Biology subjects

Ito, H.

Publications and source records attributed to Ito, H..

At least 19 recordsLinked to original sources

bioRxiv2026

HNRNPC-mediated RNA processing promotes VHL-associated excessive vasculogenesis in von Hippel-Lindau syndrome revealed from patient-derived blood vessel models

Von Hippel-Lindau Syndrome (VHLS) is an inherited disorder characterized by excessive vascularization, which contributes to the development of hemangioblastomas and benign or malignant tumors, as well as renal cell carcinoma (RCC) and cysts in multiple organs. VHLS is caused by mutations in VHL tumor suppressor gene, which encodes a component of an E3 ubiquitin ligase complex. Although therapeutic agents targeting hypoxia-inducible factor 2 alpha (HIF2A), which is stabilized by VHL loss and promotes tumor angiogenesis, have been approved for clinical use, their therapeutic response remains limited in RCC patients associated with VHLS. Therefore, there is an unmet need for the development of alternative therapeutic approaches independent of HIF2A. Here, we establish a human iPSCs-based model of VHLS-associated excessive vasculogenesis using induced pluripotent stem cells (iPSCs) derived from VHLS patients and VHL-edited isogenic iPSC lines. Vascular cells (VCs) differentiated from these VHLS-specific iPSCs exhibited excessive blood vessel formation compared to healthy donor-derived VCs, leading to vascular lesion formation characterized by abundant blood vessels and abnormal cellular growth in vivo. Mechanistically, RNA-binding proteins (RBPs) were preferentially stabilized in the patient-VCs. Among these RBPs, the stabilization of heterogeneous nuclear ribonucleoprotein C1/C2 (HNRNPC), which is a substrate for pVHL-mediated protein degradation independent of HIF2A expression, was critical for the dysregulated vascularization caused by VHL inactivation in this model. These findings provide an iPSCs-derived vascular platform to elucidate VHLS mechanisms and identify HNRNPC as a potential therapeutic target for VHL-driven vascular lesion formations through an HIF2A-independent mechanism.

cell biology↗

bioRxiv2026

Circadian Timekeeping in the Tropics: Rhythmic Transcriptome and Diurnal Regulatory Networks in Rubroshorea leprosula

Circadian rhythms allow plants to regulate internal processes to align with daily rhythms in the environment. Comparing circadian clocks across environments is essential because latitude-dependent variation in light and temperature imposes distinct selection pressures that shape the evolution and function of circadian timing systems. However, circadian clock studies have largely focused on temperate and subtropical species, leaving transcriptional circadian networks in tropical plants under relatively constant environments poorly understood. We report the first comprehensive circadian transcriptome of the ecologically important dipterocarp species Rubroshorea leprosula, a dominant species in tropical rainforests in Southeast Asia. One sapling was sampled every four hours for 48 hours under constant darkness and used for transcriptomic analyses. Only 283 of 20,748 expressed genes ([~]1.3%) exhibited significant circadian oscillations, with periods strongly concentrated between 23 and 25 h. Hierarchical clustering revealed four temporal clusters with alternate phases of expression and functional specialisation; morning clusters in processes related to light and chloroplast, midday clusters in hormone and signalling mechanisms, afternoon clusters in mitochondrial and peptide biosynthesis functions, and night clusters in protein quality control and autophagy. Comparative analysis identified clear orthologs for all major Arabidopsis circadian clock components (LHY, CCA1, PRRs, TOC1, ELF4, LUX, GI, ZTL, RVEs), with conserved synteny to Parashorea chinensis, a close relative of R. leprosula. Time-lagged cross-correlation (TLCC) network reconstruction identified a characteristic circadian topological similarity with Arabidopsis, including coupled morning and evening feedback loops and paralog expansion that maintained overall structure. Peak expression timing of these core clock genes in the tropical tree was largely consistent with that observed in Arabidopsis thaliana. In contrast to this conserved phase relationship, Rubroshorea orthologs exhibited reduced amplitudes and lower coefficients of variation in their circadian oscillations, suggesting diminished robustness of rhythmic gene expression. These findings demonstrate a conserved but regulated circadian mechanism in R. leprosula, in preparation for adaptation to tropical rainforests stable light and temperature regimes. This study lays the molecular foundation for circadian regulation in dipterocarps and offers a system for integrating rhythmic gene expression to ecological function and forest productivity in tropical communities.

plant biology↗

bioRxiv2026

Mechanism of ATXN8OS CTA/CTG repeat-associated non-AUG translation revealed by approaches ranging from cell-free translation to live-cell imaging.

