Two distinct families of protein kinases are required for plant growth under high external Mg2+ concentrations in Arabidopsis.

Protein phosphorylation events play key roles in maintaining cellular ion homeostasis in higher plants, and the regulatory roles of these events in Na(+) and K(+) transport have been studied extensively. However, the regulatory mechanisms governing Mg(2+) transport and homeostasis in higher plants remain poorly understood, despite the vital roles of Mg(2+) in cellular function. A member of subclass III sucrose nonfermenting-1-related protein kinase2 (SnRK2), SRK2D/SnRK2.2, functions as a key positive regulator of abscisic acid (ABA)-mediated signaling in response to water deficit stresses in Arabidopsis (Arabidopsis thaliana). Here, we used immunoprecipitation coupled with liquid chromatography-tandem mass spectrometry analyses to identify Calcineurin B-like-interacting protein kinase26 (CIPK26) as a novel protein that physically interacts with SRK2D. In addition to CIPK26, three additional CIPKs (CIPK3, CIPK9, and CIPK23) can physically interact with SRK2D in planta. The srk2d/e/i triple mutant lacking all three members of subclass III SnRK2 and the cipk26/3/9/23 quadruple mutant lacking CIPK26, CIPK3, CIPK9, and CIPK23 showed reduced shoot growth under high external Mg(2+) concentrations. Similarly, several ABA biosynthesis-deficient mutants, including aba2-1, were susceptible to high external Mg(2+) concentrations. Taken together, our findings provided genetic evidence that SRK2D/E/I and CIPK26/3/9/23 are required for plant growth under high external Mg(2+) concentrations in Arabidopsis. Furthermore, we showed that ABA, a key molecule in water deficit stress signaling, also serves as a signaling molecule in plant growth under high external Mg(2+) concentrations. These results suggested that SRK2D/E/I- and CIPK26/3/9/23-mediated phosphorylation signaling pathways maintain cellular Mg(2+) homeostasis.

Early senescence of the oldest leaves of Fe-deficient barley plants may contribute to phytosiderophore release from the roots.

Barley (Hordeum vulgare), which tolerates iron (Fe) deficiency, secretes a large amount of phytosiderophores from its roots. However, how barley is able to allocate resources for phytosiderophore synthesis when the carbon assimilation rate is reduced by Fe deficiency is unknown. We previously suggested that the acceleration of senescence in older leaves triggered by Fe deficiency may allow the recycling of assimilates to contribute to phytosiderophore synthesis. In this work, we show the relationship between an increase in the C/N ratio in older leaves and Fe-deficiency tolerance among three barley cultivars. The increase in the C/N ratio suggests an enhanced capacity for the retranslocation of carbohydrates or amino acids from older leaves to the sink organs. An increase in the sucrose concentration in Fe-deficient barley also suggests active redistribution of assimilates. This metabolic modulation may be supported by accelerated senescence of older leaves, as Fe deficiency increased the expression of senescence-associated genes. The older leaves of Fe-deficient barley maintained CO2 assimilation under Fe deficiency. Barley that had been Fe-deficient for 3 days preferentially allocated newly assimilated (13) C to the roots and nutrient solution. Interestingly, the oldest leaf of Fe-deficient barley released more (13) C into the nutrient solution than the second oldest leaf. Thus, the balance between anabolism and catabolism in older leaves, supported by highly regulated senescence, plays a key role in metabolic adaptation in Fe-deficient barley.