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. 2001 Jul 2;20(13):3506–3517. doi: 10.1093/emboj/20.13.3506

Table I. Amino acid changes in spt16 alleles.

Allele Amino acid changes Phenotypes Relative HO expression (% WT)    
    37°C Spt 6-AU HU A364a (genomic) A364a (plasmid) W303 (genomic)
SPT16-WT   ++ ++ ++ ++ 100 100 100
spt16-1, –2, –10 G132D – – – – ++ 100 96 36
spt16-4 P565S P570L – – – – ++ 100    
spt16-6 P920L – –   ++      
spt16-7 T848I T849I D850Y – – – – ++ 86    
spt16-8 G369D R373T – – – – ++ ++ 85    
spt16-9 G132D G836S P838S – – – –   – –   40  
spt16-9a G836S P838S ++     – –      
spt16-9b G836S ++     ++      
spt16-9c P838S ++     ++      
spt16-11 T828I P859S – – – – +/– 114    
spt16-12 A417T G568S R569K P599L – – ++ ++/– ++ 107    
spt16-16 R204W A273V C290V D318N R801Q A802T – – – –   – –/+   50  
spt16-16a R204W A273V C290V D318N – – – –   – –/+      
spt16-16b R801Q A802T ++ ++   ++      
spt16-24 T434I – – ++ ++ 63    

Sequencing of the SPT16 ORF from mutants revealed the predicted amino acid changes shown. Phenotypes were tested either in strains lacking the genomic SPT16 and containing a mutant allele on a plasmid (for growth at 37°C, the Spt phenotype and sensitivity to HU) or in strains in which the spt16 allele was integrated into the genome (for testing sensitivity to 6-AU). Effects were scored from ++ (WT) to – (mutant). HO mRNA was measured as in Figure 2.