Genetic analysis of maintenance and expression of L and M double-stranded RNAs from yeast killer virus K28

Yeast ◽  
1992 ◽  
Vol 8 (5) ◽  
pp. 373-384 ◽  
Author(s):  
Manfred J. Schmitt ◽  
Donald J. Tipper
Keyword(s):  
Genetic Analysis ◽  
Yeast Killer ◽  
Killer Virus

Evolution of defective-interfering double-stranded RNAs of the yeast killer virus.

1979 ◽  
Vol 32 (2) ◽  
pp. 692-696 ◽  
Author(s):  
W P Kane ◽  
D F Pietras ◽  
J A Bruenn
Keyword(s):  
Yeast Killer ◽  
Killer Virus

scholarly journals Ribosomal Protein L3 Mutants Alter Translational Fidelity and Promote Rapid Loss of the Yeast Killer Virus

1999 ◽  
Vol 19 (1) ◽  
pp. 384-391 ◽  
Author(s):  
Stuart W. Peltz ◽  
Amy B. Hammell ◽  
Ying Cui ◽  
Jason Yasenchak ◽  
Lara Puljanowski ◽  
...  
Keyword(s):  
Ribosomal Protein ◽  
Missense Mutations ◽  
Ribosomal Frameshift ◽  
Virus Propagation ◽  
Particle Assembly ◽  
Ribosomal Frameshifting ◽  
Peptidyl Transfer ◽  
Yeast Killer ◽  
Peptidyltransferase Center ◽  
Killer Virus

ABSTRACT Programmed −1 ribosomal frameshifting is utilized by a number of RNA viruses as a means of ensuring the correct ratio of viral structural to enzymatic proteins available for viral particle assembly. Altering frameshifting efficiencies upsets this ratio, interfering with virus propagation. We have previously demonstrated that compounds that alter the kinetics of the peptidyl-transfer reaction affect programmed −1 ribosomal frameshift efficiencies and interfere with viral propagation in yeast. Here, the use of a genetic approach lends further support to the hypothesis that alterations affecting the ribosome’s peptidyltransferase activity lead to changes in frameshifting efficiency and virus loss. Mutations in theRPL3 gene, which encodes a ribosomal protein located at the peptidyltransferase center, promote approximately three- to fourfold increases in programmed −1 ribosomal frameshift efficiencies and loss of the M1 killer virus of yeast. Themak8-1 allele of RPL3 contains two adjacent missense mutations which are predicted to structurally alter the Mak8-1p. Furthermore, a second allele that encodes the N-terminal 100 amino acids of L3 (called L3Δ) exerts atrans-dominant effect on programmed −1 ribosomal frameshifting and killer virus maintenance. Taken together, these results support the hypothesis that alterations in the peptidyltransferase center affect programmed −1 ribosomal frameshifting.

Yeast killer virus transcription initiation in vitro

Virology ◽  
1992 ◽  
Vol 187 (1) ◽  
pp. 333-337 ◽  
Author(s):  
Francis P. Barbone ◽  
Teresa L. Williams ◽  
Michael J. Leibowitz
Keyword(s):  
Transcription Initiation ◽  
Virus Transcription ◽  
Yeast Killer ◽  
Killer Virus

The internal polyadenylate tract of yeast killer virus M1 double-stranded RNA is variable in length

Virology ◽  
1986 ◽  
Vol 152 (1) ◽  
pp. 149-158 ◽  
Author(s):  
Ernest M. Hannig ◽  
Teresa L. Williams ◽  
Michael J. Leibowitz
Keyword(s):  
Double Stranded Rna ◽  
Yeast Killer ◽  
Killer Virus

scholarly journals In vivo mapping of a sequence required for interference with the yeast killer virus.

1991 ◽  
Vol 88 (4) ◽  
pp. 1271-1275 ◽  
Author(s):  
B. F. Huan ◽  
Y. Q. Shen ◽  
J. A. Bruenn
Keyword(s):  
Yeast Killer ◽  
Killer Virus

scholarly journals Evolutionary Capture of Viral and Plasmid DNA by Yeast Nuclear Chromosomes

2009 ◽  
Vol 8 (10) ◽  
pp. 1521-1531 ◽  
Author(s):  
A. Carolin Frank ◽  
Kenneth H. Wolfe
Keyword(s):  
Plasmid Dna ◽  
Nuclear Genome ◽  
Plastid Dna ◽  
Double Strand Breaks ◽  
Trna Genes ◽  
Viral Origin ◽  
Double Stranded Rna ◽  
Strand Breaks ◽  
Yeast Killer ◽  
Killer Virus

ABSTRACT A 10-kb region of the nuclear genome of the yeast Vanderwaltozyma polyspora contains an unusual cluster of five pseudogenes homologous to five different genes from yeast killer viruses, killer plasmids, the 2μm plasmid, and a Penicillium virus. By further database searches, we show that this phenomenon is not unique to V. polyspora but that about 40% of the sequenced genomes of Saccharomycotina species contain integrated copies of genes from DNA plasmids or RNA viruses. We propose the name NUPAVs (nuclear sequences of plasmid and viral origin) for these objects, by analogy to NUMTs (nuclear copies of mitochondrial DNA) and NUPTs (nuclear copies of plastid DNA, in plants) of organellar origin. Although most of the NUPAVs are pseudogenes, one intact and active gene that was formed in this way is the KHS1 chromosomal killer locus of Saccharomyces cerevisiae. We show that KHS1 is a NUPAV related to M2 killer virus double-stranded RNA. Many NUPAVs are located beside tRNA genes, and some contain sequences from a mixture of different extrachromosomal sources. We propose that NUPAVs are sequences that were captured by the nuclear genome during the repair of double-strand breaks that occurred during evolution and that some of their properties may be explained by repeated breakage at fragile chromosomal sites.

Genetic analysis of a Japanese patient with butyrylcholinesterase deficiency

1997 ◽  
Vol 61 (6) ◽  
pp. 491-496 ◽  
Author(s):  
K. HIDAKA ◽  
I. IUCHI ◽  
M. TOMITA ◽  
Y. WATANABE ◽  
Y. MINATOGAWA ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Japanese Patient

An autopsy case of gallbladder cancer developing in a Japanese man with cerebrotendinous xanthomatosis: genetic analysis of the sterol 27-hydroxylase and p53 genes

Pathology ◽  
2003 ◽  
Vol 35 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Hiroya Kato ◽  
Sukenari Koyabu ◽  
Shigenori Aoki ◽  
Takuya Tamai ◽  
Masahiro Sugawa ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Gallbladder Cancer ◽  
Cerebrotendinous Xanthomatosis ◽  
Autopsy Case ◽  
P53 Genes

Genetic analysis of non-toxic liver fibrosis in a congenic mouse intercross

2016 ◽  
Vol 54 (08) ◽  
Author(s):  
R Hall ◽  
K Hochrath ◽  
F Grünhage ◽  
F Lammert
Keyword(s):  
Liver Fibrosis ◽  
Genetic Analysis ◽  
Congenic Mouse
Sign in / Sign up

Export Citation Format

Share Document