STOP1 regulates CCX1-mediated Ca2+ homeostasis for plant adaptation to Ca2+ deprivation.

Calcium (Ca) is essential for plant growth and stress adaptation, yet its availability is often limited in acidic soils, posing a major threat to crop production. Understanding the intricate mechanisms orchestrating plant adaptation to Ca deficiency remains elusive. Here, we show that the Ca deficiency-enhanced nuclear accumulation of the transcription factor SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) in Arabidopsis thaliana confers tolerance to Ca deprivation, with the global transcriptional responses triggered by Ca deprivation largely impaired in the stop1 mutant. Notably, STOP1 activates the Ca deprivation-induced expression of CATION/Ca2+ EXCHANGER 1 (CCX1) by directly binding to its promoter region, which facilitates Ca2+ efflux from endoplasmic reticulum to cytosol to maintain Ca homeostasis. Consequently, the constitutive expression of CCX1 in the stop1 mutant partially rescues the Ca deficiency phenotype by increasing Ca content in the shoots. These findings uncover the pivotal role of the STOP1-CCX1 axis in plant adaptation to low Ca, offering alternative manipulating strategies to improve plant Ca nutrition in acidic soils and extending our understanding of the multifaceted role of STOP1.

Ammonium improved cell wall and cell membrane P reutilization and external P uptake in a putrescine and ethylene dependent pathway.

Ammonium promotes rice P uptake and reutilization better than nitrate, under P starvation conditions; however, the underlying mechanism remains unclear. In this study, ammonium treatment significantly increased putrescine and ethylene content in rice roots under P deficient conditions, by increasing the protein content of ornithine decarboxylase and 1-aminocyclopropane-1-carboxylic acid (ACC) oxidase compared with nitrate treatment. Ammonium treatment increased rice root cell wall P release by increasing pectin content and pectin methyl esterase (PME) activity, increased rice shoot cell membrane P release by decreasing phosphorus-containing lipid components, and maintained internal P homeostasis by increasing OsPT2/6/8 expression compared with nitrate treatment. Ammonium also improved external P uptake by regulating root morphology and increased rice grain yield by increasing the panicle number compared with nitrate treatment. The application of putrescine and ethylene synthesis precursor ACC further improved the above process. Our results demonstrate for the first time that ammonium increases rice P acquisition, reutilization, and homeostasis, and rice grain yield, in a putrescine- and ethylene-dependent manner, better than nitrate, under P starvation conditions.

Unearthing the alleviatory mechanisms of hydrogen sulfide in aluminum toxicity in rice.

Hydrogen sulfide (H2S) improves aluminum (Al) resistance in rice, however, the underlying mechanism remains unclear. In the present study, treatment with 30-µM Al significantly inhibited rice root growth and increased the total Al content, apoplastic and cytoplasm Al concentration in the rice roots. However, pretreatment with NaHS (H2S donor) reversed these negative effects. Pretreatment with NaHS significantly increased energy production under Al toxicity conditions, such as by increasing the content of ATP and nonstructural carbohydrates. In addition, NaHS stimulated the AsA-GSH cycle to decrease the peroxidation damage induced by Al toxicity. Pretreatment with NaHS significantly inhibited ethylene emissions in the rice and then inhibited pectin synthesis and increased the pectin methylation degree to reduce cell wall Al deposition. The phytohormones indole-3-acetic and brassinolide were also involved in the alleviation of Al toxicity by H2S. The transcriptome results further confirmed that H2S alleviates Al toxicity by increasing the pathways relating to material and energy metabolism, redox reactions, cell wall components, and signal transduction. These findings improve our understanding of how H2S affects rice responses to Al toxicity, which will facilitate further studies on crop safety.

Nitrogen in plants: from nutrition to the modulation of abiotic stress adaptation.

