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1.
Zootaxa ; 4577(1): zootaxa.4577.1.13, 2019 Apr 04.
Artigo em Inglês | MEDLINE | ID: mdl-31715745

RESUMO

The family Dipsocoridae is first reported from the Korean Peninsula based on a finding of Pachycoleus japonicum (Miyamoto, 1964) comb. nov. Detailed description of male and female genitalia of P. japonicum is provided. A new generic combination for P. japonicum is proposed. The ambiguous characters for generic concept in previous work and implications to assign genus for the species in other faunas are discussed. Biological note on the unique habitat of the species unlike congeners is presented with illustrations and photographs. A key to the Korean dipsocoromophan families (species) is also provided.

3.
Cell Metab ; 30(4): 784-799.e5, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31474566

RESUMO

Fibrosis is the final common pathway leading to end-stage renal failure. By analyzing the kidneys of patients and animal models with fibrosis, we observed a significant mitochondrial defect, including the loss of the mitochondrial transcription factor A (TFAM) in kidney tubule cells. Here, we generated mice with tubule-specific deletion of TFAM (Ksp-Cre/Tfamflox/flox). While these mice developed severe mitochondrial loss and energetic deficit by 6 weeks of age, kidney fibrosis, immune cell infiltration, and progressive azotemia causing death were only observed around 12 weeks of age. In renal cells of TFAM KO (knockout) mice, aberrant packaging of the mitochondrial DNA (mtDNA) resulted in its cytosolic translocation, activation of the cytosolic cGAS-stimulator of interferon genes (STING) DNA sensing pathway, and thus cytokine expression and immune cell recruitment. Ablation of STING ameliorated kidney fibrosis in mouse models of chronic kidney disease, demonstrating how TFAM sequesters mtDNA to limit the inflammation leading to fibrosis.

4.
Kidney Int ; 96(4): 862-870, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31492507

RESUMO

A revolution in cellular measurement technology is underway. Whereas prior studies have been able to analyze only the averaged outputs from renal tissue, we now can accurately monitor genome-wide gene expression, regulation, function, cellular history, and cellular interactions in thousands of individual cells in a single experiment. These methods are key drivers in changing our previous morphotype-based organ and disease descriptions to unbiased genomic definitions and therefore improving our understanding of kidney development, homeostasis, and disease.

5.
J Am Soc Nephrol ; 30(10): 2000-2016, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31537649

RESUMO

BACKGROUND: Although diabetic kidney disease demonstrates both familial clustering and single nucleotide polymorphism heritability, the specific genetic factors influencing risk remain largely unknown. METHODS: To identify genetic variants predisposing to diabetic kidney disease, we performed genome-wide association study (GWAS) analyses. Through collaboration with the Diabetes Nephropathy Collaborative Research Initiative, we assembled a large collection of type 1 diabetes cohorts with harmonized diabetic kidney disease phenotypes. We used a spectrum of ten diabetic kidney disease definitions based on albuminuria and renal function. RESULTS: Our GWAS meta-analysis included association results for up to 19,406 individuals of European descent with type 1 diabetes. We identified 16 genome-wide significant risk loci. The variant with the strongest association (rs55703767) is a common missense mutation in the collagen type IV alpha 3 chain (COL4A3) gene, which encodes a major structural component of the glomerular basement membrane (GBM). Mutations in COL4A3 are implicated in heritable nephropathies, including the progressive inherited nephropathy Alport syndrome. The rs55703767 minor allele (Asp326Tyr) is protective against several definitions of diabetic kidney disease, including albuminuria and ESKD, and demonstrated a significant association with GBM width; protective allele carriers had thinner GBM before any signs of kidney disease, and its effect was dependent on glycemia. Three other loci are in or near genes with known or suggestive involvement in this condition (BMP7) or renal biology (COLEC11 and DDR1). CONCLUSIONS: The 16 diabetic kidney disease-associated loci may provide novel insights into the pathogenesis of this condition and help identify potential biologic targets for prevention and treatment.

