Ribosomal protein L3 is involved in replication or maintenance of the killer double-stranded RNA genome of Saccharomyces cerevisiae.

Wickner, Reed B.; Ridley, S P; Fried, Howard M.; Ball, Steven

doi:10.1073/pnas.79.15.4706

Cited by 65 publications

(47 citation statements)

References 30 publications

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“…ItsS was mapped near the centromere of chromosome XVI (30), and we show here that it is the same as mak6. Mutations in 11 other MAK genes (mak3, 4,7,8,10,11,12,16,18,19, and 27) do not cause cold sensitivity for growth (R. B. Wickner, unpublished data), and among the low temperature-sensitive mutants of Singh and Manney, only ltsS (mak6) shows the mak-phenotype (30). The ski mutants were first discovered based on their increased production of the K1 toxin (the superkiller phenotype) (18).…”

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confidence: 57%

“…Among these genes is LTS5, whose product is necessary for both cell growth at 8°C (15) and M1 replication at 30°C (30). ItsS was mapped near the centromere of chromosome XVI (30), and we show here that it is the same as mak6.…”

mentioning

confidence: 64%

“…The correlation of cold sensitivity with M1 copy number and the existence of a gene, LTS5 (=MAK6), whose product is needed both for cell growth at 8°C (15) and for Ml dsRNA replication at 30°C (30), suggests that ski mutations cause cell cold sensitivity through increasing M copy number. The increased M dsRNA might divert most of the LTS5 product, making the cell cold sensitive for growth.…”

Section: Discussionmentioning

confidence: 99%

“…Its5 = mak6. The ItsS mutation is linked to aro7 (parental ditype = 15, nonparental ditype = 0, tetratype = 34) and causes both cold sensitivity for growth (15) and loss of M1 dsRNA (30). We have examined mutations in 12 mak genes, and of these, only mak6-1 showed cold sensitivity for growth at 8°C cosegregating with the mak-phenotype in all 24 tetrads examined.…”

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confidence: 99%

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Superkiller mutations in Saccharomyces cerevisiae suppress exclusion of M2 double-stranded RNA by L-A-HN and confer cold sensitivity in the presence of M and L-A-HN.

Ridley¹,

Sommer²,

Wickner³

1984

Mol. Cell. Biol.

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145

158

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In an mktl host, L-A-HN double-stranded RNA excludes M2 double-stranded RNA at 30°C but not at 20°C. Recessive mutations suppressing the exclusion of M2 by L-A-HN in an mktl host include six ski (superkiller) genes, three of which (ski6, ski7 and ski8) are new genes. The dominant mutations in one gene (MKS50) and recessive mutations in at least two genes (mksl and mks2) suppress M2 exclusion by L-A-HN but do not show other characteristics of ski mutations and thus define a new class of killer-related chromosomal genes. Mutations in ski2, ski3, ski4, ski6, ski7, and ski8 result in increased M copy number at 30°C and prevent the cells from growing at 8°C. Elimination of M double-stranded RNA from a coldsensitive ski-strain results in the loss of cold sensitivity. ski-[KIL-sd1] strains lack L-A-HN, carry L-A-E, and have a lower M1 copy number than do ski- [KIL-kl] strains and are only slightly cold sensitive. The LTS5 (=MAK6) product is required both for low temperature growth and for M1 maintenance or replication. We propose that the elevated levels of M in ski-strains divert the host LTS5 product away from the host and to the M replication process. We also suggest that the essential role of L-A in M replication is protection of M double-stranded RNA from the negative influence of SKI' products.The killer system of Saccharomyces cerevisiae is unique among eucaryotic virus and plasmid systems in the detail in which interactions of viral and host components have been explored and in the large number of host components shown to be involved. This probably reflects the ease with which these aspects can be investigated in S. cerevisiae rather than any difference in the degree to which viral and host functions are intertwined. Numerous examples are known of host restriction of viral growth in mammalian systems, but analysis of the host genes involved is generally not practical. We show here that overproduction of a S. cerevisiae virus, due to a host mutation, results in host pathology, apparently due to over-utilization by the virus of a specific, essential host component.

