Molecular regulatory mechanisms in plants that underlie phenotypic adaptations to low boron levels

Plants respond to low boron levels in the soil with a cessation of growth, where particularly the development of plant meristems, groups of stem cells that are responsible for postembryonic organ development, is halted. Despite the drastic consequences of boron deficiency on meristem development, our understanding of the molecular regulatory mechanisms that underly the boron deficiency-induced developmental defects in meristems is still limited. The root apical and the shoot apical meristem, from which all below and above ground organs develop, differ functionally, structurally, and molecularly, yet they both stop their development as early defects following boron limitation. Therefore, tissue-specific studies are important to gain a full mechanistic understanding of the molecular mechanisms underlying the boron deficiency-induced response in plant meristems. Boron’s function of crosslinking pectic subunits in the cell wall is best understood, and recent research has shed light on additional molecular regulatory mechanisms that contribute to the phenotypic adaptations observed when plants grow in boron limiting conditions. For example, boron interaction partners have been found in the plasma membrane, interactions of boron with phytohormones like auxin, ethylene, and cytokinin have been proposed, boron-dependent transcript level changes were observed, and functions of boron in the cytosol have been reported. One of the current challenges in boron research today is, whether the proposed additional functions of boron are mediated by cell wall defects or independent of it. In this chapter, the current knowledge of the molecular regulatory mechanisms underlying boron deficiency-induced phenotypic defects in plants will be compiled. Molecular mechanisms that are in close relation to observed root and shoot apical meristem defects will be emphasized and reported differences in both meristem types and between plant species will be highlighted.