An adenosine kinase mutation in baby hamster kidney cells causing increased sensitivity to adenosine

Abstract

A class of aravinosyladenine (araA)-resistant mutants of baby hamster kidney (BHK 21/C13) cells exhibits multiple phenotypes: resistance to araA and deoxyadenosine, extreme sensitivity to adenosine (Ado) and varying degrees of deficiency in adenosine kinase (AK) activity. One of these Ado s/araA r strains, ara-S10d, was isolated without mutagenesis and was shown to possess about 59% level of the wild-type AK activity. The AK from ara-S10d had an altered K m and pH optimum and was stimulated by K + cations. A number of Ado s to Ado r revertants were isolated from araS10d, and in all of the 7 examined, the AK activity was reduced to a nondetectable level. The altered kinetic parameters of the AK enzyme in ara-S10d cells suggest a mutation of the AK gene that leads to the synthesis of an altered enzyme. The loss of AK activity in the Ado r revertants suggests an association of the enhanced Ado sensitivity to the AK mutation.