Microsatellite repeat expansions contribute to the pathogenesis of many neurodegenerative disorders. In spinocerebellar ataxia type 8 (SCA8), abnormal expansion of CTA/CTG repeats in the 3' untranslated region of the ATXN8OS (ATXN8 Opposite Strand) gene has been implicated in disease pathology. Although the occurrence of repeat-associated non-AUG (RAN) translation from the ATXN8 transcript has been reported, whether and how RAN translation occurs from the ATXN8OS transcript has remained unexplored. Here, using a cell-free translation system and cultured cells, we showed that ATXN8OS undergoes robust AUG-independent translation in a repeat length-dependent manner. Mechanistic analyses revealed that translation of the poly L (0) frame initiates at a non-AUG codon located upstream of the repeats. Moreover, using live-cell imaging at a single mRNA level, we directly visualized ribosomal -1 frameshifting from the poly L (0) frame to the poly T-poly A (+2) frame during translation elongation. We further showed that ATXN8OS translation was enhanced upon activation of the integrated stress response. Together, these findings establish both the occurrence and the molecular mechanisms of ATXN8OS translation from expanded CTA/CTG repeats and provide insights into the pathogenic processes underlying SCA8. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=176 SRC="FIGDIR/small/700793v1_ufig1.gif" ALT="Figure 1"> View larger version (42K): org.highwire.dtl.DTLVardef@1f836fborg.highwire.dtl.DTLVardef@e1b77forg.highwire.dtl.DTLVardef@d605c3org.highwire.dtl.DTLVardef@11475d9_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2025

Reliable Detection of SGLT2 Protein through Knockout-based Antibody Characterization and Optimized Procedures

IntroductionSodium-glucose cotransporter 2 (SGLT2) is a key mediator of renal glucose reabsorption. Its pharmacological inhibition exerts cardio- and reno-protective benefits. Despite widespread clinical interest, reliable detection of SGLT2 protein remains challenging due to concerns regarding the specificity of available antibodies. MethodsThis study assessed the specificity of eight commercially available anti-SGLT2 antibodies by immunohistochemistry and Western blotting. Genetically engineered Sglt2-deficient mice and rats, generated via clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) technology, were employed as definitive negative controls. Additionally, human kidney tissues, including renal cell carcinoma samples, were analyzed. ResultsAmong the antibodies tested, few exhibited robust specificity, characterized by substantial immunostaining with minimal background in wild-type kidney tissues and complete absence of staining in Sglt2-deficient samples. In renal cell carcinoma samples, a validated antibody detected SGLT2 immunostaining in proximal tubules of non-tumor regions but not in tumor areas. Subcellular localization studies revealed that SGLT2 was enriched within proximal tubular microvilli, partially overlapping with its co-factor PDZK1IP1 (MAP17). LRP2 (megalin) and NHE3 were placed at the microvillar base and did not colocalize with SGLT2. Western blotting identified a specific SGLT2 band at approximately 55 kDa in kidney lysates using several antibodies under optimized procedures. This band was shifted to approximately 45 kDa after enzymatic removal of N-linked glycans. One antibody detected a weak band at the same molecular mass even in kidney lysates from Sglt2-deficient rodents. ConclusionsConsiderable variability exists in the specificity of commercially available anti-SGLT2 antibodies. Only a limited number of antibodies are suitable for reliable detection of SGLT2 in rodent and human samples. Rigorous antibody characterization, including the use of knockout controls and optimized experimental conditions, is essential to ensure reproducibility and prevent misinterpretation in studies investigating the biological and pathophysiological roles of SGLT2.

molecular biology↗

bioRxiv2025

A copper-dependent, redox-based hydrogen peroxide perception in plants

Redox-related molecules, such as quinones and reactive oxygen species (ROS), are important signaling molecules for all living organisms. A plant-specific leucine rich-repeat receptor-like kinase (LRR-RLK) CANNOT RESPOND TO DMBQ 1 (CARD1), also known as HYDROGEN-PEROXIDE-INDUCED Ca2+ INCREASES (HPCA1), perceives both quinones and ROS, but knowledge on key structural features is unknown. Here, we determine the structure of the CARD1 ectodomain and uncover its unique features. Structural studies, coupled with genetics and biochemical analysis, demonstrated that previously identified unique cysteine residues are not essential for signal perception in CARD1. Interestingly, CARD1 harbors a copper ion on the surface of the ectodomain via histidine-coordination that is crucial for hydrogen peroxide signaling. Our work reports the first copper-dependent redox receptor and highlights a unique perspective between a receptor and non-peptide stimuli during their perception.

plant biology↗

bioRxiv2025

Canonical translation factors eIF1A and eIF5B modulate the initiation step of repeat-associated non-AUG translation.

