13 research outputs found

    Is Mathematics the Theory of Instantiated Structural Universals?

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    This paper rejects metaphysical realism about structural universals as a basis for mathematical realism about numbers, and argues that one construal of structural universals via non-well-founded sets should be resisted by the mathematical realist

    Isolation of the <i>Bdtar2l<sup>hypo</sup></i> mutant and characterization of macroscopic phenotypes.

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    <p>(<i>A</i>) Four-day-old tissue culture grown seedlings of wild type (accession Bd21), an unrelated control transformant (control) (the unrelated transformant line was included in all our assays to control for any tissue culture regeneration effects) and the transgenic line segregating the <i>Bdtar2l<sup>hypo</sup></i> mutation. (<i>B</i>) Seminal root length quantification of the different genotypes at 4 days after germination (dag). (<i>C</i>) Schematic presentation of the <i>BdTAR2L</i> gene and the location of the T-DNA insertion in the <i>Bdtar2l<sup>hypo</sup></i> mutant. (<i>D–E</i>) Relative expression level of <i>BdTAR2L</i> in different genotypes at 4 dag as determined by qPCR and normalized with respect to the housekeeping gene, <i>BdUBC18</i>. (<i>F</i>) Root elongation in wild type, control and homozygous <i>Bdtar2l<sup>hypo</sup></i> mutants, assayed at 4 dag. (<i>G–H</i>) Quantification of seedling phenotypes at 4 dag. (<i>I</i>) Leaf number at 18 dag. (<i>J–L</i>) Different size parameters of the 5<sup>th</sup> leaf of plants, assayed at 18 dag. (<i>M</i>) Representative image of adult plants at 18 dag. Size bars are 1 cm; differences as compared to wild type are not significant unless indicated otherwise; error bars indicate standard error; * = p<0.05; ** = p<0.01; *** = p<0.001.</p

    Phenotypes of the <i>Bdtar2l<sup>qnull</sup></i> mutant in comparison to its wild type background, Bd21-3.

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    <p>(<i>A</i>) Relative expression level of <i>BdTAR2L</i> in different genotypes at 4 dag as determined by qPCR and normalized with respect to the housekeeping gene, <i>BdUBC18</i>. (<i>B–C</i>) Root elongation in wild type and <i>Bdtar2l<sup>qnull</sup></i> mutants, assayed at 4 dag. (<i>D</i>) Representative Nomarski optics images of mature root portions. Arrowheads point out top and bottom of individual cells in a cortex layer; (<i>E</i>) Quantification of mature cortex cell length at 4 dag. (<i>F</i>) Representative microscopy images of root hairs at 4 dag. (<i>G</i>) Representative light microscopy images of transverse sections across the mature root. (<i>H–I</i>) Quantification of total transverse area and stele area in sections from mature roots. (<i>J</i>) Relative seminal root length in <i>Bdtar2l<sup>qnull</sup></i> mutants during root growth progression. (<i>K</i>) Progressive breakdown of root meristem as indicated by shrinkage of the meristematic zone. (<i>L</i>) Seedling shoot length at 4 dag. (<i>M</i>) Adult shoots. Size bars are 1 cm (<i>B, M</i>) or 100 µm (<i>D,F,G</i>); differences as compared to wild type or mock are not significant unless indicated otherwise; error bars indicate standard error; * = p<0.05; *** = p<0.001.</p

    Effect of L-kynerunine (L-kyn) treatment on root elongation of different genotypes.

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    <p>(<i>A</i>) Representative images of 4-day-old seedlings, transferred onto media with indicated L-kyn concentration at 2 dag. (<i>B</i>) Quantification of root length after 2 days of indicated L-kyn treatment. (<i>C</i>) Representative Nomarski optics images of mature root portions formed during indicated L-kyn treatment. Arrowheads point out top and bottom of individual cells in the 3<sup>rd</sup> cortex layer; (<i>D</i>) Quantification of mature cortex cell length after 2 days of indicated L-kyn treatment. (<i>E–F</i>) Relative root elongation of indicated mutants and their respective wild type backgrounds after 2 days of indicated 5-methyl-tryptophan treatment. Size bars are 1 cm (<i>A</i>) or 100 µm (<i>C</i>); differences as compared to wild type or mock are not significant unless indicated otherwise; error bars indicate standard error; * = p<0.05; ** = p<0.01; *** = p<0.001.</p

    Auxin homeostasis in <i>Bdtar2l<sup>hypo</sup></i> roots and its relation to the ethylene pathway.

