Quiles-Pando, CarlosNavarro Gochicoa, María TeresaHerrera Rodríguez, María BegoñaCamacho-Cristóbal, Juan JoséGonzález-Fontes, AgustínRexach, Jesús2024-12-202024-12-202019-05-09https://doi.org/10.3390/ijms20092297https://hdl.handle.net/10433/22146This work was supported by the Ministerio de Ciencia e Innovación (BFU2012-37445 and BFU2017-88811-P) and Junta de Andalucía (BIO-266 and P09-CVI-4721), Spain.Abstract: Boron (B) is a micronutrient for plant development, and its deficiency alters many physiological processes. However, the current knowledge on how plants are able to sense the B-starvation signal is still very limited. Recently, it has been reported that B deprivation induces an increase in cytosolic calcium concentration ([Ca2+]cyt) in Arabidopsis thaliana roots. The aim of this work was to research in Arabidopsis whether [Ca2+]cyt is restored to initial levels when B is resupplied and elucidate whether apoplastic Ca2+ is the major source for B-deficiency-induced rise in [Ca2+]cyt. The use of chemical compounds a ecting Ca2+ homeostasis showed that the rise in root [Ca2+]cyt induced by B deficiency was predominantly owed to Ca2+ influx from the apoplast through plasma membrane Ca2+ channels in an IP3-independent manner. Furthermore, B resupply restored the root [Ca2+]cyt. Interestingly, expression levels of genes encoding Ca2+ transporters (ACA10, plasma membrane PIIB-type Ca2+-ATPase; and CAX3, vacuolar cation/proton exchanger) were upregulated by ethylene glycol tetraacetic acid (EGTA) and abscisic acid (ABA). The results pointed out that ACA10, and especially CAX3, would play a major role in the restoration of Ca2+ homeostasis after 24 h of B deficiency.application/pdfenAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/Apoplastic calciumBoron deficiencyCalcium signalingCytosolic calciumCameleon YC3.6Arabidopsis thalianajournal articleopen access