Is Ca2+ involved in the signal transduction pathway of boron deficiency? New hypotheses for sensing boron deprivation

•Ca2+ and Ca2+-related proteins could be involved in sensing B deficiency.•CNGCs could participate in the transient [Ca2+]cyt increase under B deprivation.•TFs and Ca2+-sensor proteins could trigger physiological responses to B deficiency.•B could have a key role for stabilization of the anchorage of AGPs. Plants sense and transmit nutrient-deprivation signals to the nucleus. This increasingly interesting research field advances knowledge of signal transduction pathways for mineral deficiencies. The understanding of this topic for most micronutrients, especially boron (B), is more limited. Several hypotheses have been proposed to explain how a B deprivation signal would be conveyed to the nucleus, which are briefly summarized in this review. These hypotheses do not explain how so many metabolic and physiological processes quickly respond to B deficiency. Short-term B deficiency affects the cytosolic Ca2+ levels as well as root expression of genes involved in Ca2+ signaling. We propose and discuss that Ca2+ and Ca2+-related proteins – channels/transporters, sensor relays, and sensor responders – might have major roles as intermediates in a transduction pathway triggered by B deprivation. This hypothesis may explain how plants sense and convey the B-deprivation signal to the nucleus and modulate physiological responses. The possible role of arabinogalactan-proteins in the B deficiency signaling pathway is also taken into account.