SNPs associations with psoriasis.

<p>SNPs associations with psoriasis.</p

Association of GRS-N with psoriasis sub-phenotypes.

<p>Association of GRS-N with psoriasis sub-phenotypes.</p

The risk of psoriasis in GRS-N quartiles relative to the first quartile.

<p>The risk of psoriasis in GRS-N quartiles relative to the first quartile.</p

Demographic and clinical characteristics of the patients.

<p>Demographic and clinical characteristics of the patients.</p

Comparison of ROC curves for prediction of psoriasis with the use of different genetic risk scores: GRS-N, GRS-HLA and GRS-N(+)HLA(-).

<p>GRS-N- GRS combining 16 SNPs at least nominally associated with psoriasis; GRS-HLA- GRS including only rs4406273 (a proxy for <i>HLA-Cw*0602</i>); GRS-N(+)HLA(-) (GRS-N without rs4406273). AUC- area under the curve.</p

Comparison of ROC curves for prediction of psoriasis with the use of different genetic risk scores (GRS).

<p>GRS-ALL- GRS combining all 38 SNPs; GRS-0.1- GRS combining 19 SNPs associated/with a trend toward association with psoriasis; GRS-N- GRS combining 16 SNPs at least nominally associated with psoriasis in our cohort; GRS-B- GRS combining 6 SNPs which remained significantly associated with psoriasis after Bonferroni correction; GRS-HLA- GRS including only rs4406273 (a proxy for <i>HLA-Cw*</i>060). AUC- area under the curve.</p

Concentration of gibberellins in wild type and mutant lines.

<p>The values are ng/g dry weight (s.e.). They are the means of three biological replicates except for the GA₁₂ and GA₉ measurements in <i>ga1-3</i>, for which 2 replicates were used. n.d. – not determined.</p

Gene Ontology (GO) categories statistically over-represented among genes differentially expressed in both <i>ga1-3</i> and <i>brm-1</i> mutants.

<p>Gene Ontology (GO) categories statistically over-represented among genes differentially expressed in both <i>ga1-3</i> and <i>brm-1</i> mutants.</p

GA responses of the <i>brm-1</i> mutant.

<p>(A, B), Elongation of <i>brm-1</i> hypocotyls and roots in response to 1 µM GA₄. Plants were grown on ½ MS medium for 8 days under long-days conditions in the presence or absence of 1 µM GA₄. GA application caused considerable elongation of the hypocotyls, but had little effect on <i>brm-1</i> root growth. Bar = 5 mm. (B), Hypocotyl length of plants grown as in A. Presented data are the means of 12 measurements ± s.d. (C), Flowering of <i>brm-1</i> plants in response to exogenous gibberellins. Plants were grown in soil under short-day conditions and treated with 10 µM GA₃. At least 15 plants of each line/condition were scored. Data are the means ± s.d. Asterisks indicate significant differences from the wild type plants (p<0.01).</p

BRM acts through distinct mechanisms to regulate GA-mediated responses.

<p>(A), Germination of the <i>brm-1</i> mutant on 10 µM PAC is rescued by the <i>triple della</i> mutation. The progeny of <i>brm-1/BRM</i> plants were analyzed 10 days after sowing. (B), Phenotypes of 3-week-old plants grown on 2.5 µM PAC. The <i>brm-1/3xdella</i> line shows an intermediate growth phenotype. Bar = 5 mm. (C), RT-qPCR analysis of relative transcript levels of the <i>OFP16, EXP5, CYS2</i> and <i>LTP2</i> genes in 18-d-old wild type, <i>brm-1</i>, <i>ga1-3</i>, <i>ga1-3/brm-1</i>, <i>ga1-3/3xdella</i> and <i>ga1-3/brm-1/3xdella</i> lines. Transcript levels in the wild type were set to 1. Data are the means ± s.d. of 3 biological replicates. (D), Model of the role of BRM in regulating the expression of GA-responsive genes. BRM positively regulates the <i>GA3ox1</i> and <i>SCL3</i> genes involved in GA biosynthesis and signaling, and probably through this influences the expression of many GA-responsive genes in the opposite manner to DELLA repressors. In addition, BRM seems to act on a subset of GA-responsive genes independently of DELLA repressors. Also in this case, the effect exerted by BRM is typically in the opposite direction to that of DELLAs and is observed both for genes up- and down-regulated by the SWI/SNF complex (blue and red lines, respectively).</p