Abstract
Plants have two isoprenoid biosynthetic pathways, the cytosolic mevalonate (MVA) pathway and the plastidic 2-C-methyl-D-erythritol-4-phosphate (MEP) pathway. Since the discovery of the MEP pathway, metabolic cross-talk between them has been a great problem. Although many feeding experiments have been reported to demonstrate the existence of the cross-talk, it remains to be solved whether the native cross-talk, not exogenously applied metabolites, compensate for the complete blockage of one isoprenoid biosynthetic pathway. We have previously isolated Arabidopsis mutants in HMG1 and HMG2 encoding HMG-CoA reductase in the MVA pathway. To estimate the contribution of the native cross-talk, we generated hmg1 hmg2 double mutant. However, no double homozygote mutant was obtained. Crossing experiment and microscopic observations suggested that the cause is a defect in the male gametophytogenesis. Our data demonstrate that the native cross-talk from the plastid can not compensate the complete blockage of the MVA pathway at least in the male gametophytegenesis.
