoprotein was not required for progression from chromatin to previrions.
对两个无基因(agnogene)突变体的分析表明,小噬菌斑形成的突变表型必定是成熟途径后期缺陷的结果。这两个突变体分别是整个无基因缺失的dl2304和携带2个碱基插入的in2379。两个突变体均以野生型动力学从可用于复制的分子池中去除。虽然dl2304从染色质到前病毒颗粒 - 病毒颗粒的进展速率有所降低,但产生比dl2304更小噬菌斑的in2379却以野生型动力学进展。因此,从染色质到前病毒颗粒的进展不需要agnoprotein。