6.
Nat Commun ; 10(1): 3842, 2019 Aug 26.
Artigo em Inglês | MEDLINE | ID: mdl-31451708

RESUMO

Chronic kidney disease (CKD), defined by low estimated glomerular filtration rate (eGFR), contributes to global morbidity and mortality. Here we conduct a transethnic Genome-Wide Association Study of eGFR in 280,722 participants of the Million Veteran Program (MVP), with replication in 765,289 participants from the Chronic Kidney Disease Genetics (CKDGen) Consortium. We identify 82 previously unreported variants, confirm 54 loci, and report interesting findings including association of the sickle cell allele of betaglobin among non-Hispanic blacks. Our transcriptome-wide association study of kidney function in healthy kidney tissue identifies 36 previously unreported and nine known genes, and maps gene expression to renal cell types. In a Phenome-Wide Association Study in 192,868 MVP participants using a weighted genetic score we detect associations with CKD stages and complications and kidney stones. This investigation reinterprets the genetic architecture of kidney function to identify the gene, tissue, and anatomical context of renal homeostasis and the clinical consequences of dysregulation.

7.
Neuroimage Clin ; 23: 101859, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31150957

RESUMO

Accurate, reliable prediction of risk for Alzheimer's disease (AD) is essential for early, disease-modifying therapeutics. Multimodal MRI, such as structural and diffusion MRI, is likely to contain complementary information of neurodegenerative processes in AD. Here we tested the utility of the multimodal MRI (T1-weighted structure and diffusion MRI), combined with high-throughput brain phenotyping-morphometry and structural connectomics-and machine learning, as a diagnostic tool for AD. We used, firstly, a clinical cohort at a dementia clinic (National Health Insurance Service-Ilsan Hospital [NHIS-IH]; N = 211; 110 AD, 64 mild cognitive impairment [MCI], and 37 cognitively normal with subjective memory complaints [SMC]) to test the diagnostic models; and, secondly, Alzheimer's Disease Neuroimaging Initiative (ADNI)-2 to test the generalizability. Our machine learning models trained on the morphometric and connectome estimates (number of features = 34,646) showed optimal classification accuracy (AD/SMC: 97% accuracy, MCI/SMC: 83% accuracy; AD/MCI: 97% accuracy) in NHIS-IH cohort, outperforming a benchmark model (FLAIR-based white matter hyperintensity volumes). In ADNI-2 data, the combined connectome and morphometry model showed similar or superior accuracies (AD/HC: 96%; MCI/HC: 70%; AD/MCI: 75% accuracy) compared with the CSF biomarker model (t-tau, p-tau, and Amyloid ß, and ratios). In predicting MCI to AD progression in a smaller cohort of ADNI-2 (n = 60), the morphometry model showed similar performance with 69% accuracy compared with CSF biomarker model with 70% accuracy. Our comparisons of the classifiers trained on structural MRI, diffusion MRI, FLAIR, and CSF biomarkers showed the promising utility of the white matter structural connectomes in classifying AD and MCI in addition to the widely used structural MRI-based morphometry, when combined with machine learning.

8.
Nat Commun ; 10(1): 2461, 2019 06 05.
Artigo em Inglês | MEDLINE | ID: mdl-31165727

RESUMO

Epigenetic changes might provide the biological explanation for the long-lasting impact of metabolic alterations of diabetic kidney disease development. Here we examined cytosine methylation of human kidney tubules using Illumina Infinium 450 K arrays from 91 subjects with and without diabetes and varying degrees of kidney disease using a cross-sectional design. We identify cytosine methylation changes associated with kidney structural damage and build a model for kidney function decline. We find that the methylation levels of 65 probes are associated with the degree of kidney fibrosis at genome wide significance. In total 471 probes improve the model for kidney function decline. Methylation probes associated with kidney damage and functional decline enrich on kidney regulatory regions and associate with gene expression changes, including epidermal growth factor (EGF). Altogether, our work shows that kidney methylation differences can be detected in patients with diabetic kidney disease and improve kidney function decline models indicating that they are potentially functionally important.