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confidence: 57%

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confidence: 64%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Superkiller mutations in Saccharomyces cerevisiae suppress exclusion of M2 double-stranded RNA by L-A-HN and confer cold sensitivity in the presence of M and L-A-HN.

Ridley¹,

Sommer²,

Wickner³

1984

Mol. Cell. Biol.

Self Cite

145

158

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“…The Kil-phenotype of some of the gcd mutations is of interest in this connection since a disturbance in protein synthesis can lead to a loss of M dsRNA (7,22). In addition, the MAK8 gene, which is required for maintenance of M dsRNA, encodes ribosomal protein L3 (39).…”

Section: Discussionmentioning

confidence: 99%

Multiple GCD genes required for repression of GCN4, a transcriptional activator of amino acid biosynthetic genes in Saccharomyces cerevisiae.

Harashima¹,

Hinnebusch²

1986

Mol. Cell. Biol.

104

116

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GCN4 encodes a positive regulator of multiple unlinked genes encoding amino acid biosynthetic enzymes in Saccharomyces cerevisiae. Expression of GCN4 is coupled to amino acid availability by a control mechanism involving GCD1 as a negative effector and GCNI, GCN2, and GCN3 as positive effectors of GCN4 expression. We used reversion of a gcn2 gcn3 double mutation to isolate new alleles of GCDI and mutations in four additional GCD genes which we designate GCDIO, GCDII, GCD12, and GCDI3. All of the mutations lead to constitutive derepression of HIS4 transcription in the absence of the GCN2+ and GCN3+ alleles. By contrast, the gcd mutations require the wild-type GCN4 allele for their derepressing effect, suggesting that each acts by influencing the level of GCN4 activity in the cell. Consistent with this interpretation, mutations in each GCD gene lead to constitutive derepression of a GCN4::1acZ gene fusion. Thus, at least five gene products are required to maintain the normal repressed level of GCN4 expression in nonstarvation conditions. Interestingly, the gcd mutations are pleiotropic and also affect growth rate in nonstarvation conditions. In addition, certain alleles lead to a loss of M double-stranded RNA required for the killer phenotype. This pleiotropy suggests that the GCD gene products contribute to an essential cellular function, in addition to, or in conjunction with, their role in GCN4 regulation.

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Structure and nuclear localization signal of the SK13 antiviral protein of Saccharomyces cerevisiae

Rhee

Icho

Wickner

1989

Yeast

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The yeast chromosomal genes SKI2, SKI3, SKI4, SKI6, SKI7 and SKI8 repress the replication of double-stranded RNA viruses, protecting the host from the otherwise lethal effects of the virus. We cloned and sequenced the SKI3 gene and found that it encodes a 163 kDa protein including a typical nuclear localization signal. Cell fractionation experiments show that the SKI3 gene product is indeed tightly associated with nuclei and that the putative nuclear localization sequence directs beta-galactosidase into the nucleus. However, fusion of a part of the SKI3 protein lacking this signal with beta-galactosidase also directs beta-galactosidase into the nucleus, suggesting the presence of a second nuclear localization signal. The SKI3 gene is only essential in the presence of an M double-stranded RNA virus.

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Ribosomal protein L3 is involved in replication or maintenance of the killer double-stranded RNA genome of Saccharomyces cerevisiae.

Cited by 65 publications

References 30 publications

Superkiller mutations in Saccharomyces cerevisiae suppress exclusion of M2 double-stranded RNA by L-A-HN and confer cold sensitivity in the presence of M and L-A-HN.

Superkiller mutations in Saccharomyces cerevisiae suppress exclusion of M2 double-stranded RNA by L-A-HN and confer cold sensitivity in the presence of M and L-A-HN.

Multiple GCD genes required for repression of GCN4, a transcriptional activator of amino acid biosynthetic genes in Saccharomyces cerevisiae.

Structure and nuclear localization signal of the SK13 antiviral protein of Saccharomyces cerevisiae

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