Nucleotide repeat expansions, such as the GGGGCC repeats in C9orf72, associated with C9-ALS, are linked to neurodegenerative diseases. These repeat sequences undergo a non-canonical translation known as repeat-associated non-AUG (RAN) translation. Unlike canonical translation, RAN translation initiates from non-AUG codons and occurs in all reading frames. To identify potential regulators of RAN translation, we employed a bottom-up approach using a human factor-based reconstituted cell-free translation system to recapitulate RAN translation. This approach revealed that omission of either eIF1A or eIF5B enhanced the translation in all reading frames of C9orf72-mediated RAN translation (C9-RAN), suggesting that eIF1A and eIF5B act as repressors of RAN translation. eIF1A and eIF5B are known to contribute to the fidelity of translation initiation. In HEK293T cells, double knockdown of eIF1A and eIF5B further promoted C9-RAN compared to single knockdowns, indicating that these factors regulate C9-RAN through distinct initiation steps. Furthermore, under eIF1A knockdown conditions, the enhancement of RAN translation via the integrated stress response (ISR) was not observed in HEK293T cells, indicating that eIF1A is involved in the ISR-mediated non-AUG translation. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=78 SRC="FIGDIR/small/654993v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@160e2adorg.highwire.dtl.DTLVardef@1c1cc8forg.highwire.dtl.DTLVardef@5d01d0org.highwire.dtl.DTLVardef@220507_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2025

Low temperature abolishes human cellular circadian rhythm through Hopf bifurcation

Circadian clocks orchestrate behavior, physiology, and metabolism in harmony with the Earths 24-h cycle. Low temperatures are known to disrupt circadian clocks in plants and poikilotherms; however, their effects on human circadian rhythms remain poorly understood. Here, we demon-strate that cold exposure abolishes the circadian rhythm in cultured human cells through diminishing the oscillation amplitude, which was restored upon rewarming. In addition, the oscillation amplitude of the 24-h temperature cycles was enhanced through resonance, reflecting the intrinsic frequency of the circadian clock. From a theoretical perspective, these dynamics correspond to Hopf bifurcation, which is confirmed by a mathematical model for the mammalian circadian clock. In contrast, the circadian amplitude of human hair follicle cells was resistant to temperature changes, indicating robust temperature homeostasis. These findings suggest that Hopf bifurcation in the circadian clock for temperature regulation is shared by homeothermic and poik-ilothermic species.

systems biology↗

bioRxiv2025

Sinusoidal regulation denoises circadian machinery

The rhythms transmitted from the circadian clock inevitably fluctuate because of molecular noise. The level of period fluctuations, observed not in the circadian clock, but in the output system that receives the transmitted rhythm, varies according to the organism and cell type, ranging from 0.5% to 10%. However, it remains unclear how the signal transduction involved in this transmission affects the fluctuations in the oscillation period of the output system. To address this, we investigated a coupled system consisting of a circadian clock and its output. We numerically and analytically demonstrated that the rhythmic regulation through which the clock controls downstream gene expression affects the level of fluctuations in the output system. Moreover, Gibbs sampling based on the analytically obtained fluctuation formula confirmed that the sine-wave-like regulatory functions effectively minimized the fluctuation of the output system. These theoretical insights provide new perspectives on signal transduction as a denoising mechanism embodied in the circadian system. Author summaryRecent single-cell observations have revealed that individual cells exhibit circadian rhythms with intrinsic variability. In particular, the period fluctuation, evaluated using the coefficient of variation (CV), was studied. In this study, we investigated how signal transduction from the central clock affects period fluctuations in the output system. We identified a key factor influencing these fluctuations: the waveform of the regulatory function by which the circadian clock governs the downstream output. We numerically demonstrated that the fluctuations vary widely depending on the regulatory function and that the sinusoidal function significantly reduced fluctuations in the output system. Furthermore, Gibbs sampling revealed that sine-like regulatory functions effectively minimized fluctuations. These findings suggest a preference for near-sinusoidal waveforms in the regulation of circadian rhythms.