Assuntos
Citosina/metabolismo , Metilação de DNA , Nefropatias Diabéticas/genética , Rim/metabolismo , Idoso , Estudos de Casos e Controles , Ilhas de CpG , Estudos Transversais , Nefropatias Diabéticas/metabolismo , Nefropatias Diabéticas/patologia , Progressão da Doença , Epigênese Genética , Feminino , Fibrose , Regulação da Expressão Gênica , Taxa de Filtração Glomerular , Humanos , Rim/patologia , Masculino , Pessoa de Meia-Idade
9.
JCI Insight ; 4(11)2019 06 06.
Artigo em Inglês | MEDLINE | ID: mdl-31167971

RESUMO

In patients with diabetes mellitus, poor metabolic control has a long-lasting impact on kidney disease development. Epigenetic changes, including cytosine methylation, have been proposed as potential mediators of the long-lasting effect of adverse metabolic events. Our understanding of the presence and contribution of methylation changes to disease development is limited because of the lack of comprehensive base-resolution methylome information of human kidney tissue samples and site-specific methylation editing. Base resolution, whole-genome bisulfite sequencing methylome maps of human diabetic kidney disease (DKD) tubule samples, and associated gene expression measured by RNA sequencing highlighted widespread methylation changes in DKD. Pathway analysis highlighted coordinated (methylation and gene expression) changes in immune signaling, including tumor necrosis factor alpha (TNF). Changes in TNF methylation correlated with kidney function decline. dCas9-Tet1-based lowering of the cytosine methylation level of the TNF differentially methylated region resulted in an increase in the TNF transcript level, indicating that methylation of this locus plays an important role in controlling TNF expression. Increasing the TNF level in diabetic mice increased disease severity, such as albuminuria. In summary, our results indicate widespread methylation differences in DKD kidneys and highlights epigenetic changes in the TNF locus and its contribution to the development of nephropathy in patients with diabetes mellitus.

10.
Nat Med ; 25(5): 805-813, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-31011203

RESUMO

Chronic inflammation is postulated to be involved in the development of end-stage renal disease in diabetes, but which specific circulating inflammatory proteins contribute to this risk remain unknown. To study this, we examined 194 circulating inflammatory proteins in subjects from three independent cohorts with type 1 and type 2 diabetes. In each cohort, we identified an extremely robust kidney risk inflammatory signature (KRIS), consisting of 17 proteins enriched in tumor necrosis factor-receptor superfamily members, that was associated with a 10-year risk of end-stage renal disease. All these proteins had a systemic, non-kidney source. Our prospective study findings provide strong evidence that KRIS proteins contribute to the inflammatory process underlying end-stage renal disease development in both types of diabetes. These proteins point to new therapeutic targets and new prognostic tests to identify subjects at risk of end-stage renal disease, as well as biomarkers to measure responses to treatment of diabetic kidney disease.


Assuntos
Nefropatias Diabéticas/sangue , Nefropatias Diabéticas/etiologia , Falência Renal Crônica/sangue , Falência Renal Crônica/etiologia , Adulto , Idoso , Biomarcadores/sangue , Proteínas Sanguíneas/genética , Proteínas Sanguíneas/metabolismo , Estudos de Coortes , Diabetes Mellitus Tipo 1/sangue , Diabetes Mellitus Tipo 1/complicações , Diabetes Mellitus Tipo 1/genética , Diabetes Mellitus Tipo 2/sangue , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/genética , Nefropatias Diabéticas/genética , Progressão da Doença , Feminino , Humanos , Mediadores da Inflamação/sangue , Falência Renal Crônica/genética , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Prospectivos , Proteômica , Receptores do Fator de Necrose Tumoral/sangue , Receptores do Fator de Necrose Tumoral/genética , Fatores de Risco
11.
Psychiatry Res ; 275: 46-52, 2019 05.
Artigo em Inglês | MEDLINE | ID: mdl-30878856

