Additional file 3: of Cloning and characterization of an ABA-independent DREB transcription factor gene, HcDREB2, in Hemarthria compressa

Nucleotide sequence and deduced amino-acid sequence of HcDREB cDNA. (DOC 31 kb

Average expression stability values (M₁) of 11 candidate reference genes calculated by geNorm.

<p>(a) drought stress, (b) salt stress, (c) heat stress, (d) waterlogging stress, (e) ABA treatment. Lower M₁ values indicate more stable expression.</p

Primer specificity and amplicon size.

<p>(A) Agarose gel (2.0%) electrophoresis indicates amplification of a single PCR product of the expected size for 13 genes. (B) Melting curves of 13 genes show single peaks. M represents 100 bp DNA marker.</p

Expression stability values for perennial ryegrass candidate reference genes calculated using BestKeeper under five treatments.

<p>Note: Expression stability and ranking of 11 candidate reference genes calculated with BestKeeper under drought, salt, heat, waterlogging stresses and ABA treatment. Eleven reference genes are identified as the most stable genes, as evaluated by the lowest values of the coefficient of variance (CV) and standard deviation (SD).</p

Agarose gel results of <i>SOD</i>, <i>POD</i>, <i>elF4A</i>, and <i>60S</i> PCR amplicons in perennial ryegrass leaves exposed to drought stress treatment.

<p>Agarose gel results of <i>SOD</i>, <i>POD</i>, <i>elF4A</i>, and <i>60S</i> PCR amplicons in perennial ryegrass leaves exposed to drought stress treatment.</p

Additional file 6: of Genome-wide association study of rust traits in orchardgrass using SLAF-seq technology

(XLSX 50 kb

Stability ranking of 11 candidate reference genes.

<p>Stability ranking of 11 candidate reference genes.</p

List of primer sequences and related information for 13 genes (11 references gene and 2 object genes).

<p>List of primer sequences and related information for 13 genes (11 references gene and 2 object genes).</p

Median cycle threshold (C_T) values for each reference gene for all samples.

<p>The filled diamond symbol indicates median C_T values. The bars indicate standard deviation.</p

Blocking the Class I Histone Deacetylase Ameliorates Renal Fibrosis and Inhibits Renal Fibroblast Activation via Modulating TGF-Beta and EGFR Signaling

<div><h3>Background</h3><p>Histone deacetylase (HDAC) inhibitors are promising anti-fibrosis drugs; however, nonselective inhibition of class I and class II HDACs does not allow a detailed elucidation of the individual HDAC functions in renal fibrosis. In this study, we investigated the effect of MS-275, a selective class I HDAC inhibitor, on the development of renal fibrosis in a murine model of unilateral ureteral obstruction (UUO) and activation of cultured renal interstitial fibroblasts.</p> <h3>Methods/Findings</h3><p>The UUO model was established by ligation of the left ureter and the contralateral kidney was used as a control. At seven days after UUO injury, kidney developed fibrosis as indicated by deposition of collagen fibrils and increased expression of collagen I, fibronectin and alpha-smooth muscle actin (alpha-SMA). Administration of MS-275 inhibited all these fibrotic responses and suppressed UUO-induced production of transforming growth factor-beta1 (TGF-beta), increased expression of TGF-beta receptor I, and phosphorylation of Smad-3. MS-275 was also effective in suppressing phosphorylation and expression of epidermal growth factor receptor (EGFR) and its downstream signaling molecule, signal transducer and activator of transcription-3. Moreover, class I HDAC inhibition reduced the number of renal tubular cells arrested in the G2/M phase of the cell cycle, a cellular event associated with TGF-beta1overproduction. In cultured renal interstitial fibroblasts, MS-275 treatment inhibited TGF-beta induced phosphorylation of Smad-3, differentiation of renal fibroblasts to myofibroblasts and proliferation of myofibroblasts.</p> <h3>Conclusions and Significance</h3><p>These results demonstrate that class I HDACs are critically involved in renal fibrogenesis and renal fibroblast activation through modulating TGF-beta and EGFR signaling and suggest that blockade of class I HDAC may be a useful treatment for renal fibrosis.</p> </div