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Saiardi, A.

Publications and source records attributed to Saiardi, A..

15 recordsLinked to original sources

Species Context Reverses PPIP5K Control of Fungal Morphogenesis and Actin Organization

Inositol pyrophosphates are conserved signaling molecules synthesized by the bifunctional PPIP5K enzymes, but how their cellular functions diversify across species remains poorly understood. Here, we compared the PPIP5K enzyme Asp1 in the fission yeasts Schizosaccharomyces pombe and Schizosaccharomyces japonicus and in the distantly related fungus Ustilago maydis. All three homologs retained a conserved kinase-phosphatase architecture and catalytic activity. However, whereas Asp1 produced broadly similar effects on actin organization and morphogenesis in S. pombe and U. maydis, its regulatory output was reversed in S. japonicus. In S. pombe and U. maydis, Asp1 positively supported Arp2/3-dependent actin functions, as loss of Asp1 increased sensitivity to the Arp2/3 inhibitor CK666. In contrast, deletion of asp1 in S. japonicus conferred strong CK666 resistance and caused excessive, spatially deregulated actin-patch organization. This opposing cytoskeletal phenotype was mirrored at the level of morphogenesis: Asp1 restricted the yeast-to-hypha transition in S. japonicus, whereas Asp1 was required for pseudohyphal growth in S. pombe and for filamentous development in U. maydis. However, the negative regulatory activity observed in S. japonicus was not an intrinsic property of the SjAsp1 protein. When expressed in S. pombe, SjAsp1 promoted invasive pseudohyphal growth, reproducing the regulatory output of the S. pombe Asp1 morphogenesis pathway rather than that of its native species. Similarly, SjAsp1 supported Arp2/3 functions when expressed in S. pombe. Thus, SjAsp1 adopted the functional behavior imposed by the host cellular environment. S. pombe Asp1 was originally identified as a suppressor of Arp2/3-complex mutant phenotypes, establishing a genetic connection between Asp1 and the actin nucleator. Extending this link, affinity enrichment with inositol pyrophosphates reagents recovered all seven subunits of the S. pombe Arp2/3 complex, providing biochemical support for a potential association between inositol pyrophosphate and Arp2/3. Together, these findings identify S. japonicus as a functional outlier in which a conserved PPIP5K pathway produces an opposing biological output. They further demonstrate that this divergence is determined primarily by species-specific cellular networks rather than by intrinsic differences in the Asp1 protein.

cell biology↗

Isotopic tracing of scyllo-inositol uncovers its incorporation into phosphatidylinositols in mammalian cells

Inositols are a family of cyclic sugar alcohols comprising nine stereoisomers. Myo-inositol is the most abundant isomer found in humans and has been studied most extensively. It plays an important role in osmoregulation and is incorporated into membrane-anchored phosphatidylinositols. Scyllo-inositol is the second most abundant inositol isomer in the human brain and aberrant concentrations are associated with various diseases; however, its biological functions remain poorly understood. Here, the development and application of [13C6]scyllo-inositol as an isotopic tracer to study its metabolism is reported. A concise and robust synthetic route was established to obtain [13C6]scyllo-inositol from [13C6]myo-inositol in good yield. The uptake of [13C6]scyllo-inositol and responses of endogenous inositol isomers were measured in multiple cell lines by HILIC-MS/MS, showcasing the advantages of isotopic tracing. [13C6]scyllo-inositol proved to be a versatile isotopic tracer, when coupled with MS-based lipidomics and 2D NMR experiments. These experiments provide evidence that scyllo-inositol is incorporated into phosphatidylinositols in different cell lines. The results suggest a previously underappreciated role of scyllo-inositol in mammalian cells. The utilization of [13C6]scyllo-inositol will help to elucidate the role of scyllo-inositol metabolism in healthy and diseased states. SignificanceScyllo-inositol is a cyclic sugar alcohol found predominantly in the human brain. Changes in its concentration are associated with different diseases, and scyllo-inositol has been investigated as a potential drug against Alzheimers disease in clinical trials. However, its metabolic fate in mammalian cells is not well understood. We report here a synthetic strategy to obtain [13C6]scyllo-inositol and demonstrate, through isotopic tracing, its incorporation into phosphatidylinositols in different human-derived cell lines. This new stable isotopic tracer enables the investigation of the biological role of scyllo-inositol in mammals and beyond. HighlightsO_LIConcise synthesis of [13C6]scyllo-inositol C_LIO_LI[13C6]scyllo-inositol uptake and response of endogenous inositol isomers studied in multiple cell lines C_LIO_LIUse of [13C6]scyllo-inositol as an isotopic tracer in metabolomics and lipidomics experiments C_LIO_LIEvidence for scyllo-inositol incorporation into phosphatidylinositol in mammalian cells C_LI

biochemistry↗

Inositol hexakisphosphate Functions as a Cofactor and Modulator of ADAR1 Activity

