Revertants of a trans-dominant S49 mouse lymphoma mutant that affects expression of cAMP-dependent protein kinase.
Phenotypic revertants were isolated from an S49 mouse lymphoma tissue culture cell mutant that lacks cAMP-dependent protein kinase (cA-PK) activity (kin-). The mutant phenotype is trans-dominant and results from a lesion that probably lies outside the cA-PK subunit structural genes. The nature of the event that produces the kin- phenotype is unknown. However, the mechanism that is responsible for its behavior is genetically encoded because: spontaneous revertants arise at low frequency; reversion frequency is increased by mutagen treatment; mutagen-specific classes of revertant phenotypes are induced; and some revertants are temperature-sensitive for expression of cA-PK subunit polypeptides. Additional evidence is provided that argues against structural lesions in cA-PK catalytic (C) subunits as explanatory of the kin- phenotype. Kin- cells do not express an immunologically detectable C polypeptide, whereas C expression is restored in revertant cells. Revertants in which phenotype and cA-PK activity levels are only partially restored to that of wild-type cells contain a commensurately reduced amount of C polypeptide. Finally, the structure of C polypeptide in partial revertants is unaltered from that of wild-type C. The evidence supports the hypothesis that the kin- lesion defines a regulatory gene responsible for setting intracellular levels of cA-PK C subunit expression.
D000818:Animals; D002460:Cell Line; D005786:Gene Expression Regulation; D005796:Genes; D005799:Genes, Dominant; D005809:Genes, Regulator; D008223:Lymphoma; D051379:Mice; D009154:Mutation; D010641:Phenotype; D011494:Protein Kinases / Q000096:biosynthesis / Q000235:genetics*; D013696:Temperature
D011494:Protein Kinases