systems biology↗

bioRxiv2024

Arabidopsis SUFB and CLP protease regulate SUFBC2D to manipulate iron-sulfur cluster biosynthesis in chloroplast

Iron-sulfur (Fe-S) clusters are essential cofactors for Fe-S proteins. SUFBC2D complex is the scaffold responsible for Fe-S cluster assembly in chloroplasts. However, the regulatory mechanism on SUFBC2D remains elusive. In this study, we report that the transcription of SUFB responds rapidly to leaf senescence, whereas the transcription of SUFC and SUFD does not. Intriguingly, their protein contents remain stable during leaf senescence. We further found that leaf death was occurred only when SUFB RNAi was induced, and SUFB and SUFC contents decreased much faster in the SUFB-RNAi lines than in the SUFC-RNAi lines, indicating that SUFB had a faster turnover rate than SUFC. Moreover, overexpressing SUFB increased the contents of SUFC and SUFD, and SUFBC2D, whereas overexpressing SUFC did not increase SUFB and SUFD. Our findings reveal that SUFB stabilizes SUFC and SUFD via forming SUFBC2D, whereas SUFC lacks this function. Furthermore, SUFB expression was sharply downregulated when the plants were subjected to iron deficiency, whereas SUFC and SUFD expression was not. Interestingly, the contents of all three SUF members decreased, indicating that plants degrade SUFBC2D in response to iron deficiency by downregulating SUFB transcription. We subsequently studied the degradation mechanism of SUFBC2D. Our results indicated that all SUFs are substrates of the caseinolytic protease (CLP) because they all accumulated in the CLP impaired mutant, and they physically interact with CLPS1, the substrate recognition adaptor of CLP. Collectively, our findings provide novel insights into how plants regulate SUFBC2D complex via SUFB to adapt to leaf senescence and iron deficiency.

plant biology↗

bioRxiv2024

Diversity of ancestral brainstem noradrenergic neurons across species and multiple biological factors

The brainstem cell group, locus coeruleus (LC), is present across vertebrates and influences cardiorespiratory, metabolic, immune, and cognitive functions by activating in two putatively distinct firing patterns. Yet, the degree to which the LC firing rates and patterns are homogenous across species has never been assessed due to inherently limited sample sizes. To remedy this, we pooled cross-species data from 20 laboratories to show that firing rates differ across species and are modulated by sex, age, and type of in vitro or in vivo preparation. Contrary to the prevailing dual-mode firing pattern schema, we observed patterns spread across a low-dimensional manifold, with subregions enriched for specific biological factors and neurodegenerative disease models. Our findings show considerable diversity in an ancestral vertebrate neuromodulatory system.

neuroscience↗

bioRxiv2024

Longitudinal analysis of glioblastoma response to oncolytic HSV1 guides PLX3397 combination for enhanced viral permissiveness

Clinical trial data underscores the need to improve oncolytic virus (OV) distribution within tumors, a challenge compounded by the lack of predictive biomarkers and limited opportunities for post-treatment analysis. To decipher the factors influencing treatment outcomes, we employed multimodal bioluminescence imaging (MM-BLI) in conjunction with magnetic resonance imaging (MRI) to monitor OV infection, replication, and tumor viability in orthotopic brain glioma mouse models. This approach revealed two distinct therapeutic responses: "Responders" with tumor regression and "Non-Responders" with tumor progression. In-depth analysis of individual brains from both groups uncovered dynamic interactions between the OV and the tumor microenvironment, highlighting the involvement of Iba-1+ microglia and tumor necrosis in hindering OV distribution within the tumor. To address this, we incorporated a CSF-1 receptor inhibitor (PLX3397), which improved tumor control by enhancing OVs direct cytopathic effects and reducing microglial interference. Our findings highlight microglia as a significant barrier to effective OV therapy, suggesting that targeting brain-resident immune cells could enhance the therapeutic efficacy of OVs in resistant brain tumors.

bioengineering↗

bioRxiv2024

Targeting of retrovirus-derived Rtl8a/8b reduces social response and increases apathy-like behavior associated with GABRB2 reduction