Adenosine-to-inosine (A-to-I) RNA editing by ADAR1 is a key post-transcriptional modification, and mutations in ADAR1 lead to Aicardi-Goutieres syndrome (AGS), an autoimmune disorder. Despite its biological and clinical relevance, the regulation of ADAR1 activity remains incompletely understood. Using a combination of biochemical approaches, inositol-pentakisphosphate 2-kinase (IPPK)-knockout cells, molecular dynamics simulations, and a cell-permeable inositol hexakisphosphate (IP6) prodrug (Pro-IP6), we demonstrate that IP6 depletion drastically reduces global RNA editing, while supplementation with Pro-IP6 restores and even enhances editing levels. Furthermore, we identify the C6-phosphate of IP6 as a critical determinant of ADAR1 catalytic efficiency, functioning within a hydrogen-bonding network that indirectly coordinates a Zn{superscript 2}-ion. Finally, we show that the AGS-associated ADAR1 mutation N907S impairs RNA editing activity, most likely by altering the hydrogen-bond interaction network linking IP6 to the ADAR1 catalytic center. Together, these findings identify IP6 as an essential cofactor and regulator of ADAR1 activity and highlight cofactor availability and interaction networks as strategies for therapeutically modulating RNA editing.

molecular biology↗

A Screening Approach Unveils an Unknown Mn2+ - dependent Endopolyphosphatase Activity in Yeast

Inorganic polyphosphate (polyP) is a ubiquitous biopolymer composed of multiple orthophosphates connected by energy-rich phosphoanhydride bonds. In organisms, polyP is digested by two types of enzymes: exopolyphosphatases, which shorten the chain from the ends by cleaving off monophosphate units, and endopolyphosphatases, which cut the chain internally. While several continuous methods are available to monitor exopolyphosphatase activity, endopolyphosphatase activity assays are less common and typically involve multiple tedious steps. Here, we introduce FRET-polyP8, a novel probe for real-time detection of endopolyphosphatase activity. The FRET assay enabled rapid, highly sensitive, single-step detection of specific endopolyphosphatase activity both from isolated proteins and cell extracts. The simple read-out additionally enabled enzyme inhibitor screening. Furthermore, a novel Mn2+-dependent endopolyphosphatase activity in bakers yeast was detected in a quadruple mutant, highlighting the ability to screen for metal-dependence of new endopolyphosphatase activity. This approach thus represents a significant addition to existing methodologies, facilitating the discovery and classification of new endopoly-phosphatases and their inhibitors to advance our understanding of polyP metabolism and regulation.

biochemistry↗

Nuclear Speckle Dynamics are Controlled by Polyphosphate Inhibition of CLK Proteins

Nuclear speckles (NS) are membrane-less nuclear organelles that act as critical hubs for pre-mRNA splicing. Defects in splicing are linked to several human diseases, including cancer, Alzheimers disease, and dystrophies. While CLK kinases regulate the mobilization of splicing factors from NS, the molecular mechanisms underlying NS assembly and dissolution remain unclear. Using an adaptation of the Biotinylation by Antibody Recognition (BAR) technique, we identify polyphosphate (polyP) as a novel and essential regulator of NS dynamics. Polyphosphate, a highly conserved polyanion composed of a chain of phosphate molecules, is involved in several functions in mammalian cells. Here, we show that polyP interacts with the NS core component SRRM2, and polyP depletion disrupts NS organization releasing splicing factors into the nucleoplasm. RNA-seq analysis reveals that polyP depletion increases exon inclusion, particularly in long genes with multiple exons, highlighting its role in splicing regulation. Mechanistically, we demonstrate that polyP acts as a physiological inhibitor of CLK3 kinase, preventing the phosphorylation of SR proteins and thereby maintaining NS stability. Our findings not only expand our understanding of NS biology but also provide new insights into the polyP involvement in splicing-related diseases. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=90 SRC="FIGDIR/small/633116v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@1dc44b6org.highwire.dtl.DTLVardef@2339e4org.highwire.dtl.DTLVardef@ade454org.highwire.dtl.DTLVardef@69482b_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Inositol Hexaphosphate (InsP6) Activates the HDAC1/3 Epigenetic Axis toMaintain Intestinal Barrier Function

