R B Wickner

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Host function of MAK16: G1 arrest by a mak16 mutant of Saccharomyces cerevisiae
    R B Wickner
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892
    Proc Natl Acad Sci U S A 85:6007-11. 1988
  2. ncbi request reprint Sequence of MKT1, needed for propagation of M2 satellite dsRNA of the L-A virus of Saccharomyces cerevisiae
    M Vermut
    Section on Genetics of Simple Eukaryotes, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830
    Yeast 10:1477-9. 1994
  3. ncbi request reprint Mak21p of Saccharomyces cerevisiae, a homolog of human CAATT-binding protein, is essential for 60 S ribosomal subunit biogenesis
    H K Edskes
    Laboratory of Biochemistry and Genetics, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    J Biol Chem 273:28912-20. 1998
  4. ncbi request reprint [URE3] and [PSI] are prions of yeast and evidence for new fungal prions
    D C Masison
    National Institutes of Health, Bethesda, MD 20892 0830, USA
    Curr Issues Mol Biol 2:51-9. 2000
  5. ncbi request reprint Prions of yeast as epigenetic phenomena: high protein "copy number" inducing protein "silencing"
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Adv Genet 46:485-525. 2002
  6. doi request reprint Amyloids and yeast prion biology
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Biochemistry 52:1514-27. 2013
  7. doi request reprint Viruses and prions of Saccharomyces cerevisiae
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Adv Virus Res 86:1-36. 2013
  8. doi request reprint The yeast prions [PSI+] and [URE3] are molecular degenerative diseases
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD, USA
    Prion 5:258-62. 2011
  9. pmc Study of amyloids using yeast
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Methods Mol Biol 849:321-46. 2012
  10. pmc Prion amyloid structure explains templating: how proteins can be genes
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    FEMS Yeast Res 10:980-91. 2010

Collaborators

Detail Information

Publications81

  1. pmc Host function of MAK16: G1 arrest by a mak16 mutant of Saccharomyces cerevisiae
    R B Wickner
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892
    Proc Natl Acad Sci U S A 85:6007-11. 1988
    ..This region contains potential phosphorylation sites for "casein kinases," protein kinases specific for serine or threonine residues in an acidic environment...
  2. ncbi request reprint Sequence of MKT1, needed for propagation of M2 satellite dsRNA of the L-A virus of Saccharomyces cerevisiae
    M Vermut
    Section on Genetics of Simple Eukaryotes, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830
    Yeast 10:1477-9. 1994
    ..We report that MKT1 encodes a 92,979 Da protein with serine-rich regions and the retroviral protease signature, DTG, but with no substantial homology to proteins presently in the databases...
  3. ncbi request reprint Mak21p of Saccharomyces cerevisiae, a homolog of human CAATT-binding protein, is essential for 60 S ribosomal subunit biogenesis
    H K Edskes
    Laboratory of Biochemistry and Genetics, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    J Biol Chem 273:28912-20. 1998
    ..The virus propagation phenotype of mak21-1 is suppressed by ski2 or ski6 mutations, each of which derepresses translation of non-poly(A) mRNA...
  4. ncbi request reprint [URE3] and [PSI] are prions of yeast and evidence for new fungal prions
    D C Masison
    National Institutes of Health, Bethesda, MD 20892 0830, USA
    Curr Issues Mol Biol 2:51-9. 2000
    ..Recently, two new potential prions have been described, one in yeast and the other in the filamentous fungus, Podospora...
  5. ncbi request reprint Prions of yeast as epigenetic phenomena: high protein "copy number" inducing protein "silencing"
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Adv Genet 46:485-525. 2002
    ..Since these prions are nonchromosomal genes, they are proteins acting as genes, a parallel to the fact that nucleic acids can catalyze enzymatic reactions...
  6. doi request reprint Amyloids and yeast prion biology
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Biochemistry 52:1514-27. 2013
    ....