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    <p>(<i>A</i>) Free auxin (IAA) content in wild type and <i>Bdtar2l<sup>hypo</sup></i> root segments at 4 dag. The root tip comprised the terminal 8 mm of the roots, the elongated parts all above this. (<i>B</i>) Expression levels of the homologs of various genes encoding rate limiting enzymes in alternative auxin biosynthesis pathways in wild type and <i>Bdtar2l<sup>hypo</sup></i> roots at 4 dag. (<i>C</i>) Expression levels of <i>YUCCA</i> homologs in wild type and <i>Bdtar2l<sup>hypo</sup></i> roots at 4 dag. (<i>D</i>) Expression levels of <i>BdTAR1L</i> and <i>BdTAR2L</i> in wild type at 3 dag and after 3 h of ACC treatment. (<i>E</i>) Expression levels of <i>YUCCA</i> homologs in wild type at 3 dag and after 3 h of ACC treatment. All expression levels were determined by qPCR and normalized with respect to the housekeeping gene, <i>BdUBC18</i>; differences as compared to wild type or mock are not significant unless indicated otherwise; error bars indicate standard error; * = p<0.05; ** = p<0.01; *** = p<0.001.</p

    A schematic overview of the regulation of tryptophan-dependent auxin (indole-3-acetic acid) biosynthesis via indole-3-pyruvic acid (IPA) by ethylene action in Arabidopsis (<i>A</i>) and Brachypodium (<i>B</i>).

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    <p>A schematic overview of the regulation of tryptophan-dependent auxin (indole-3-acetic acid) biosynthesis via indole-3-pyruvic acid (IPA) by ethylene action in Arabidopsis (<i>A</i>) and Brachypodium (<i>B</i>).</p

    Sankar_et_al_data_file_4

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    Archive of tables (tab-delimited) of the normalized data used in machine learning for the Ler sections from data file 2, combined with the cell type assignment

    Study design.

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    <p>Thirty-three BXD lines plus the 2 parental strains and their reciprocal F1 progeny were phenotyped. Mice were submitted to either one of 2 experiments. In Experiment 1 (left), EEG/EMG signals and LMA were recorded under standard 12:12 h light–dark conditions (white and black bars under top-left panel) for 2 baseline days (B1, B2), a 6 h SD (red bar) from ZT0–6 (ZT0 = light onset), followed by 2 recovery days (R1, R2). The deep sleep-wake phenome consists of 341 sleep-wake state-, LMA-, and EEG-related phenotypes quantified in each mouse, among which time spent in NREM sleep (gray area spans mean maximum and minimum NREM sleep time among BXD lines, respectively, for consecutive 90 min intervals). Mice in Experiment 2 (right) were used to collect cortex, liver, and blood samples at ZT6. Half of the mice were challenged with an SD as in Experiment 1, the other half were left undisturbed and served as controls (labeled Ctr). Cortex and liver samples were used to quantify gene expression by RNA-seq, blood samples for a targeted analysis of 124 metabolites by LC/MS, or with FIA/MS. For <i>ph</i>QTLs, <i>m</i>QTLs, and <i>e</i>QTLs, a high-density genotype dataset (Genome; approximately 11,000 SNPs) was created, merging identified RNA-seq variants with a publicly available database (<a href="http://www.genenetwork.org/" target="_blank">www.genenetwork.org</a>). The entirety of the multilevel dataset was integrated in a systems genetics analysis to chart molecular pathways underlying the many facets of sleep and the EEG, using newly developed computational tools to interactively visualize the results and pathways, and to prioritize candidate genes. EEG/EMG, electroencephalography/electromyogram; <i>e</i>QTL, expression quantitative trait locus; FIA/MS, flow injection analysis/mass spectrometry; LC/MS, liquid chromatography/mass spectrometry; LMA, locomotor activity; <i>m</i>QTL, metabolic quantitative trait locus; NREM, non-REM; <i>ph</i>QTL, phenotypic quantitative trait locus; RNA-seq, RNA sequencing; SD, sleep deprivation; ZT, zeitgeber time.</p

    EEG delta power in NREM sleep after SD is associated with <i>Kif16b</i> and <i>Wrn</i>.