Retrotransposon Gag-like (RTL) 8A, 8B and 8C are eutherian-specific genes derived from a certain retrovirus. They clustered as a triplet of genes on the X chromosome, but their function remains unknown. Here, we demonstrate that Rtl8a and Rtl8b play important roles in the brain: their double knockout (DKO) mice not only exhibit reduced social responses and increased apathy-like behavior, but also become obese from young adulthood. Mouse RTL8A/8B proteins are expressed in the prefrontal cortex and hypothalamus and localize to both the nucleus and cytoplasm of neurons, presumably due to the N-terminal nuclear localization signal-like sequence at the N-terminus. An RNAseq study in the cerebral cortex revealed reduced expression of several GABA type A receptor subunits, in particular the {beta}2 subunit of Gabrb2, in DKO. We confirmed the reduction of GABRB2 protein in the DKO cerebral cortex by Western blotting. As GABRB2 has been implicated in the etiology of several neurodevelopmental disorders, it is likely that the reduction of GABRB2 is one of the major causes of the neuropsychiatric defects in the DKO mice.

molecular biology↗

bioRxiv2024

Targeting fatty acid synthase suppresses tumor development in NF2/CDKN2A-deficient malignant pleural mesothelioma

Malignant pleural mesothelioma (MPM) is an uncommon yet deadly cancer linked to asbestos exposure. The lack of effective early diagnosis and treatment leads to reduced life expectancy among patients with MPM. This study is aimed to identify a novel molecular target inhibitor to develop more effective therapeutics for MPM. Our drug screening assay showed that the fatty acid synthase (FASN) inhibitor cerulenin demonstrates strong and selective anti-proliferative properties against NF2/CDKN2A(p16)-deficient MPM cells, surpassing the effects of cisplatin or pemetrexed. FASN protein is frequently detected in NF2/p16-deficient MPM tumor-derived tissues (15/15, 100%), but rarely in NF2/p16-intact MPM tumors (8/25, 32%). Notably, cerulenin administration successfully reduced the growth of NF2/p16-deficient MPM tumors in xenografted mice. Cerulenin inhibits mitochondrial fission by targeting dynamin-related protein 1 (DRP1) in NF2/p16-deficient cells. Moreover, the disruption of the FASN gene leads to increased ubiquitination of DRP1. These findings suggest that FASN might play a role in the tumorigenesis of MPM cells through the regulation of mitochondrial dynamics. This research offers a novel perspective on the potential development of precision medicine for MPM.

cancer biology↗

bioRxiv2024

Encoding seizures with partial synchronization: A spiking neural network for biosignal monitoring on a mixed signal neuromorphic processor

Long-term monitoring of biomedical signals is essential for the modern clinical management of neurological conditions such as epilepsy. However, developing wearable systems that are able to monitor, analyze, and detect epileptic seizures with long-lasting operation times using current technologies is still an open challenge. Brain-inspired spiking neural networks (SNNs) represent a promising signal processing and computing framework as they can be deployed on ultra-low power neuromorphic computing systems, for this purpose. Here, we introduce a novel SNN architecture, co-designed and validated on a mixed-signal neuromorphic chip, that shows potential for always-on monitoring of epileptic activity. We demonstrate how the hardware implementation of this SNN captures the phenomenon of partial synchronization within neural activity during seizure periods. We assess the network using a full-custom asynchronous mixed-signal neuromorphic platform, processing analog signals in real-time from an Electroencephalographic (EEG) seizure dataset. The neuromorphic chip comprises an analog front-end (AFE) signal conditioning stage and an asynchronous delta modulation (ADM) circuit directly integrated on the same die, which can produce the stream of spikes as input to the SNN, directly from the analog EEG signals. We show a linear classifier in a post processing stage that is sufficient to reliably classify and detect seizures, from the local features extracted by the SNN, indicating the feasibility of full on-chip seizure monitoring in the future. This research marks a significant advancement toward developing embedded intelligent "wear and forget" units for resource-constrained environments. These units could autonomously detect and log relevant EEG events of interest in out-of-hospital environments, offering new possibilities for patient care and management of neurological disorders.

neuroscience↗

bioRxiv2024

Arf GTPase-Activating proteins ADAP1 and ARAP1 regulate incorporation of CD63 in multivesicular bodies

