Root cells take up K + from the soil solution, and a fraction of the absorbed K + is translocated to the shoot after being loaded into xylem vessels. K + uptake and translocation are spatially separated processes. K + uptake occurs in the cortex and epidermis whereas K + translocation starts at the stele. Both uptake and translocation processes are expected to be linked, but the connection between them is not well characterized. Here, we studied K + uptake and translocation using Rb + as a tracer in wild-type Arabidopsis thaliana and in T-DNA insertion mutants in the K + uptake or translocation systems. The relative amount of translocated Rb + to the shoot was positively correlated with net Rb + uptake rates, and the akt1 athak5 T-DNA mutant plants were more efficient in their allocation of Rb + to shoots. Moreover, a mutation of SKOR and a reduced plant transpiration prevented the full upregulation of AtHAK5 gene expression and Rb + uptake in K + -starved plants. Lastly, Rb + was found to be retrieved from root xylem vessels, with AKT1 playing a significant role in K + -sufficient plants. Overall, our results suggest that K + uptake and translocation are tightly coordinated via signals that regulate the expression of K + transport systems.

Potassium (K ) is a macronutrient known for its high mobility and positive charge, which allows efficient and fast control of the electrical balance and osmotic potential in plant cells. Such features allow K to remarkably contribute to plant stress adaptation. Some agricultural lands are deficient in K , imposing a stress that reduces crop yield and makes fertilization a common practice. However, individual stress conditions in the field are rare, and crops usually face a combination of different stresses. As plant response to a stress combination cannot always be deduced from individual stress action, it is necessary to gain insights into the specific mechanisms that connect K homeostasis with other stress effects to improve plant performance in the context of climate change. Surprisingly, plant responses to environmental stresses under a K -limiting scenario are poorly understood. In the present review, we summarize current knowledge and find substantial gaps regarding specific outcomes of K deficiency in addition to other environmental stresses. In this regard, combined nutrient deficiencies of K and other macronutrients are covered in the first part of the review and interactions arising from K deficiency with salinity, drought and biotic factors in the second part. Information available so far suggests a prominent role of potassium and nitrate transport systems and their regulatory proteins in the response of plants to several stress combinations. Thus, such molecular pathways, which are located at the crossroad between K homeostasis and environmental stresses, could be considered biotechnological targets in future studies.

The high-affinity K+ transporter HAK5 is the major contributor to root K+ uptake from dilute solutions in K+-starved Arabidopsis plants. Its functionality is tightly regulated and its activity is enhanced under K+ starvation by the transcriptional induction of the AtHAK5 gene, and by the activation of the transporter via the AtCBL1–AtCIPK23 complex. In the present study, the 26 members of the Arabidopsis CIPK protein kinase family were screened in yeast for their capacity to activate HAK5-mediated K+ uptake. Among them, AtCIPK1 was the most efficient activator of AtHAK5. In addition, AtCIPK9, previously reported to participate in K+ homeostasis, also activated the transporter. In roots, the genes encoding AtCIPK1 and AtCIPK9 were induced by K+ deprivation and atcipk1 and atcipk9 Arabidopsis KO mutants showed a reduced AtHAK5-mediated Rb+ uptake. Activation of AtHAK5 by AtCIPK1 did not occur under hyperosmotic stress conditions, where AtCIPK1 function has been shown to be required to maintain plant growth. Taken together, our data contribute to the identification of the complex regulatory networks that control the high-affinity K+ transporter AtHAK5 and root K+ uptake.

Root K+ acquisition is a key process for plant growth and development, extensively studied in the model plant Arabidopsis thaliana. Because important differences may exist among species, translational research supported by specific studies is needed in crops such as tomato. Here we present a reverse genetics study to demonstrate the role of the SlHAK5 K+ transporter in tomato K+ nutrition, Cs+ accumulation and its fertility. slhak5 KO lines, generated by CRISPR‐Cas edition, were characterized in growth experiments, Rb+ and Cs+ uptake tests and root cells K+‐induced plasma membrane depolarizations. Pollen viability and its K+ accumulation capacity were estimated by using the K+‐sensitive dye Ion Potassium Green 4. SlHAK5 is the major system for high‐affinity root K+ uptake required for plant growth at low K+, even in the presence of salinity. It also constitutes a pathway for Cs+ entry in tomato plants with a strong impact on fruit Cs+ accumulation. SlHAK5 also contributes to pollen K+ uptake and viability and its absence produces almost seedless fruits. Knowledge gained into SlHAK5 can serve as a model for other crops with fleshy fruits and it can help to generate tools to develop low Cs+ or seedless fruits crops.

The high-affinity K+ transporter HAK5 from Arabidopsis is essential for K+ acquisition and plant growth at low micromolar K+ concentrations. Despite its functional relevance in plant nutrition, information about functional domains of HAK5 is scarce. Its activity is enhanced by phosphorylation via the AtCIPK23/AtCBL1-9 complex. Based on the recently published 3D-structure of the bacterial ortholog KimA from Bacillus subtilis, we have modeled AtHAK5 and, by a mutational approach, identified residues G67, Y70, G71, D72, D201, and E312 as essential for transporter function. According to the structural model, residues D72, D201, and E312 may bind K+, whereas residues G67, Y70, and G71 may shape the selective filter for K+, which resembles that of K+shaker-like channels. In addition, we show that phosphorylation of residue S35 by AtCIPK23 is required for reaching maximal transport activity. Serial deletions of the AtHAK5 C-terminus disclosed the presence of an autoinhibitory domain located between residues 571 and 633 together with an AtCIPK23-dependent activation domain downstream of position 633. Presumably, autoinhibition of AtHAK5 is counteracted by phosphorylation of S35 by AtCIPK23. Our results provide a molecular model for K+ transport and describe CIPK-CBL-mediated regulation of plant HAK transporters.