Effects of lovastatin on auxin transport and root development in Arabidopsis thaliana
Sterol biosynthesis underlies significant physiological functions in plants, including the production of membrane structural sterols and hormones such as brassinosteroids and cytokinins. Inhibition of sterol biosynthesis has been shown to disrupt multiple aspects of Arabidopsis thaliana development. Here, the effects of lovastatin, an inhibitor of HMG-CoA reductase, on root development were investigated, focusing on auxin-cytokinin distribution and transport. Lovastatin inhibited primary root growth, especially cell elongation, in a dose-dependent manner. Additionally, lateral root density was considerably increased and lateral root primordia (LRP) emerged ectopically. In accordance to the above defects, auxin/cytokinin imbalance was recorded by the ectopic presence of the synthetic auxin marker DR5 and a significant decrease of cytokinins, as revealed by depletion of the TCS (two-component signaling) marker. Because auxin distribution appeared disturbed, auxin transport impairment was further examined. Plasma membrane localization of PIN auxin efflux carriers declined significantly, showing additional diffuse cytoplasmic localization in LRP cells. However, the cell-specific localization patterns of several PINs and their abundance at the transcript and protein level appeared unaffected or slightly increased. Fluorescence recovery after photobleaching (FRAP) analysis regarding membrane kinetics of PIN2 revealed altered PIN2 membrane dynamics and transmission electron microscopy (TEM) observations showed structural defects at the plasma membrane-cell wall interface. Together, these results support that sterol biosynthesis is essential for maintaining plasma membrane organization, which, in turn, is key factor for the distribution of hormones that control root development. HighlightsLovastatin treatment inhibits root growth and causes deregulated formation of lateral roots. Consistently, lovastatin causes altered patterns of auxin distribution relevant to PIN protein mis-localization and decreases cytokinin levels. These changes could be attributed to reduced structural sterols as exemplified from alteration in PIN2 membrane dynamics.