While HDAC inhibition shows promise in cancer treatment, pan-HDAC inhibitors cause gastrointestinal issues in 48% of patients. Understanding HDAC activation mechanisms is crucial to treat diverse diseases beyond cancer. Our study reveals the essential role of inositol polyphosphate multikinase (IPMK) and inositol hexakisphosphate (InsP6 or phytic acid), enriched in vegan diets, in activating the HDAC3 epigenetic axis and maintaining intestinal barrier integrity. IPMK binds to HDAC3, driving InsP6 synthesis, which selectively activates HDAC3 at 10nM concentration by recruiting the DAD domain of its corepressor protein. IPMK deletion diminishes HDAC3 activation, leading to histone hyperacetylation and MMP gene transcription, compromising intestinal barrier integrity. InsP6 treatment is sufficient to rescue these effects. In inflammatory bowel disease, diminished IPMK levels exacerbated intestinal permeability, while oral InsP6 treatment mitigated gut permeability by restoring the HDAC3 epigenetic axis, indicating the clinical implications of the IPMK-HDAC3 epigenetic axis and therapeutic potential of phytic acid.

cell biology↗

Phosphate overplus response in Chlamydomonas reinhardtii: polyphosphate dynamics to monitor phosphate uptake and turnover

Many micro-organisms store inorganic phosphate (Pi) in the form of polyphosphate (polyP) and exhibit in-cell polyP accumulation, a phenomenon known as phosphate overplus response, when resupplied with Pi after a period of deprivation. Quantitative and qualitative methods were used to follow the dynamics of polyP synthesis and turnover in four strains of Chlamydomonas reinhardtii during Pi deprivation followed by nutrient resupply. The lowest level of in-cell polyP during Pi deprivation, which also correlates with the cessation of growth, is the key parameter for the timing of Pi resupply to maximise the Pi overplus response Additional nutrients do not affect the size of the overplus response, but they are important for continued growth and maximal Pi removal from the media. Tracking polyP allows the correct time for nutrient resupply to be determined and therefore a reproducible Pi overplus response to be achieved. Depending on whether maximum cellular phosphorus (P) content or maximum Pi removal is desired different strategies may be required - e,g., Pi deprivation until growth cessation then resupplying complete nutrients gives the best trade-off between high in-cell P accumulation, high Pi uptake and algal biomass growth. Although polyP levels are maintained after Pi resupply, the polymer is dynamically remodelled. IP6 increases during this time. This increase does not precede polyP synthesis as predicted by a model where inositol phosphates switch on polyP synthesis. One strain tested, CC-5325, shows enhanced Pi uptake and levels of polyP and total in-cell P, suggesting that strain selection is also important. ImportanceThere is strong interest in using microalgae to sustainably control and recover nutrients, especially P, from wastewater. This would help to meet environmental discharge consents and recycle nutrients into agriculture or other applications. Like bacteria and yeasts, microalgae exhibit a Pi overplus phenomenon when Pi-deprived cells are resupplied with P, but microalgae do not require an additional carbon source and can simultaneously uptake nitrogen as well. Use of microalgae in wastewater treatment is limited by the unpredictability of their response and sensitivity to environmental factors, but engineered systems can greatly benefit from better understanding Pi dynamics and polyP accumulation. In the literature there is a lack of consensus regarding protocols to maximise the Pi overplus. In this work we provide robust measurements of quantitative physiological parameters, which should allow reproducibility in laboratory studies and provide design parameters for algal-based nutrient recovery systems from waste waters.

microbiology↗

β-Lapachone Regulates Mammalian Inositol Pyrophosphate Levels in an NQO1- and Oxygen-dependent Manner