Arf GTPase-Activating proteins (ArfGAPs) mediate the hydrolysis of GTP bound to ADP-ribosylation factors. ArfGAPs are critical for cargo sorting in the Golgi-to-ER traffic. However, the role of ArfGAPs in sorting into intralumenal vesicles (ILVs) in multivesicular bodies (MVBs) in post-Golgi traffic remains unclear. Exosomes are extracellular vesicles (EVs) of endosomal origin. EVs mediate cell-to-cell communication, and CD63 is an EV marker. CD63 is enriched in intralumenal vesicles (ILVs) in MVBs of cells. However, the secretion of CD63 positive EVs has not been consistent with the data on CD63 localization in MVBs, and how CD63-containing EVs are formed is yet to be understood. To elucidate the mechanism of CD63 transport to ILVs, we focused on CD63 localization in MVBs and searched for the ArfGAPs involved in CD63 localization. We observed that ADAP1 and ARAP1 depletion inhibited CD63 localization to enlarged endosomes after Rab5Q79L overexpression. We tested epidermal growth factor (EGF) and CD9 localization in MVBs. We observed that ADAP1 and ARAP1 depletion affected the localization of EGF and CD9 differently. Our results indicate that there may be different populations of MVBs and that ADAP1 and ARAP1 regulate CD63 incorporation into ILVs in different MVBs. Summary StatementADAP1 and ARAP1 regulate CD63 localization in endosomes.

cell biology↗

bioRxiv2023

Akaluc bioluminescence offers superior sensitivity to track in vivo dynamics of SARS-CoV-2 infection

Monitoring in vivo viral dynamics can improve our understanding of pathogenicity and tissue tropism. For positive-sense, single-stranded RNA viruses, several studies have attempted to monitor viral kinetics in vivo using reporter genomes. The application of such recombinant viruses can be limited by challenges in accommodating bioluminescent reporter genes in the viral genome. Conventional luminescence also exhibits relatively low tissue permeability and thus less sensitivity for visualization in vivo. Here we show that unlike NanoLuc bioluminescence, the improved method, termed AkaBLI, allows visualization of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in Syrian hamsters. By successfully incorporating a codon-optimized Akaluc luciferase gene into the SARS-CoV-2 genome, we visualized in vivo infection, including the tissue-specific differences associated with particular variants. Additionally, we could evaluate the efficacy of neutralizing antibodies and mRNA vaccination by monitoring changes in Akaluc signals. Overall, AkaBLI is an effective technology for monitoring viral dynamics in live animals.

microbiology↗

bioRxiv2023

Variability in radiocesium activity concentration in growing hardwood shoots in Fukushima, Japan

The radiocesium contamination caused by the Fukushima Daiichi Nuclear Power Plant accident has made it difficult to use coppice woods as bed logs for mushroom cultivation. Evaluating the variability in the radiocesium activity concentration of logs is necessary in order to predict how many coppice woodlands are available for producing mushroom bed logs. To clarify the variability in radiocesium activity concentrations and to estimate the sample size required to estimate these concentrations with sufficient accuracy, we modeled the log-transformed radiocesium activity concentrations in growing shoots of hardwoods. We designed two models: (1) a model with mean concentrations that varied among stands with a standard deviation that was the same among stands, and (2) a model with varying means and standard deviations. We fit the data pertaining to only Quercus serrata to both models and calculated the widely applicable information criterion values. Consequently, we adopted the simpler model (1). Applying the selected model to data for all species, we examined the relationship between the number of measurement individuals and the predictive distribution of the expected concentration. Based on previous recommendations and measurement costs, we proposed that five individuals would be appropriate for estimating radiocesium activity concentration in a stand.

plant biology↗

bioRxiv2023

Carotenoid metabolism negatively regulates auxin-mediated root growth

Root development is essential for plant survival. The lack of carotenoid biosynthesis in the phytoene desaturase 3 (pds3) mutant results in short primary roots (PR) and reduced lateral root (LR) formation. In this study, we show that short-term inhibition of PDS by fluridone suppressed PR growth in WT, but to a lesser extent in auxin mutants. Such an inhibition of PDS activity increased endogenous indole-3-acetic acid (IAA) levels, promoted auxin signaling, and partially complemented the PR growth of auxin deficient mutant, YUCCA 3 5 7 8 9 quadruple mutant (yucQ). The exogenous application of retinaldehyde (retinal), an apocarotenoid derived from {beta}-carotene, complemented the fluridone-induced suppression of root growth, as well as the short roots of the pds3 mutant. Retinal also partially complemented the auxin-induced suppression of root growth. These results suggest that retinal may play a role in regulating root growth by modulating endogenous auxin levels. One-sentence summaryThe short-term inhibition of carotenoid biosynthesis mediates the production of {beta}-carotene-derived apocarotenoid retinal which negatively regulates auxin levels and signaling to control root growth.

plant biology↗