  7. doi request reprint Viruses and prions of Saccharomyces cerevisiae
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Adv Virus Res 86:1-36. 2013
    ..Here, we emphasize the L-A dsRNA virus and its killer-toxin-encoding satellites, the 20S and 23S ssRNA naked viruses, and the several infectious proteins (prions) of yeast...
  8. doi request reprint The yeast prions [PSI+] and [URE3] are molecular degenerative diseases
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD, USA
    Prion 5:258-62. 2011
    ..Recently, we showed that the array of [PSI] and [URE3] prions includes a majority of lethal or very toxic variants, a result not expected if either prion were an adaptive cellular response to stress...
  9. pmc Study of amyloids using yeast
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Methods Mol Biol 849:321-46. 2012
    ....
  10. pmc Prion amyloid structure explains templating: how proteins can be genes
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    FEMS Yeast Res 10:980-91. 2010
    ..The prion domain sequences generally vary more rapidly in evolution than does the remainder of the molecule, producing a barrier to prion transmission, perhaps selected in evolution by this protection...
  11. pmc The relationship of prions and translation
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Wiley Interdiscip Rev RNA 1:81-9. 2010
    ..Another connection of prions with translation is the influence on prion propagation and generation of ribosome-associated chaperones, the Ssbs, and a chaperone activity intrinsic to the 60S ribosomal subunits...
  12. pmc Double-stranded RNA viruses of Saccharomyces cerevisiae
    R B Wickner
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 0830, USA
    Microbiol Rev 60:250-65. 1996
  13. pmc Prion diseases of yeast: amyloid structure and biology
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, United States
    Semin Cell Dev Biol 22:469-75. 2011
    ..Moreover, we have pointed out that this amyloid architecture can explain how one protein can faithfully transmit any of several conformations to new protein monomers. This explains how proteins can be genes...
  14. ncbi request reprint Prions: Portable prion domains
    R B Wickner
    Laboratory of Biochemistry and Genetics, NIDDK, NIH, Bethesda, 20892 0830, USA
    Curr Biol 10:R335-7. 2000
    ....
  15. pmc Prion variants, species barriers, generation and propagation
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    J Biol 8:47. 2009
    ..Protein sequence alteration can prevent accurate structural templating at filament ends producing prion variants...
  16. pmc Protein inheritance (prions) based on parallel in-register beta-sheet amyloid structures
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Bioessays 30:955-64. 2008
    ..This property of self-reproduction, in turn, allows these proteins to act as de facto genes, encoding heritable information...
  17. ncbi request reprint Prion genetics: new rules for a new kind of gene
    Reed B Wickner
    Laboraory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Annu Rev Genet 38:681-707. 2004
    ..A recently identified prion is based on obligatory self-activation of an enzyme in trans. Although prions can be detrimental, they may also be beneficial to their hosts...
  18. ncbi request reprint Prion domains: sequences, structures and interactions
    Eric D Ross
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Nat Cell Biol 7:1039-44. 2005
    ..Ure2p and Sup35p, two yeast prion proteins, can still form prions when the prion domains are shuffled, indicating a parallel in-register beta-sheet structure...
  19. ncbi request reprint How to find a prion: [URE3], [PSI+] and [beta]
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Methods 39:3-8. 2006
    ..We detail methods used in studies of [URE3] and [beta], a self-activating protease, some of which are of broad application...
  20. pmc Yeast prions: evolution of the prion concept
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, The National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Prion 1:94-100. 2007
    ..Thus amino acid content and not sequence determine these prions. Shuffleability also suggests amyloids with a parallel in-register beta-sheet structure...
  21. pmc Prions of fungi: inherited structures and biological roles
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Nat Rev Microbiol 5:611-8. 2007
    ....
  22. ncbi request reprint Prions: proteins as genes and infectious entities
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Genes Dev 18:470-85. 2004
  23. pmc Amyloid of Rnq1p, the basis of the [PIN+] prion, has a parallel in-register beta-sheet structure
    Reed B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 225, 8 Center Drive, MSC 0830, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 105:2403-8. 2008
    ....
