Abstract
AbstractPreviously, Segev and Gerst found that mutants in any of the four ribosomal protein genesrpl1b, rpl2b, rps11a, orrps26bhad a petite phenotype—i.e., the mutants were deficient in respiration. Strikingly, mutants of their paralogsrpl1a, rpl2a, rps11b, andrps26awere grande—i.e., competent for respiration. It is remarkable that these paralogs should have opposite phenotypes, because three of the paralog pairs (Rpl1a/Rpl1b, Rpl2a/Rpl2b, Rps11a/Rps11b) are 100% identical to each other in amino acid sequence, while Rps26a and Rps26b differ in 2 amino acids out of 119. However, while attempting to use this paralog-specific petite phenotype in an unrelated experiment, I found that therpl1b, rpl2b, rps11a, andrps26bdeletion mutants are competent for respiration, contrary to Segev and Gerst.
Publisher
Cold Spring Harbor Laboratory