Temperature-sensitive phenotype of a mutant Sendai virus strain is caused by its insufficient accumulation of the M protein.
We investigated the process interrupting the production of a temperature-sensitive mutant strain of Sendai virus, Cl.151, at the nonpermissive temperature (38 degrees C). The amount of virus M protein increased up to 6-fold when the cells persistently infected with Cl.151 strain at 38 degrees C are transferred to 32 degrees C, while the amount of nucleocapsid proteins did not alter. Cl.151 strain could restore virus production at 38 degrees C not only by the supplementation of M protein of wild type (Z) strain but also by the supplementation of M protein of Cl.151 strain. Neither the amount of M mRNA nor the rate of synthesis of M protein was altered by temperature in cells infected with the Cl.151 strain. However, we found that M protein of Cl.151 virus, which has 3-amino acid alterations from the wild type, was highly unstable at 38 degrees C when expressed under the control of an actin promoter. These results clearly show that Sendai virus M protein has a critical role in the production of virus particles without affecting virus gene expression.
Kondo
T
T
Institute for Molecular and Cellular Biology, Osaka University, Japan.
Yoshida
T
T
Miura
N
N
Nakanishi
M
M
D000596:Amino Acids / Q000235:genetics; D000818:Animals; D001483:Base Sequence; D002642:Chick Embryo; D017931:DNA Primers; D008969:Molecular Sequence Data; D009154:Mutation; D010222:Parainfluenza Virus 1, Human / Q000235:genetics* / Q000378:metabolism; D010641:Phenotype; D012333:RNA, Messenger / Q000378:metabolism; D013696:Temperature; D014763:Viral Matrix Proteins / Q000378:metabolism*
D000596:Amino Acids; D017931:DNA Primers; D012333:RNA, Messenger; D014763:Viral Matrix Proteins