RESUMO

To provide appropriate solutions for problematic smartphone use, we need to first understand its types. This study aimed to identify types of problematic smartphone use based on psychiatric symptoms, using the decision tree method. We recruited 5,372 smartphone users from online surveys conducted between February 3 and February 22, 2016. Based on scores on the Korean Smartphone Addiction Proneness Scale for Adults (S-Scale), 974 smartphone users were assigned to the smartphone-dependent group and 4398 users were assigned to the normal group. The data-mining technique of C5.0 decision tree was applied. We used 15 input variables, including demographic and psychological factors. Four psychiatric variables emerged as the most important predictors: self-control (Sc; 66%), anxiety (Anx; 25%), depression (Dep; 7%), and dysfunctional impulsivities (Imp; 3%). We identified the following five types of problematic smartphone use: (1) non-comorbid, (2) self-control, (3) Sc + Anx, (4) Sc + Anx + Dep, and (5) Sc + Anx + Dep + Imp. We found that 74% of smartphone-dependent users had psychiatric symptoms. The ratio of participants belonging to the non-comorbid and self-control types was 64%. We proposed that these types of problematic smartphone use may be used for the development of an appropriate service for controlling and preventing such behaviors in adults.

12.
J Am Soc Nephrol ; 30(4): 594-609, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30850438

RESUMO

BACKGROUND: Cytosine methylation of regulatory regions, such as promoters and enhancers, plays a key role in regulating gene expression, however, its role in kidney development has not been analyzed. METHODS: To identify functionally important epigenome-modifying enzymes and genome regions where methylation modifications are functionally important for kidney development, we performed genome-wide methylation analysis, expression profiling, and systematic genetic targeting of DNA methyltransferases (Dnmt1, Dnmt3a, and Dnmt3b) and Ten-eleven translocation methylcytosine hydroxylases (Tet2) in nephron progenitor cells (Six2 Cre) in mice. RESULTS: Genome-wide methylome analysis indicated dynamic changes on promoters and enhancers during development. Six2 Cre Dnmt3a f/f, Six2 Cre Dnmt3b f/f, and Six2 Cre Tet2 f/f mice showed no significant structural or functional renal abnormalities. In contrast, Six2 Cre Dnmt1 f/f mice died within 24 hours of birth, from a severe kidney developmental defect. Genome-wide methylation analysis indicated a marked loss of methylation of transposable elements. RNA sequencing detected endogenous retroviral transcripts. Expression of intracellular viral sensing pathways (RIG-I), early embryonic, nonrenal lineage genes and increased cell death contributed to the phenotype development. In podocytes, loss of Dnmt1, Dnmt3a, Dnmt3b, or Tet2 did not lead to functional or structural differences at baseline or after toxic injury. CONCLUSIONS: Genome-wide cytosine methylation and gene expression profiling showed that by silencing embryonic, nonrenal lineage genes and transposable elements, DNMT1-mediated cytosine methylation is essential for kidney development.

13.
Nat Commun ; 10(1): 380, 2019 01 22.
Artigo em Inglês | MEDLINE | ID: mdl-30670690

RESUMO

Knowledge of cell type composition in disease relevant tissues is an important step towards the identification of cellular targets of disease. We present MuSiC, a method that utilizes cell-type specific gene expression from single-cell RNA sequencing (RNA-seq) data to characterize cell type compositions from bulk RNA-seq data in complex tissues. By appropriate weighting of genes showing cross-subject and cross-cell consistency, MuSiC enables the transfer of cell type-specific gene expression information from one dataset to another. When applied to pancreatic islet and whole kidney expression data in human, mouse, and rats, MuSiC outperformed existing methods, especially for tissues with closely related cell types. MuSiC enables the characterization of cellular heterogeneity of complex tissues for understanding of disease mechanisms. As bulk tissue data are more easily accessible than single-cell RNA-seq, MuSiC allows the utilization of the vast amounts of disease relevant bulk tissue RNA-seq data for elucidating cell type contributions in disease.