1Inositol pyrophosphates (PP-InsPs) are energetic signalling molecules with important functions in mammals. As their biosynthesis depends on ATP concentration, PP-InsPs are tightly connected to cellular energy homeostasis. Consequently, an increasing number of studies involves PP-InsPs in metabolic disorders, such as type 2 diabetes, aspects of tumorigenesis, and hyperphosphatemia. Research conducted in yeast suggests that the PP-InsP pathway is activated in response to reactive oxygen species (ROS). However, the precise modulation of PP-InsPs during cellular ROS signalling is unknown. Here, we report how mammalian PP-InsP levels are changing during exposure to exogenous (H2O2) and endogenous ROS. Using capillary electrophoresis electrospray ionization mass spectrometry (CE-ESI-MS), we found that PP-InsP levels decrease upon exposure to oxidative stressors in HCT116 cells. Application of quinone drugs, particularly {beta}-lapachone ({beta}-lap), under normoxic and hypoxic conditions enabled us to produce ROS in cellulo and to show that {beta}-lap treatment caused PP-InsP changes that are oxygen dependent. Experiments in MDA-MB-231 breast cancer cells deficient of NAD(P)H:quinone oxidoreductase-1 (NQO1) demonstrated that {beta}-lap requires NQO1-bioactivation to regulate the cellular metabolism of PP-InsPs. Critically, significant reductions in cellular ATP concentrations were not directly mirrored in reduced PP-InsP levels as shown in NQO1-deficient MDA-MB-231 cells treated with {beta}-lap. The data presented here unveil new aspects of {beta}-lap pharmacology and its impact on PP-InsP levels. Our identification of different quinone drugs as modulators of PP-InsP synthesis will allow to better appreciate their overall impact on cellular function. 2 Significance StatementInositol pyrophosphates (PP-InsPs) are messenger molecules regulating various functions in mammals. They are associated with the oxidative stress response, but the underlying mechanism is unclear. We investigate PP-InsP signalling in mammalian cells subjected to reactive oxygen species (ROS). Applying the quinone {beta}-lapachone ({beta}-lap) generated intracellular ROS resulting in decreased PP-InsP levels. This indicates a key role of PP-InsPs in cellular signalling under oxidative stress. Moreover, {beta}-lap mediated PP-InsP signalling required oxygen and the enzyme NAD(P)H:quinone oxidoreductase-1 (NQO1). Since quinone drugs are cytotoxic, our data provide a basis for further investigations into the role of PP-InsPs during quinone-dependent chemotherapies. This is of special relevance since a phase II clinical trial demonstrated {beta}-lap efficacy in a combination chemotherapy against pancreatic cancer.

biochemistry↗

Inositol pyrophosphate profiling reveals regulatory roles of IP6K2-dependent enhanced IP7 metabolism in enteric nervous system

Inositol pyrophosphates (PP-IPs) regulate diverse physiological processes; to better understand their functional roles, assessing their tissue-specific distribution is important. Here, we profiled PP-IP levels in mammalian organs using a novel HILIC-MS/MS protocol and discovered that the gastrointestinal tract (GIT) contained the highest levels of IP7 and its precursor IP6. Although their absolute levels in the GIT is diet-dependent, elevated IP7 metabolism still exists under dietary regimes devoid of exogenous IP7. Of the major GIT cells, enteric neurons selectively express the IP7-synthesizing enzyme IP6K2. IP6K2-knockout mice exhibited significantly impaired IP7 metabolism in the various organs including the proximal GIT. Additionally, HILIC-MS/MS analysis displayed that genetic ablation of IP6K2 significantly impaired IP7 metabolism in the gut and duodenal muscularis externa containing myenteric plexus. Whole transcriptome analysis of duodenal muscularis externa further suggested that IP6K2 inhibition induced the gene sets associated with mature neurons such as inhibitory, GABAergic and dopaminergic neurons, concomitantly with suppression of those for neural progenitor/stem cells and glial cells. In addition, IP6K2 inhibition explicitly affected transcript levels of certain genes modulating neuronal differentiation and functioning, implying critical roles of IP6K2-IP7 axis in developmental and functional regulation of enteric nervous system. These results collectively reveal an unexpected role of mammalian IP7--a highly active IP6K2-IP7 pathway is conducive to enteric nervous system.