  24. pmc Prions in Saccharomyces and Podospora spp.: protein-based inheritance
    R B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Microbiol Mol Biol Rev 63:844-61, table of contents. 1999
    ..Both [URE3] and [PSI] are cured by growth of cells in millimolar guanidine HCl. [URE3] is also cured by overexpression of fragments of Ure2p or fusion proteins including parts of Ure2p...
  25. ncbi request reprint Prions of yeast are genes made of protein: amyloids and enzymes
    R B Wickner
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Cold Spring Harb Symp Quant Biol 69:489-96. 2004
  26. pmc Yeast MAK3 N-acetyltransferase recognizes the N-terminal four amino acids of the major coat protein (gag) of the L-A double-stranded RNA virus
    J C Tercero
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, Maryland 20892
    J Bacteriol 175:3192-4. 1993
    ..In yeast cells, only three mitochondrial proteins are known to have the MAK3 acetylation signal, suggesting an explanation for the slow growth of mak3 mutants on nonfermentable carbon sources...
  27. pmc The ski7 antiviral protein is an EF1-alpha homolog that blocks expression of non-Poly(A) mRNA in Saccharomyces cerevisiae
    L Benard
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    J Virol 73:2893-900. 1999
    ..ski1/xrn1Delta ski2Delta and ski1/xrn1Delta ski7Delta mutants were viable but temperature sensitive for growth...
  28. pmc Two prion-inducing regions of Ure2p are nonoverlapping
    M L Maddelein
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Mol Cell Biol 19:4516-24. 1999
    ..The region from 66 to 80 and the region around residue 224 are both necessary for this second prion-inducing activity. Thus, each of two nonoverlapping parts of Ure2p is sufficient to induce the appearance of the [URE3] prion...
  29. pmc Evidence that the SKI antiviral system of Saccharomyces cerevisiae acts by blocking expression of viral mRNA
    W R Widner
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
    Mol Cell Biol 13:4331-41. 1993
    ..In support of this idea, we find that Ski2p represses production of beta-galactosidase from RNA polymerase I [no cap and no poly(A)] transcripts but not from RNA polymerase II (capped) transcripts...
  30. pmc Ski6p is a homolog of RNA-processing enzymes that affects translation of non-poly(A) mRNAs and 60S ribosomal subunit biogenesis
    L Benard
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 0830, USA
    Mol Cell Biol 18:2688-96. 1998
    ..We speculate that the derepressed translation of non-poly(A) mRNAs is due to abnormal (but full-size) 60S subunits...
  31. pmc Mks1p is a regulator of nitrogen catabolism upstream of Ure2p in Saccharomyces cerevisiae
    H K Edskes
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Genetics 153:585-94. 1999
    ..Either overproduction of Mks1p or deletion of MKS1 interferes with pseudohyphal growth...
  32. pmc Elimination of L-A double-stranded RNA virus of Saccharomyces cerevisiae by expression of gag and gag-pol from an L-A cDNA clone
    R P Valle
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
    J Virol 67:2764-71. 1993
    ..Our hypotheses on exclusion of L-A proteins may also apply to resistance to plant viruses produced by expression of viral replicases in transgenic plants...
  33. pmc Decoying the cap- mRNA degradation system by a double-stranded RNA virus and poly(A)- mRNA surveillance by a yeast antiviral system
    D C Masison
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA
    Mol Cell Biol 15:2763-71. 1995
    ..The SKI2-SKI3-SKI8 system is more effective against cap+ poly(A)- mRNA, suggesting a (nonessential) role in blocking translation of fragmented cellular mRNAs...
  34. pmc A novel Rtg2p activity regulates nitrogen catabolism in yeast
    M M Pierce
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Building 8, Room 225, 8 Center Drive MSC0830, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 98:13213-8. 2001
    ..These characteristics suggest that Rtg2p acts in the upstream part of the nitrogen catabolism regulation pathway...
