Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able to suppress the original mutation. Q. On the basis of this information, are the R1 and SuB mutations intragenic suppressors or intergenic suppressors? Explain your reasoning.
Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to
Q. On the basis of this information, are the R1 and SuB mutations intragenic suppressors or intergenic suppressors? Explain your reasoning.
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