molecular biology↗

Stable isotopomers of myo-inositol to uncover the complex MINPP1-dependent inositol phosphate network

The water-soluble inositol phosphates (InsPs) represent a functionally diverse group of small-molecule messengers central to a myriad of cellular processes. However, we have an incomplete understanding of InsP metabolism because the available analytical toolset for inositol phosphates is rather limited. Here, we have synthesized and utilized fully and unsymmetrically 13C-labeled myo-inositol and inositol phosphates. These probes were applied in combination with nuclear magnetic resonance spectroscopy (NMR) and capillary electrophoresis mass spectrometry (CE-MS) to further annotate central aspects of InsP metabolism in human cells. The labeling strategy provided detailed structural information via NMR - down to individual enantiomers - which overcomes a crucial blind spot in the analysis of InsPs. We uncovered a novel branch of InsP dephosphorylation in human cells which is dependent on MINPP1, a phytase-like enzyme, that contributes to cellular homeostasis. Full characterization of MINPP1 activity in vitro and in cells, provided a clear picture of this multifunctional phosphatase. Metabolic labeling with stable isotopomers thus constitutes a powerful tool for investigating InsP networks in a variety of different biological contexts.

biochemistry↗

Inositol pyrophosphate-controlled kinetochore architecture and mitotic entry in S. pombe

Inositol pyrophosphates (IPPs) comprise a specific class of signaling molecules that regulate central biological processes in eukaryotes. The conserved Vip1/PPIP5K family controls intracellular IP8 levels, the highest phosphorylated form of IPPs present in yeasts, as it has both inositol kinase and pyrophosphatase activities. Previous studies have shown that the fission yeast S. pombe Vip1/PPIP5K family member Asp1 impacts chromosome transmission fidelity via modulation of spindle function. We now demonstrate that an IP8 analogue is targeted by endogenous Asp1 and that cellular IP8 is subject to cell cycle control. Mitotic entry requires Asp1 kinase function and IP8 levels are increased at the G2/M transition. In addition, the kinetochore, the conductor of chromosome segregation assembled on chromosomes is modulated by IP8. Members of the yeast CCAN kinetochore-subcomplex such as Mal2/CENP-O localize to the kinetochore depending on the intracellular IP8-level: higher than wild-type IP8 levels reduces Mal2 kinetochore targeting, while a reduction in IP8 has the opposite effect. As our perturbations of the inositol polyphosphate and IPP pathways demonstrate that kinetochore architecture depends solely on IP8 and not on other IPPs, we conclude that chromosome transmission fidelity is controlled by IP8 via an interplay between entry into mitosis, kinetochore architecture and spindle dynamics.

cell biology↗

Analysis of Inositol Phosphate Metabolism by Capillary Electrophoresis Electrospray Ionization Mass Spectrometry (CE-ESI-MS)

The analysis of myo-inositol phosphates (InsPs) and myo-inositol pyrophosphates (PP-InsPs) is a daunting challenge due to the large number of possible isomers, the absence of a chromophore, the high charge density, the low abundance, and the instability of the esters and anhydrides. Given their importance in biology, an analytical approach to follow and understand this complex signaling hub is highly desirable. Here, capillary electrophoresis (CE) coupled to electrospray ionization mass spectrometry (ESI-MS) is implemented to analyze complex mixtures of InsPs and PP-InsPs with high sensitivity. Stable isotope labeled (SIL) internal standards allow for matrix-independent quantitative assignment. The method is validated in wild-type and knockout mammalian cell lines and in model organisms. SIL-CE-ESI-MS enables for the first time the accurate monitoring of InsPs and PP-InsPs arising from compartmentalized cellular synthesis pathways, by feeding cells with either [13C6]-myo-inositol or [13C6]-D-glucose. In doing so, we uncover that there must be unknown inositol synthesis pathways in mammals, highlighting the unique potential of this method to dissect inositol phosphate metabolism and signalling.

biochemistry↗

ITPK1 is an InsP6/ADP phosphotransferase that controls systemic phosphate homeostasis in Arabidopsis