  35. ncbi request reprint Structure and nuclear localization signal of the SKI3 antiviral protein of Saccharomyces cerevisiae
    S K Rhee
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
    Yeast 5:149-58. 1989
    ..The SKI3 gene is only essential in the presence of an M double-stranded RNA virus...
  36. pmc MAK10, a glucose-repressible gene necessary for replication of a dsRNA virus of Saccharomyces cerevisiae, has T cell receptor alpha-subunit motifs
    Y J Lee
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892
    Genetics 132:87-96. 1992
    ..The highest levels of expression were seen in tup1 and cyc8 mutants, known to be defective in glucose repression. These results suggest that the mitochondrial genome and L-A dsRNA compete for the MAK10 protein...
  37. pmc Prion filament networks in [URE3] cells of Saccharomyces cerevisiae
    V V Speransky
    Laboratory of Structural Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Cell Biol 153:1327-36. 2001
    ..These observations support and further specify the concept of the [URE3] prion as a self-propagating amyloid...
  38. ncbi request reprint MAK3 encodes an N-acetyltransferase whose modification of the L-A gag NH2 terminus is necessary for virus particle assembly
    J C Tercero
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892
    J Biol Chem 267:20277-81. 1992
    ..We propose that MAK3 encodes an N-acetyltransferase whose modification of the L-A major coat protein NH2 terminus is essential for viral assembly, and that unassembled coat protein is unstable...
  39. pmc Yeast virus propagation depends critically on free 60S ribosomal subunit concentration
    Y Ohtake
    Section of Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA
    Mol Cell Biol 15:2772-81. 1995
    ....
  40. pmc 3' poly(A) is dispensable for translation
    A M Searfoss
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, 8 Center Drive, MSC 0830, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 97:9133-7. 2000
    ....
  41. pmc Mechanism of inactivation on prion conversion of the Saccharomyces cerevisiae Ure2 protein
    Ulrich Baxa
    Laboratory of Structural Biology, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 99:5253-60. 2002
    ..These observations suggest that the amyloid content of these filaments is confined to their prion domain-containing backbones and imply that Ure2p is inactivated in [URE3] cells by a steric blocking mechanism...
  42. pmc The crystal structure of the nitrogen regulation fragment of the yeast prion protein Ure2p
    T C Umland
    Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0560, USA
    Proc Natl Acad Sci U S A 98:1459-64. 2001
    ..Residues within this regulatory fragment that have been indicated by mutational studies to influence prion generation have been mapped onto the three-dimensional structure, and possible implications for prion activity are discussed...
  43. ncbi request reprint The MAK11 protein is essential for cell growth and replication of M double-stranded RNA and is apparently a membrane-associated protein
    T Icho
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
    J Biol Chem 263:1467-75. 1988
    ....
  44. ncbi request reprint The double-stranded RNA genome of yeast virus L-A encodes its own putative RNA polymerase by fusing two open reading frames
    T Icho
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892
    J Biol Chem 264:6716-23. 1989
    ..The coding sequence of ORF2 shows a pattern characteristic of viral RNA-dependent RNA polymerases of icosahedral (+)-strand RNA viruses. Thus, the 180-kDa protein is analogous to gag-pol fusion proteins...
  45. pmc Curing of the [URE3] prion by Btn2p, a Batten disease-related protein
    Dmitry S Kryndushkin
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    EMBO J 27:2725-35. 2008
    ..Btn2p curing requires cell division, and our results suggest that Btn2p is part of a system, reminiscent of the mammalian aggresome, that collects aggregates preventing their efficient distribution to progeny cells...
  46. pmc Measurement of amyloid fibril mass-per-length by tilted-beam transmission electron microscopy
    Bo Chen
    Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 106:14339-44. 2009
    ....