Nitrogen is one of the most important nutrient for plant growth and development; it is strongly associated with a variety of abiotic stress responses. As sessile organisms, plants have evolved to develop efficient strategies to manage N to support growth when exposed to a diverse range of stressors. This review summarizes the recent progress in the field of plant nitrate (NO3-) and ammonium (NH4+) uptake, which are the two major forms of N that are absorbed by plants. We explore the intricate relationship between NO3-/NH4+ and abiotic stress responses in plants, focusing on stresses from nutrient deficiencies, unfavorable pH, ions, and drought. Although many molecular details remain unclear, research has revealed a number of core signaling regulators that are associated with N-mediated abiotic stress responses. An in-depth understanding and exploration of the molecular processes that underpin the interactions between N and abiotic stresses is useful in the design of effective strategies to improve crop growth, development, and productivity.

STOP1 activates NRT1.1-mediated nitrate uptake to create a favorable rhizospheric pH for plant adaptation to acidity.

Protons (H+) in acidic soils arrest plant growth. However, the mechanisms by which plants optimize their biological processes to diminish the unfavorable effects of H+ stress remain largely unclear. Here, we showed that in the roots of Arabidopsis thaliana, the C2H2-type transcription factor STOP1 in the nucleus was enriched by low pH in a nitrate-independent manner, with the spatial expression pattern of NITRATE TRANSPORTER 1.1 (NRT1.1) established by low pH required the action of STOP1. Additionally, the nrt1.1 and stop1 mutants, as well as the nrt1.1 stop1 double mutant, had a similar hypersensitive phenotype to low pH, indicating that STOP1 and NRT1.1 function in the same pathway for H+ tolerance. Molecular assays revealed that STOP1 directly bound to the promoter of NRT1.1 to activate its transcription in response to low pH, thus upregulating its nitrate uptake. This action improved the nitrogen use efficiency (NUE) of plants and created a favorable rhizospheric pH for root growth by enhancing H+ depletion in the rhizosphere. Consequently, the constitutive expression of NRT1.1 in stop1 mutants abolished the hypersensitive phenotype to low pH. These results demonstrate that STOP1-NRT1.1 is a key module for plants to optimize NUE and ensure better plant growth in acidic media.

A transcription factor STOP1-centered pathway coordinates ammonium and phosphate acquisition in Arabidopsis.

Phosphorus (P) is an indispensable macronutrient required for plant growth and development. Natural phosphate (Pi) reserves are finite, and a better understanding of Pi utilization by crops is therefore vital for worldwide food security. Ammonium has long been known to enhance Pi acquisition efficiency in agriculture; however, the molecular mechanisms coordinating Pi nutrition and ammonium remains unclear. Here, we reveal that ammonium is a novel initiator that stimulates the accumulation of a key regulatory protein, STOP1, in the nuclei of Arabidopsis root cells under Pi deficiency. We show that Pi deficiency promotes ammonium uptake mediated by AMT1 transporters and causes rapid acidification of the root surface. Rhizosphere acidification-triggered STOP1 accumulation activates the excretion of organic acids, which help to solubilize Pi from insoluble iron or calcium phosphates. Ammonium uptake by AMT1 transporters is downregulated by a CIPK23 protein kinase whose expression is directly modulated by STOP1 when ammonium reaches toxic levels. Taken together, we have identified a STOP1-centered regulatory network that links external ammonium with efficient Pi acquisition from insoluble phosphate sources. These findings provide a framework for developing possible strategies to improve crop production by enhancing the utilization of non-bioavailable nutrients in soil.

Improved Plant Nitrate Status Involves in Flowering Induction by Extended Photoperiod.