In plants, phosphate (Pi) homeostasis is regulated by the interaction of Pi starvation response transcription factors (PHRs) with stand-alone SPX proteins, which act as sensors for inositol pyrophosphates (PP-InsPs). Recently, ITPK1 was shown to generate the PP-InsP InsP7 from InsP6 in vitro, but the importance of this activity in Pi signaling remained unknown. Here, we show that uncontrolled Pi accumulation in ITPK1-deficient plants is accompanied by impaired Pi-dependent InsP7 and InsP8 synthesis. Reciprocal grafting demonstrates that Pi starvation responses are mainly controlled by ITPK1 activity in shoots. Nuclear magnetic resonance assays and PAGE analyses with recombinant protein reveal that besides InsP6 phosphorylation, ITPK1 is also able to catalyze ATP synthesis using 5-InsP7 but not any other InsP7 isomer as a P-donor when ATP is low. Additionally, we show that the dynamic changes in InsP7 and InsP8 to cellular Pi are conserved from land plant species to human cells, suggesting that Pi-dependent PP-InsP synthesis is a common component of Pi signaling across kingdoms. Together, our study demonstrates how Pi-dependent changes in nutritional and energetic states modulate ITPK1 activities to fine-tune the synthesis of PP-InsPs.

plant biology↗

MINPP1 prevents intracellular accumulation of the cation chelator inositol hexakisphosphate and is mutated in Pontocerebellar Hypoplasia

Inositol polyphosphates are vital metabolic and secondary messengers, involved in diverse cellular functions. Therefore, tight regulation of inositol polyphosphate metabolism is essential for proper cell physiology. Here, we describe an early-onset neurodegenerative syndrome caused by loss-of-function mutations in the multiple inositol polyphosphate phosphatase 1 gene (MINPP1). Patients were found to have a distinct type of Pontocerebellar Hypoplasia with typical basal ganglia involvement on neuroimaging. We found that patient-derived and genome edited MINPP1-/- induced pluripotent stem cells (iPSCs) are not able to differentiate efficiently into neurons. MINPP1 deficiency results in an intracellular imbalance of the inositol polyphosphate metabolism. This metabolic defect is characterized by an accumulation of highly phosphorylated inositols, mostly inositol hexakiphosphate (IP6), detected in HEK293, fibroblasts, iPSCs and differentiating neurons lacking MINPP1. In mutant cells, higher IP6 level is expected to be associated with an increased chelation of intracellular cations, such as iron or calcium, resulting in decreased levels of available ions. These data suggest the involvement of IP6-mediated chelation on Pontocerebellar Hypoplasia disease pathology and thereby highlight the critical role of MINPP1 in the regulation of human brain development and homeostasis.

genetics↗

ITPK1-Dependent Inositol Polyphosphates Regulate Auxin Responses in Arabidopsis thaliana

The combinatorial phosphorylation of myo-inositol results in the generation of different inositol phosphates (InsP), of which phytic acid (InsP6) is the most abundant species in eukaryotes. InsP6 is also the precursor of higher phosphorylated forms called inositol pyrophosphates (PP-InsPs), such as InsP7 and InsP8, which are characterized by a diphosphate moiety and are also ubiquitously found in eukaryotic cells. While PP-InsPs regulate various cellular processes in animals and yeast, their biosynthesis and functions in plants has remained largely elusive because plant genomes do not encode canonical InsP6 kinases. Recently, it was shown that Arabidopsis ITPK1 catalyzes the phosphorylation of InsP6 to the natural 5-InsP7 isomer in vitro. Here, we demonstrate that Arabidopsis ITPK1 contributes to the synthesis of InsP7 in planta. We further find a critical role of ITPK1 in auxin-related processes including primary root elongation, leaf venation, thermomorphogenic and gravitropic responses, and sensitivity towards exogenously applied auxin. Notably, 5-InsP7 binds to recombinant auxin receptor complex, consisting of the F-Box protein TIR1, ASK1 and the transcriptional repressor IAA7, with high affinity. Furthermore, a specific increase in 5-InsP7 in a heterologous yeast expression system results in elevated interaction of the TIR1 homologs AFB1 and AFB2 with various AUX/IAA-type transcriptional repressors. We also identified a physical interaction between ITPK1 and TIR1, suggesting a dedicated channeling of an activating factor, such as 5-InsP7, to the auxin receptor complex. Our findings expand the mechanistic understanding of auxin perception and lay the biochemical and genetic basis to uncover physiological processes regulated by 5-InsP7.

plant biology↗