  47. pmc Primary sequence independence for prion formation
    Eric D Ross
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 102:12825-30. 2005
    ..These results suggest that [PSI+] formation is driven primarily by the amino acid composition of the Sup35p prion domain, and that the Sup35p oligopeptide repeats are not required for prion maintenance...
  48. ncbi request reprint Localized mutagenesis and evidence for post-transcriptional regulation of MAK3. A putative N-acetyltransferase required for double-stranded RNA virus propagation in Saccharomyces cerevisiae
    J C Tercero
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892
    J Biol Chem 267:20270-6. 1992
    ..Mutation of any of the underlined conserved residues (94GI----AA, 123N----A, 130Y----A, 134GF----SL, 144Y----A, and 149G----A) inactivated the gene, supporting the hypothesis that MAK3 encodes an N-acetyltransferase...
  49. ncbi request reprint [PSI] and [URE3] as yeast prions
    R B Wickner
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, Bethesda, MD 20892 0830, USA
    Yeast 11:1671-85. 1995
    ..3) Overproduction of Sup35p and Ure2p increases the frequency of cells acquiring [PSI] or [URE3], respectively...
  50. pmc Amyloid of the prion domain of Sup35p has an in-register parallel beta-sheet structure
    Frank Shewmaker
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 103:19754-9. 2006
    ..Certain sites in the M domain also exhibit intermolecular distances of approximately 0.5 nm. These results indicate that an in-register parallel beta-sheet structure underlies the [PSI(+)] prion phenomenon...
  51. ncbi request reprint Characterization of beta-sheet structure in Ure2p1-89 yeast prion fibrils by solid-state nuclear magnetic resonance
    Ulrich Baxa
    Laboratory of Structural Biology, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892 8025, USA
    Biochemistry 46:13149-62. 2007
    ....
  52. ncbi request reprint A new kind of prion: a modified protein necessary for its own modification
    B T Roberts
    National Institute of Diabetes, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Cell Cycle 3:100-3. 2004
    ..The importance of this system is that many protein-modifying enzymes may act on themselves, and if conditions are right, may become prions as well...
  53. pmc Scrambled prion domains form prions and amyloid
    Eric D Ross
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Mol Cell Biol 24:7206-13. 2004
    ....
  54. pmc Conservation of a portion of the S. cerevisiae Ure2p prion domain that interacts with the full-length protein
    Herman K Edskes
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 99:16384-91. 2002
    ..A nearly identical region is highly conserved among many of the yeasts examined in this study, despite the wide divergence of sequences found in other parts of the N-terminal domains...
  55. ncbi request reprint Ageing in yeast does not enhance prion generation
    Frank Shewmaker
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Yeast 23:1123-8. 2006
    ..From normal strains lacking the prions, we isolated old cells and measured the frequency of de novo [URE3] and [PSI(+)] prion generation. We find no evidence that ageing of yeast increases the frequency of prion occurrence...
  56. ncbi request reprint CLG1, a new cyclin-like gene of Saccharomyces cerevisiae
    Y Matsumoto
    Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases
    Yeast 9:929-31. 1993
    ..A disruption mutation of this open reading frame has no apparent phenotype under the conditions tested. ORFD, an open reading frame adjacent to the CDC48 gene, is even more similar to HCS26...
  57. ncbi request reprint Prions and RNA viruses of Saccharomyces cerevisiae
    R B Wickner
    National Institute of Diabetes, Digestive and Kidney Disease, National Institute of Health, Bethesda, Maryland 20892 0830, USA
    Annu Rev Genet 30:109-39. 1996
    ..SKI1/XRN1 is a 5'--> 3' exoribonuclease that degrades uncapped mRNAs. The viral Gag protein decapitates cellular mRNAs apparently to decoy this enzyme from working on viral mRNA...
  58. ncbi request reprint Filaments of the Ure2p prion protein have a cross-beta core structure
    Ulrich Baxa
    Laboratory of Structural Biology, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Struct Biol 150:170-9. 2005
    ..Local area electron diffraction and X-ray diffraction from partially aligned specimens showed that the 4.7A reflection is meridional and therefore the underlying structure is cross-beta...