The floral transition stage is pivotal for sustaining plant populations and is affected by several environmental factors, including photoperiod. However, the mechanisms underlying photoperiodic flowering responses are not fully understood. Herein, we have shown that exposure to an extended photoperiod effectively induced early flowering in Arabidopsis plants, at a range of different nitrate concentrations. However, these photoperiodic flowering responses were attenuated when the nitrate levels were suboptimal for flowering. An extended photoperiod also improved the root nitrate uptake of by NITRATE TRANSPORTER 1.1 (NRT1.1) and NITRATE TRANSPORTER 2.1 (NRT2.1), whereas the loss of function of NRT1.1/NRT2.1 in the nrt1.1-1/2.1-2 mutants suppressed the expression of the key flowering genes CONSTANS (CO) and FLOWERING LOCUS T (FT), and reduced the sensitivity of the photoperiodic flowering responses to elevated levels of nitrate. These results suggest that the upregulation of root nitrate uptake during extended photoperiods, contributed to the observed early flowering. The results also showed that the sensitivity of photoperiodic flowering responses to elevated levels of nitrate, were also reduced by either the replacement of nitrate with its assimilation intermediate product, ammonium, or by the dysfunction of the nitrate assimilation pathway. This indicates that nitrate serves as both a nutrient source for plant growth and as a signaling molecule for floral induction during extended photoperiods.

A reevaluation of the contribution of NRT1.1 to nitrate uptake in Arabidopsis under low-nitrate supply.

NRT1.1 has been previously characterized as a dual-affinity nitrate transporter in Arabidopsis, though several lines of evidence have raised questions regarding its high-affinity function in nitrate uptake. Here, we show that the induction of NRT2.1- and NRT2.2-mediated nitrate uptake interferes with measurements of the contribution of NRT1.1 to high-affinity uptake using nrt1.1 mutants. Therefore, a nrt1.1/2.1/2.2 triple mutant was generated to reevaluate the role of NRT1.1 in high-affinity nitrate uptake. This triple mutant has a lower rate of nitrate uptake than the nrt2.1/2.2 double mutant under low external nitrate supply, resulting in a lower growth rate than that of the double mutant. Therefore, we conclude that NRT1.1-mediated high-affinity nitrate uptake is necessary for plant growth under low-nitrate conditions.

Effects of split applications of nitrogen fertilizers on the Cd level and nutritional quality of Chinese cabbage.

Cadmium (Cd) contamination in soil is an increasingly serious problem. Management of plant nutrients has been proposed as a potentially promising strategy for minimizing Cd accumulation in crops grown in contaminated soil. This study investigated the effects of split applications of nitrogen (N) fertilizers on the Cd concentration in Chinese cabbage (Brassica chinensis L.) plants grown in Cd-contaminated soil. Compared with single applications, split applications of ammonium or urea resulted in significantly lower Cd concentrations, and higher biomass production and antioxidant-associated nutritional quality in the edible plant parts. However, when nitrate was used as the N fertilizer, there were no significant differences between the split and single applications for the same parameters. We conclude that a split application could be more beneficial than a single application method when ammonium or urea is used as the N fertilizer for vegetable cultivation in Cd-contaminated soil.

Alleviation of proton toxicity by nitrate uptake specifically depends on nitrate transporter 1.1 in Arabidopsis.

Protons in acid soil are highly rhizotoxic to plants, but the mechanism of tolerance of plants to protons is largely unknown. Nitrate uptake by root cells is accompanied by the uptake of protons. Therefore, nitrate uptake transporters (NRTs) may be involved in plant tolerance to proton toxicity. We investigated the root nitrate uptake response to proton stress in Arabidopsis and its association with proton tolerance using NRT-related mutants and pharmacological methods. Lack of NRT1.1 in knockout nrt1.1 mutants led to impaired proton tolerance in nitrate-sufficient growth medium, whereas no difference was seen between wild-type plants and NRT1.2-, NRT2.1-, NRT2.2-, and NRT2.4-null mutants. Another nrt1.1 point mutant, which is defective in nitrate uptake but has a normal nitrate-sensing function, also had impaired proton tolerance compared with the wild-type plant. Furthermore, proton stress induced NRT1.1-mediated nitrate uptake. These results indicate that NRT1.1-conferred proton tolerance depends on nitrate uptake activity. In addition, the rooting medium was alkalified by wild-type plants, but not by knockout nrt1.1 mutants, and in pH-buffered medium, there were no differences in proton tolerance between wild-type plants and knockout nrt1.1 mutants. We conclude that NRT1.1-mediated nitrate uptake plays a crucial role in plant proton tolerance by alkalifying the rhizosphere.