scholarly journals The DNA-binding Protein Hdf1p (a Putative Ku Homologue) Is Required for Maintaining Normal Telomere Length in Saccharomyces Cerevisiae

1996 ◽  
Vol 24 (4) ◽  
pp. 582-585 ◽  
Author(s):  
S. E. Porter ◽  
P. W. Greenwell ◽  
K. B. Ritchie ◽  
T. D. Petes
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Telomere Length ◽  
Binding Protein ◽  
Dna Binding Protein

scholarly journals Zuotin, a putative Z-DNA binding protein in Saccharomyces cerevisiae.

1992 ◽  
Vol 11 (10) ◽  
pp. 3787-3796 ◽  
Author(s):  
S. Zhang ◽  
C. Lockshin ◽  
A. Herbert ◽  
E. Winter ◽  
A. Rich
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Z Dna

scholarly journals The release element of the yeast polymerase I transcription terminator can function independently of Reb1p.

1995 ◽  
Vol 15 (11) ◽  
pp. 5929-5936 ◽  
Author(s):  
S W Jeong ◽  
W H Lang ◽  
R H Reeder
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Binding Site ◽  
Mutational Analysis ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Lac Repressor ◽  
Transcription Terminator ◽  
Polymerase I ◽  
Apparent Ability

The Saccharomyces cerevisiae polymerase I (polI) transcription terminator utilizes a DNA-binding protein (Reb1p) as part of a signal that causes the polymerase to pause prior to release from the template. To study the release element of the terminator, independent of the Reb1p pause signal, we have replaced the Reb1p binding site with the binding site for the lac repressor, which acts as a self-contained heterologous pause signal for polI. Release efficiency is maximal when the lac repressor causes polI to pause in exactly the same position that Reb1p would have caused it to pause, suggesting that polI must be precisely positioned for transcript release to occur. Mutational analysis shows that the release element is a region rich in T residues which codes for the extreme 3' end of the transcript and which has no apparent ability to form hairpins when transcribed into RNA. We discuss possible mechanisms whereby this polI release element might function.

scholarly journals A mutation in the gene encoding the Saccharomyces cerevisiae single-stranded DNA-binding protein Rfa1 stimulates a RAD52-independent pathway for direct-repeat recombination.

1995 ◽  
Vol 15 (3) ◽  
pp. 1632-1641 ◽  
Author(s):  
J Smith ◽  
R Rothstein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Binding ◽  
Binding Protein ◽  
Large Subunit ◽  
Direct Repeat ◽  
Fold Increase ◽  
Dna Binding Protein ◽  
Yeast Saccharomyces Cerevisiae ◽  
Single Stranded Dna ◽  
Mutant Strains

In the yeast Saccharomyces cerevisiae, recombination between direct repeats is synergistically reduced in rad1 rad52 double mutants, suggesting that the two genes define alternate recombination pathways. Using a classical genetic approach, we searched for suppressors of the recombination defect in the double mutant. One mutation that restores wild-type levels of recombination was isolated. Cloning by complementation and subsequent physical and genetic analysis revealed that it maps to RAF1. This locus encodes the large subunit of the single-stranded DNA-binding protein complex, RP-A, which is conserved from S. cerevisiae to humans. The rfa1 mutation on its own causes a 15-fold increase in direct-repeat recombination. However, unlike most other hyperrecombination mutations, the elevated levels in rfa1 mutants occur independently of RAD52 function. Additionally, rfa1 mutant strains grow slowly, are UV sensitive, and exhibit decreased levels of heteroallelic recombination. DNA sequence analysis of rfa1 revealed a missense mutation that alters a conserved residue of the protein (aspartic acid 228 to tyrosine [D228Y]). Biochemical analysis suggests that this defect results in decreased levels of RP-A in mutant strains. Overexpression of the mutant subunit completely suppresses the UV sensitivity and partially suppresses the recombination phenotype. We propose that the defective complex fails to interact properly with components of the repair, replication, and recombination machinery. Further, this may permit the bypass of the recombination defect of rad1 rad52 mutants by activating an alternative single-stranded DNA degradation pathway.

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