  59. ncbi request reprint Architecture of Ure2p prion filaments: the N-terminal domains form a central core fiber
    Ulrich Baxa
    Laboratories of Structural Biology, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, and Biochemistry and Genetics, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 278:43717-27. 2003
    ....
  60. pmc A prion of yeast metacaspase homolog (Mca1p) detected by a genetic screen
    Julie Nemecek
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 225, MSC 0830, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 106:1892-6. 2009
    ..The prion state, which we name [MCA], was transmitted to the chromosomally encoded Mca1p based on genetic, cytological and biochemical tests...
  61. pmc Ure2p function is enhanced by its prion domain in Saccharomyces cerevisiae
    Frank Shewmaker
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Genetics 176:1557-65. 2007
    ..Finally, we demonstrate that the prion domain may affect the interaction of Ure2p with other components of the nitrogen regulation system, specifically the negative regulator of nitrogen catabolic genes, Gzf3p...
  62. pmc Nucleotide exchange factors for Hsp70s are required for [URE3] prion propagation in Saccharomyces cerevisiae
    Dmitry Kryndushkin
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Mol Biol Cell 18:2149-54. 2007
    ..Sse1p and Fes1p are nucleotide exchange factors for Ssa1p. Interestingly, deletion of either SSE1 or FES1 completely blocked [URE3] propagation. In addition, deletion of SSE1 also interfered with [PSI(+)] propagation...
  63. doi request reprint Amyloids of shuffled prion domains that form prions have a parallel in-register beta-sheet structure
    Frank Shewmaker
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Biochemistry 47:4000-7. 2008
    ..This result confirms our inference that shuffleability indicates parallel in-register structure...
  64. pmc Two prion variants of Sup35p have in-register parallel beta-sheet structures, independent of hydration
    Frank Shewmaker
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive andKidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Biochemistry 48:5074-82. 2009
    ..Transmission of the [PSI(+)] prion by amyloid fibrils of Sup35NM and transmission of the [URE3] prion by amyloid fibrils of recombinant full-length Ure2p are similar whether they have been lyophilized or not (wet or dry)...
  65. pmc Yeast prions [URE3] and [PSI+] are diseases
    Toru Nakayashiki
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 225, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 102:10575-80. 2005
    ..The absence of [URE3] and [PSI+] in wild strains indicates that each prion has a net deleterious effect on its host...
  66. pmc Prion variants and species barriers among Saccharomyces Ure2 proteins
    Herman K Edskes
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    Genetics 181:1159-67. 2009
    ..This implies that conservation of its prion domain is not for the purpose of forming prions. Indeed the Ure2p prion domain has been shown to be important, though not essential, for the nitrogen catabolism regulatory role of the protein...
  67. pmc The functional curli amyloid is not based on in-register parallel beta-sheet structure
    Frank Shewmaker
    Laboratory of Biochemistry and Genetics, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 0830, USA
    J Biol Chem 284:25065-76. 2009
    ..Solid state NMR and electron microscopy data are consistent with a beta-helix-like structure but are not sufficient to establish such a structure definitively...
  68. pmc Heritable activity: a prion that propagates by covalent autoactivation
    B Tibor Roberts
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Genes Dev 17:2083-7. 2003
    ..We propose that other enzymes whose active, modified, form is necessary for their maturation might also be prions...
  69. ncbi request reprint Prions of yeast fail to elicit a transcriptional response
    Eric D Ross
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Yeast 21:963-72. 2004
    ....
  70. ncbi request reprint [URE3] prion propagation is abolished by a mutation of the primary cytosolic Hsp70 of budding yeast
    B Tibor Roberts
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Yeast 21:107-17. 2004
    ..The ssa2-10 allele is compatible with propagation of [PSI(+)]. However, in combination with a deletion of SSA1, ssa2-10 eliminates the nonsense-suppression phenotype of [PSI(+)] cells...
