We have investigated the genetic control of murine
catalase expression by analyzing
catalase transcription and translation products from the tissues of control (Csa) and acatalasemic (Csb) mouse strains. Csb animals possess nearly normal
catalase enzyme activity levels in liver, while displaying approximately 20 and 1% of normal activity levels in kidney and red blood cells, respectively. Immunoblot analyses of
catalase in these tissues have revealed reduced levels of immunologically reactive
catalase protein in Csb kidney and red blood cells, paralleling the reduction of
catalase enzyme activity in these tissues. In order to determine the molecular basis for Csb
acatalasemia, we have isolated a
cDNA clone for murine
catalase and have used this probe to analyze Csa and Csb genomic
DNA and
catalase mRNA. These studies have revealed: 1) no restriction fragment length polymorphisms between Csa and Csb genomic DNAs; 2) no differences in the levels of Csa and Csb
catalase mRNA within a single tissue; and 3) no differences in the sizes of Csa and Csb
catalase mRNAs. These observations suggest that the genetic defect that produces the tissue-specific reduction of
catalase expression in Csb mice is not due to a marked rearrangement of
DNA within the Csb
catalase structural gene. Furthermore, the Csb mutation does not act at the level of gene transcription or mRNA stability, but rather at the level of mRNA translation and/or
catalase protein turnover.