Two methods were developed for the isolation of mammalian somatic cell mutants defective in peroxisome biogenesis: (i) colony autoradiographic screening with a phenotypic marker, dihydroxyacetonephosphate
acyltransferase (DHAP-ATase) deficiency; (28),(29) and (ii) the photo-sensitized selection method using 9(1,-pyrene)nonanol (P9OH) and an exposure to long wave-length ultraviolet (UV) light which kills wildtype cells incorporating P9OH as a fatty alcohol into plasmalogens and survive cell mutants deficient in such activity.
In the chloroplast the enzyme catalyzes the linkage of dihydroxyacetonephosphate
and glycerine-3-phosphate to fructose1,6-bisphosphate and initiates the regeneration of ribulose1,5-bisphosphate, the CO2-acceptor of the Calvin cycle.
These observations are in agreement with a previous study that reported the predictive value of dihydroxyacetonephosphate
acyltransferase (DHAPAT) activity and residual peroxisomal VL-CFA [beta]-oxidation activity, measured with 1-[[sup.14]C]-C24:0 as substrate, for the life expectancy of PBD patients (8).