  71. ncbi request reprint Is the prion domain of soluble Ure2p unstructured?
    Michael M Pierce
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 0830, USA
    Biochemistry 44:321-8. 2005
    ..These results suggest that the N-terminal prion domain is unstructured in the soluble protein and does not have a specific interaction with the C-terminus...
  72. ncbi request reprint The N-terminal prion domain of Ure2p converts from an unfolded to a thermally resistant conformation upon filament formation
    Ulrich Baxa
    Laboratory of Structural Biology, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Mol Biol 339:259-64. 2004
    ..In contrast, no thermal signal was associated with the N-terminal domains: in the soluble state of Ure2p, because they are unfolded; in the filamentous state, because their robust amyloid conformation resists heating to 100 degrees C...
  73. ncbi request reprint Prions of Saccharomyces and Podospora
    Ulrich Baxa
    Laboratory of Biochemistry, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA
    Contrib Microbiol 11:50-71. 2004
  74. pmc The repeat domain of the melanosome fibril protein Pmel17 forms the amyloid core promoting melanin synthesis
    Ryan P McGlinchey
    Laboratorie of Biochemistry, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Proc Natl Acad Sci U S A 106:13731-6. 2009
    ..We suggest that RPT is the amyloid core domain of the Pmel17 filaments so critical for melanin formation...
  75. ncbi request reprint Protein synthesis assayed by electroporation of mRNA in Saccharomyces cerevisiae
    Anjanette M Searfoss
    National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland 20892, USA
    Methods Enzymol 351:631-9. 2002
  76. ncbi request reprint Nitrogen source and the retrograde signalling pathway affect detection, not generation, of the [URE3] prion
    Herman K Edskes
    Laboratory of Biochemistry and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 0830, USA
    Yeast 23:833-40. 2006
    ..Moreover, the presence of both ammonia and glutamate blocks USA uptake in a known [URE3] strain, so that detection of the prion is prevented, rather than its generation...
  77. ncbi request reprint Transmissible spongiform encephalopathies: prion proof in progress
    Herman K Edskes
    Nature 430:977-9. 2004
  78. pmc A model for Ure2p prion filaments and other amyloids: the parallel superpleated beta-structure
    Andrey V Kajava
    Centre de Recherches de Biochimie Macromoleculaire, Centre National de la Recherche Scientifique FRE 2593, 1919 Route de Mende, 34293 Montpellier 5, France
    Proc Natl Acad Sci U S A 101:7885-90. 2004
    ..47 nm) and is readily adaptable to other amyloids, for instance the core of Sup35p filaments and glutamine expansions in huntingtin...
  79. ncbi request reprint The structural basis of recognition and removal of cellular mRNA 7-methyl G 'caps' by a viral capsid protein: a unique viral response to host defense
    Jinghua Tang
    Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    J Mol Recognit 18:158-68. 2005
    ..Along with His154, the reaction requires a cluster of positive charge adjoining the trench and residues Tyr 452, Tyr150 and either Tyr or Phe at position 538. A tentative mechanism for decapping is proposed...
  80. pmc Interactions among prions and prion "strains" in yeast
    Michael E Bradley
    Laboratory for Molecular Biology, Department of Biological Sciences, University of Illinois, 900 South Ashland Avenue, Chicago 60607, USA
    Proc Natl Acad Sci U S A 99:16392-9. 2002
    ..These results reinforce earlier reports that heterologous prions interact, but suggest that such interactions can not only positively, but also negatively, influence the de novo generation of prions...
  81. ncbi request reprint L-A virus at 3.4 A resolution reveals particle architecture and mRNA decapping mechanism
    Hisashi Naitow
    Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Struct Biol 9:725-8. 2002
    ..The L-A virus decaps cellular mRNA to efficiently translate its own uncapped mRNA. Our structure reveals a trench at the active site of the decapping reaction and suggests a role for nearby residues in the reaction...