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    <p>(A) NREM sleep EEG spectra in the first 3 h after SD (ZT6–9) for the 2 BXD lines that displayed the lowest and highest EEG activity in the fast delta frequency band (2.5–4.25 Hz, δ2; top, see panel E) and for the 2 BXD lines that displayed the smallest and largest increase (or gain) in EEG power in the slow delta band (1.0–2.25 Hz, δ1; bottom, see panel E). Spectra were “1/f-corrected” (and therefore not directly comparable to the values in panel E) for better visualization of activity in higher frequency bands (theta [5–9 Hz, θ], sigma [11–16 Hz, σ], beta [18–30 Hz, β], and slow [32–55 Hz, γ1] and fast gamma [55–80 Hz, γ2]). Subsequent analyses were performed without this correction. (B) QTL mapping and prioritization for δ2 power identified a significant association on chromosome 2 and <i>Kif16b</i> in cortex as top-ranked gene (top). For the δ1 increase after SD, we obtained a suggestive QTL on chromosome 8 and a significant prioritization score for the DNA-helicase <i>Wrn</i>. (C) Hiveplot visualization of network connections for the δ1 and δ2 power after SD (top-left panels) and the SD-induced increase in δ1 and δ2 power over baseline (bottom-left panels). Note the marked differences in the networks and QTLs regulating the expression of these 2 delta bands. Right hiveplots highlight <i>Kif16b</i> in the δ2 power–associated network (top), and <i>Wrn</i> in the network associated with the δ1 increase (bottom). Only <i>Kif16b</i> expression in the cortex was linked to the chromosome 2 <i>cis</i>-<i>e</i>QTL and was not associated with any metabolite. <i>Wrn</i> expression was significantly linked to the chromosome 8 <i>cis-e</i>QTL and to the long phosphatidylcholine, PC-ae-C38:5. (D) <i>Kif16b</i> is highly significantly down-regulated in cortex (left), while it remains unchanged in liver after SD (<i>p</i> = 0.15; not shown). Also, <i>Wrn</i> expression was strongly down-regulated by SD in cortex (right) and only marginally so, albeit significantly, in liver (<i>p</i> = 0.02; not shown). (E) Strain distribution patterns. BXD lines carrying a <i>B6-</i>allele on the chromosome 2–associated region showed higher δ2 power after SD (left) and a significantly higher <i>Kif16b</i> expression (<i>p</i> = 1.3e−15; second to left) than <i>D2-</i>allele carriers. <i>D2-</i>allele carriers of the chromosome 8–associated region showed a larger δ1 increase after SD (second to right) as well as a significantly larger decrease in <i>Wrn</i> expression after SD (right) than <i>B6-</i>allele carriers. For color-coding of genotypes, see <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2005750#pbio.2005750.g004" target="_blank">Fig 4</a>. CPM, counts per million; Ctr, control; EEG, electroencephalography; <i>e</i>QTL, expression quantitative trait locus; FDR, false discovery rate; <i>Kif16b</i>, <i>Kinesin family member 16B</i>; NREM, non-REM; PC-ae, phosphatidylcholine acyl-alkyl; QTL, quantitative trait locus; SD, sleep deprivation; <i>Wrn</i>, <i>Werner syndrome RecQ like helicase</i>; ZT, zeitgeber time</p

    Genetic diversity in the BXD panel greatly impacts behavioral, metabolic, and molecular traits.

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    <p>The phenome was divided into 3 phenotypic categories: (i) LMA, (ii) EEG features (labeled EEG), and (iii) sleep-wake state characteristics (labeled State), which were subdivided further (see <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2005750#sec015" target="_blank">Materials and methods</a>). The 5 classes of metabolites and the gene expression represent intermediate molecular phenotypic categories. (A) Heritability for EEG/behavioral and metabolite phenotypes. Dots represent single phenotypes within each category and subcategory indicated along the x-axis. Red dots represent phenotypes recorded in baseline (labeled bsl; B1 and B2), blue in recovery (labeled rec; R1 and R2), purple during SD, and green dots refer to the recovery-to-baseline contrasts. Values represent narrow-sense heritability. (B) Overview of significant and highly suggestive (FDR < 0.1) QTLs obtained for all 341 EEG/behavioral phenotypes (<i>ph</i>QTLs: LMA in red, EEG in blue, and sleep-wake state in green) and 124 blood metabolite levels in baseline and recovery (<i>m</i>QTLs; purple). Note that overlap of neighboring QTLs renders color shading darker. (C) Venn diagram of genes under significant <i>cis-e</i>QTL effect in liver and cortex for the two experimental conditions (SD and controls [labeled Ctr]). EEG, electroencephalography; <i>e</i>QTL, expression quantitative trait locus; FDR, false discovery rate; LMA, locomotor activity; <i>m</i>QTL, metabolic quantitative trait locus; <i>ph</i>QTL, phenotypic quantitative trait locus; QTL, quantitative trait locus; SD, sleep deprivation.</p
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