Phenylboronic acid-induced defects in maize roots are independent of rhamnogalacturonan-II dimerization

Soil boron deficiency is a global abiotic stress, negatively impacting on crop yield. In the dicot model species Arabidopsis thaliana, inhibition of root elongation is one of the earliest symptoms of boron deficiency. In the monocot model maize (Zea mays L.), boron deficiency-induced root defects are widely unexplored. In this study, we assessed boron deficiency-induced defects in the primary root system of maize and tested the suitability of phenylboronic acid (PBA) as boron deficiency mimic by performing phenotypic, histological, molecular, and biochemical analyses. Our analyses showed that boron deficiency and PBA resulted in similar defects in primary root elongation and lateral root density. The PBA-induced defects, however, were much stronger than those induced by boron deficiency, particularly regarding lateral root development. We provide evidence that the PBA-induced defects were caused by the boric acid moiety and show that both boron deficiency and PBA altered the levels of auxin and reactive oxygen species. Strikingly, PBA did not affect rhamnogalacturonan-II (RG-II) dimerization. Interference of boron-mediated RG-II crosslinking, however, was previously proposed to be the mode of action of PBA in planta. Our study shows that PBA is particularly suited for the molecular dissection of lateral root development in maize and suggests that PBA does not mimic known molecular boron deficiency responses.