scholarly journals Selenomethionine, p-cyanophenylalanine pairs provide a convenient, sensitive, non-perturbing fluorescent probe of local helical structure

2016 ◽  
Vol 52 (10) ◽  
pp. 2055-2058 ◽  
Author(s):  
Ivan Peran ◽  
Matthew D. Watson ◽  
Osman Bilsel ◽  
Daniel P. Raleigh

Selenomethionine is a short range quencher of p-cyanophenylalanine fluorescence and these residues provide a site-specific probe of protein helical structure.

2011 ◽  
Vol 9 (1) ◽  
pp. 50-57 ◽  
Author(s):  
Isaac N. Ugwumba ◽  
Kiyoshi Ozawa ◽  
Laura de la Cruz ◽  
Zhi-Qiang Xu ◽  
Anthony J. Herlt ◽  
...  

2011 ◽  
Vol 107 (14) ◽  
Author(s):  
Anita Zeidler ◽  
Philip S. Salmon ◽  
Henry E. Fischer ◽  
Jörg C. Neuefeind ◽  
J. Mike Simonson ◽  
...  

2012 ◽  
Vol 215 (16) ◽  
pp. 2751-2759 ◽  
Author(s):  
H. Mitamura ◽  
K. Uchida ◽  
Y. Miyamoto ◽  
T. Kakihara ◽  
A. Miyagi ◽  
...  
Keyword(s):  

1989 ◽  
Vol 9 (4) ◽  
pp. 1507-1512 ◽  
Author(s):  
H Zhu ◽  
H Conrad-Webb ◽  
X S Liao ◽  
P S Perlman ◽  
R A Butow

All mRNAs of yeast mitochondria are processed at their 3' ends within a conserved dodecamer sequence, 5'-AAUAAUAUUCUU-3'. A dominant nuclear suppressor, SUV3-I, was previously isolated because it suppresses a dodecamer deletion at the 3' end of the var1 gene. We have tested the effects of SUV3-1 on a mutant containing two adjacent transversions within a dodecamer at the 3' end of fit1, a gene located within the 1,143-base-pair intron of the 21S rRNA gene, whose product is a site-specific endonuclease required in crosses for the quantitative transmission of that intron to 21S alleles that lack it. The fit1 dodecamer mutations blocked both intron transmission and dodecamer cleavage, neither of which was suppressed by SUV3-1 when present in heterozygous or homozygous configurations. Unexpectedly, we found that SUV3-1 completely blocked cleavage of the wild-type fit1 dodecamer and, in SUV3-1 homozygous crosses, intron conversion. In addition, SUV3-1 resulted in at least a 40-fold increase in the amount of excised intron accumulated. Genetic analysis showed that these phenotypes resulted from the same mutation. We conclude that cleavage of a wild-type dodecamer sequence at the 3' end of the fit1 gene is essential for fit1 expression.


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