Novel signals in the regulation of Pi starvation responses in plants: facts and promises

Puga, María Isabel; Rojas-Triana, Mónica; Lorenzo, Laura de; Leyva, Antonio; Rubio, Vicente; Paz‐Ares, Javier

doi:10.1016/j.pbi.2017.05.007

Cited by 156 publications

(145 citation statements)

References 84 publications

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“…Plants have evolved multiple strategies to maintain cellular Pi homeostasis in Pi deficient conditions. Components involved in this process include PHR family transcription factors, their SPX domain interaction partners, phosphate transporters, ubiquitin ligases controlling phosphate transporter protein levels, microRNAs and ferroxidase enzymes (Puga et al, 2017). The recent finding that eukaryotic SPX domains are cellular receptors for PP-InsPs (Wild et al, 2016) Wild et al, 2016;Qi et al, 2017) and phosphate transporters (Wild et al, 2016;Potapenko et al, 2018) (Rubio et al, 2001;Bustos et al, 2010) can partially rescue the vih1-2 vih2-4 mutant phenotype.…”

Section: Discussionmentioning

confidence: 99%

Two bifunctional inositol pyrophosphate kinases/phosphatases control plant phosphate homeostasis

Zhu

Lau

Harmel

et al. 2018

Preprint

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Many eukaryotic proteins regulating phosphate (Pi) homeostasis contain SPX domains. We have previously shown that these domains act as cellular receptors for inositol pyrophosphate (PP-InsP) signaling molecules, suggesting that PP-InsPs may regulate Pi homeostasis. Here we report that simultaneous deletion of two diphosphoinositol pentakisphosphate kinases VIH1 and 2 in Arabidopsis impairs plant growth and leads to constitutive Pi starvation responses. We demonstrate that VIH1 and VIH2 are bifunctional cytosolic enzymes able to generate and break-down PP-InsPs. Point-mutants targeting the kinase and phosphatase active sites have opposing effects on plant Pi content and Pi starvation responses, while VIH1 and VIH2 protein levels remain constant in different Pi growth conditions. Enzymatic assays reveal that ATP-Mg 2+ substrate levels can shift the relative kinase and phosphatase activities of fulllength diphosphoinositol pentakisphosphate kinases. Deletion of phosphate starvation response transcription factors rescues vih1 vih2 mutant phenotypes, placing diphosphoinositol pentakisphosphate kinases and PP-InsPs in plant phosphate signal transduction cascades. We propose that VIH1 and VIH2 relay changes in cellular ATP concentration to changes in PP-InsP levels, allowing plants to maintain cellular Pi concentrations constant and to trigger Pi starvation responses.

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Section: Discussionmentioning

confidence: 99%

Two bifunctional inositol pyrophosphate kinases/phosphatases control plant phosphate homeostasis

Zhu

Lau

Harmel

et al. 2018

Preprint

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“…Instead, it depends on the concentration of Pi in the growth medium. This phenomenon was described as the so‐called –Pi local response, in opposition to the –Pi systemic responses that are governed by the Pi concentration inside the plant tissues (Puga et al ., ). While the –Pi systemic response is mainly controlled by the two master regulatory genes PHOSPHATE STARVATION RESPONSE 1 ( PHR1 ) and PHR1‐like 1 ( PHL1 ), the –Pi local response is not (Balzergue et al ., ).…”

Section: Introductionmentioning

confidence: 97%

Under phosphate starvation conditions, Fe and Al trigger accumulation of the transcription factor STOP1 in the nucleus of Arabidopsis root cells

et al. 2019

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Summary Low‐phosphate (Pi) conditions are known to repress primary root growth of Arabidopsis at low pH and in an Fe‐dependent manner. This growth arrest requires accumulation of the transcription factor STOP1 in the nucleus, where it activates the transcription of the malate transporter gene ALMT1; exuded malate is suspected to interact with extracellular Fe to inhibit root growth. In addition, ALS3 – an ABC‐like transporter identified for its role in tolerance to toxic Al – represses nuclear accumulation of STOP1 and the expression of ALMT1. Until now it was unclear whether Pi deficiency itself or Fe activates the accumulation of STOP1 in the nucleus. Here, by using different growth media to dissociate the effects of Fe from Pi deficiency itself, we demonstrate that Fe is sufficient to trigger the accumulation of STOP1 in the nucleus, which, in turn, activates the expression of ALMT1. We also show that a low pH is necessary to stimulate the Fe‐dependent accumulation of nuclear STOP1. Furthermore, pharmacological experiments indicate that Fe inhibits proteasomal degradation of STOP1. We also show that Al acts like Fe for nuclear accumulation of STOP1 and ALMT1 expression, and that the overaccumulation of STOP1 in the nucleus of the als3 mutant grown in low‐Pi conditions could be abolished by Fe deficiency. Altogether, our results indicate that, under low‐Pi conditions, Fe2/3+ and Al3+ act similarly to increase the stability of STOP1 and its accumulation in the nucleus where it activates the expression of ALMT1.

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“…The implication of miR399 in the phosphate starvation response (PSR) of Arabidopsis plants is well documented (Chiou et al , ; Hsieh et al , ; Puga et al , ; Ham et al , ). In brief, Pi deprivation rapidly increases miR399 accumulation, which causes degradation of PHOSPHATE2 ( PHO2 ) transcripts encoding a ubiquitin‐conjugating E2 enzyme responsible for the ubiquitination and proteasome degradation of Pi transporters (Aung et al , ; Chiou et al , ; Liu et al , ).…”

Section: Introductionmentioning

confidence: 99%

Phosphate excess increases susceptibility to pathogen infection in rice

Campos-Soriano

Bundó

Bach‐Pages

et al. 2020

Molecular Plant Pathology

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Phosphorus (P) is an essential nutrient for plant growth and productivity. Due to soil fixation, however, phosphorus availability in soil is rarely sufficient to sustain high crop yields. The overuse of fertilizers to circumvent the limited bioavailability of phosphate (Pi) has led to a scenario of excessive soil P in agricultural soils. Whereas adaptive responses to Pi deficiency have been deeply studied, less is known about how plants adapt to Pi excess and how Pi excess might affect disease resistance. We show that high Pi fertilization, and subsequent Pi accumulation, enhances susceptibility to infection by the fungal pathogen Magnaporthe oryzae in rice. This fungus is the causal agent of the blast disease, one of the most damaging diseases of cultivated rice worldwide. Equally, MIR399f overexpression causes an increase in Pi content in rice leaves, which results in enhanced susceptibility to M. oryzae. During pathogen infection, a weaker activation of defence‐related genes occurs in rice plants over‐accumulating Pi in leaves, which is in agreement with the phenotype of blast susceptibility observed in these plants. These data support that Pi, when in excess, compromises defence mechanisms in rice while demonstrating that miR399 functions as a negative regulator of rice immunity. The two signalling pathways, Pi signalling and defence signalling, must operate in a coordinated manner in controlling disease resistance. This information provides a basis to understand the molecular mechanisms involved in immunity in rice plants under high Pi fertilization, an aspect that should be considered in management of the rice blast disease.

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Novel signals in the regulation of Pi starvation responses in plants: facts and promises

Cited by 156 publications

References 84 publications

Two bifunctional inositol pyrophosphate kinases/phosphatases control plant phosphate homeostasis

Two bifunctional inositol pyrophosphate kinases/phosphatases control plant phosphate homeostasis

Under phosphate starvation conditions, Fe and Al trigger accumulation of the transcription factor STOP1 in the nucleus of Arabidopsis root cells

Phosphate excess increases susceptibility to pathogen infection in rice

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