Assuntos
Perfilação da Expressão Gênica/métodos , Expressão Gênica , Teste de Histocompatibilidade/métodos , Análise de Célula Única/métodos , Animais , Doença , Humanos , Ilhotas Pancreáticas/citologia , Rim/citologia , Camundongos , Modelos Teóricos , Ratos , Análise de Sequência de RNA/métodos
14.
PLoS Genet ; 15(1): e1007874, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30625149

RESUMO

Extensive cell-to-cell variation exists even among putatively identical cells, and there is great interest in understanding how the properties of transcription relate to this heterogeneity. Differential expression from the two gene copies in diploid cells could potentially contribute, yet our ability to measure from which gene copy individual RNAs originated remains limited, particularly in the context of tissues. Here, we demonstrate quantitative, single molecule allele-specific RNA FISH adapted for use on tissue sections, allowing us to determine the chromosome of origin of individual RNA molecules in formaldehyde-fixed tissues. We used this method to visualize the allele-specific expression of Xist and multiple autosomal genes in mouse kidney. By combining these data with mathematical modeling, we evaluated models for allele-specific heterogeneity, in particular demonstrating that apparent expression from only one of the alleles in single cells can arise as a consequence of low-level mRNA abundance and transcriptional bursting.


Assuntos
Desequilíbrio Alélico/genética , Hibridização in Situ Fluorescente/métodos , Rim/metabolismo , RNA Longo não Codificante/genética , Alelos , Animais , Regulação da Expressão Gênica no Desenvolvimento/genética , Camundongos , Especificidade de Órgãos , RNA Longo não Codificante/isolamento & purificação
15.
Nat Genet ; 51(1): 51-62, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30578418

RESUMO

In this trans-ethnic multi-omic study, we reinterpret the genetic architecture of blood pressure to identify genes, tissues, phenomes and medication contexts of blood pressure homeostasis. We discovered 208 novel common blood pressure SNPs and 53 rare variants in genome-wide association studies of systolic, diastolic and pulse pressure in up to 776,078 participants from the Million Veteran Program (MVP) and collaborating studies, with analysis of the blood pressure clinical phenome in MVP. Our transcriptome-wide association study detected 4,043 blood pressure associations with genetically predicted gene expression of 840 genes in 45 tissues, and mouse renal single-cell RNA sequencing identified upregulated blood pressure genes in kidney tubule cells.


Assuntos
Pressão Sanguínea/genética , Grupos Étnicos/genética , Adolescente , Animais , Feminino , Expressão Gênica/genética , Estudo de Associação Genômica Ampla/métodos , Humanos , Túbulos Renais/fisiologia , Masculino , Camundongos , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único/genética , Transcriptoma/genética , Regulação para Cima/genética
16.
Rev Sci Instrum ; 89(11): 115006, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30501353

RESUMO

A monitoring device is proposed to investigate the charge accumulation effects in a high-aspect-ratio trench structure. This monitoring device is made of an anodic aluminum oxide (AAO) template, which is a self-organized material with parallel pores, to demonstrate a high aspect ratio trench structure. A top electrode and bottom electrode were formed in the AAO contact structure for measuring electric potentials. These electrodes can be assumed to be electrically floating due to the very high input resistance of the measurement circuit. Therefore, the electric potentials resulting from the charge accumulation can be measured. In this paper, the fabrication process of the proposed device and experimental demonstrations are presented.

17.
Nat Med ; 24(11): 1721-1731, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30275566

RESUMO

Chronic kidney disease (CKD), a condition in which the kidneys are unable to clear waste products, affects 700 million people globally. Genome-wide association studies (GWASs) have identified sequence variants for CKD; however, the biological basis of these GWAS results remains poorly understood. To address this issue, we created an expression quantitative trait loci (eQTL) atlas for the glomerular and tubular compartments of the human kidney. Through integrating the CKD GWAS with eQTL, single-cell RNA sequencing and regulatory region maps, we identified novel genes for CKD. Putative causal genes were enriched for proximal tubule expression and endolysosomal function, where DAB2, an adaptor protein in the TGF-ß pathway, formed a central node. Functional experiments confirmed that reducing Dab2 expression in renal tubules protected mice from CKD. In conclusion, compartment-specific eQTL analysis is an important avenue for the identification of novel genes and cellular pathways involved in CKD development and thus potential new opportunities for its treatment.

