Why excess boron becomes toxic?: closing in on the molecular mechanism of boron toxicity

Abstract

Boron (B) is an essential micronutrient for plants that contributes to cell elongation through mediating cross-linking of the pectic polysaccharide rhamnogalacturonan II (RG-II). However, as with many of other nutrients, excess level of B becomes toxic to plants, resulting in the impaired growth and consequently the reduction in yield of seeds. So far, numerous studies have described physiological defects caused by excess B, while the molecular mechanisms underlying B toxicity remains poorly understood. Hence I characterized the mutants of Arabidopsis thaliana exhibiting extremely reduced root growth and abnormal root morphology under the excess B condition and identified a chromosomal protein complex condensin II and an active proteolytic device 26S proteasome as novel factors required for the tolerance to B toxicity. Through the functional analyses of these factors, I found that excess B induces DNA damage. In addition, I revealed the generation and suppressing mechanism of excess B-dependent DNA damage. Here I report the new aspects of B toxicity at molecular level.