| Literature DB >> 3027418 |
M H Hou-Jong, S H Larsen, A Roman.
Abstract
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.Entities:
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Year: 1987 PMID: 3027418 PMCID: PMC254043 DOI: 10.1128/JVI.61.3.937-939.1987
Source DB: PubMed Journal: J Virol ISSN: 0022-538X Impact factor: 5.103