18.
PLoS Biol ; 16(9): e2005233, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30226866

RESUMO

While Notch signaling has been proposed to play a key role in fibrosis, the direct molecular pathways targeted by Notch signaling and the precise ligand and receptor pair that are responsible for kidney disease remain poorly defined. In this study, we found that JAG1 and NOTCH2 showed the strongest correlation with the degree of interstitial fibrosis in a genome-wide expression analysis of a large cohort of human kidney samples. Transcript analysis of mouse kidney disease models, including folic-acid (FA)-induced nephropathy, unilateral ureteral obstruction (UUO), or apolipoprotein L1 (APOL1)-associated kidney disease, indicated that Jag1 and Notch2 levels were higher in all analyzed kidney fibrosis models. Mice with tubule-specific deletion of Jag1 or Notch2 (Kspcre/Jag1flox/flox and Kspcre/Notch2flox/flox) had no kidney-specific alterations at baseline but showed protection from FA-induced kidney fibrosis. Tubule-specific genetic deletion of Notch1 and global knockout of Notch3 had no effect on fibrosis. In vitro chromatin immunoprecipitation experiments and genome-wide expression studies identified the mitochondrial transcription factor A (Tfam) as a direct Notch target. Re-expression of Tfam in tubule cells prevented Notch-induced metabolic and profibrotic reprogramming. Tubule-specific deletion of Tfam resulted in fibrosis. In summary, Jag1 and Notch2 play a key role in kidney fibrosis development by regulating Tfam expression and metabolic reprogramming.

19.
Clin Orthop Surg ; 10(3): 368-373, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30174814

RESUMO

Background: The purpose of this study was to compare clinical and radiological results of arthrodesis performed by the anterior approach and by the transfibular approach in ankle osteoarthritis. Methods: Sixty patients underwent open arthrodesis (38 by the anterior approach and 22 by the transfibular approach). The visual analogue scale score and the American Orthopedic Foot and Ankle Society (AOFAS) score were examined clinically, and radiological examination was performed on the alignment of the lower extremity and bone union. Results: Both groups showed significant improvement in AOFAS score (from 39.8 to 58.3 in the anterior approach group and from 44.5 to 60.7 in the transfibular approach group). There was no significant difference in AOFAS score at the last follow-up in both groups. The time to fusion was 13.5 weeks in the anterior approach group and 11.8 weeks in the transfibular approach group. Nonunion occurred in four cases in the anterior approach group and in one case in the transfibular approach group. Conclusions: Ankle arthrodesis by the anterior approach and the transfibular approach showed comparably good clinical results.

20.
Plant Cell Physiol ; 2018 Aug 07.
Artigo em Inglês | MEDLINE | ID: mdl-30099525

RESUMO

Leaf senescence is regulated by diverse developmental and environmental factors to maximize plant fitness. The red to far-red light ratio (R:FR) detected by plant phytochromes is reduced under vegetation shade, thus initiating leaf senescence. However, the role of phytochromes in promoting leaf senescence under FR-enriched conditions is not fully understood. In this study, we investigated the role of phyA and phyB in regulating leaf senescence under FR in Arabidopsis thaliana (Arabidopsis). FR enrichment and intermittent FR pulses promoted the senescence of Arabidopsis leaves. Additionally, phyA and phyB mutants showed enhanced and repressed senescence phenotypes in FR, respectively, indicating that phyA and phyB antagonistically regulate FR-dependent leaf senescence. Transcriptomic analysis using phyA and phyB mutants in FR identified differentially expressed genes (DEGs) involved in leaf senescence-related processes, such as responses to light, phytohormones, and temperature, photosynthesis, and defense, showing opposite expression patterns in phyA and phyB mutants. These contrasting expression profiles of DEGs support the antagonism between phyA and phyB in FR-dependent leaf senescence. Among the genes showing antagonistic regulation, we confirmed that the expression of WRKY6, which encodes a senescence-associated transcription factor, was negatively and positively regulated by phyA and phyB, respectively. The wrky6 mutant showed a repressed senescence phenotype compared with the wild type in FR, indicating that WRKY6 plays a positive role in FR-dependent leaf senescence. Our results imply that antagonism between phyA and phyB is involved in fine-tuning leaf senescence under varying FR conditions in Arabidopsis.

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