MOESM1 of Disruption of the transcription factors Thi2p and Nrm1p alleviates the post-glucose effect on xylose utilization in Saccharomyces cerevisiae

Additional file 1: Figure S1. Fermentation characteristics of xylose-utilizing strains. Figure S2. The transcriptional difference of genes involved in fructose, mannose, galactose, sucrose, and starch metabolism in GX stage versus X stage in both BSGX001 and XH7. Table S1. The primers used in this study. Table S2. Gene cluster analysis of transcriptome difference of GX stage versus X stage in both BSGX001 and XH7. Table S3. Gene cluster analysis of transcription reaction in THI2 deletion strains versus WT strains. Table S4. The ribosomal related genes with significantly different expression levels between GX stage and X stage in both BSGX001 and XH7

Molecular Characterization of the <i>ORF3</i> and <i>S1</i> Genes of Porcine Epidemic Diarrhea Virus Non S-INDEL Strains in Seven Regions of China, 2015

<div><p>In an effort to trace the evolution of porcine epidemic diarrhea virus (PEDV), <i>S1</i> and <i>ORF3</i> genes of viruses identified in 41 pig farms from seven regions (North, Northeast, Northwest, Central, East, South West, and South, respectively) of China in 2015 were sequenced and analyzed. Sequence analysis revealed that the 41 <i>ORF3</i> genes and 29 <i>S1</i> genes identified in our study exhibited nucleotide homologies of 98.2%–100% and 96.6%–100%, respectively; these two genes exhibited low nucleotide sequence similarities with classical CV777 strain and early Chinese strain LZC. Phylogenetic analysis indicated that the identified PEDV strains belonged to global non S-INDEL strains, and exhibited genetic diversity; <i>S1</i> gene of the HLJ2015/DP1-1 strain harbored an unique deletion of 12 nucleotides (A¹¹³⁰CAACTCCACTG¹¹⁴¹); while the Chinese PEDV S-INDEL reference strains included two types of the “CV777” S-INDEL as well as the “US” S-INDEL, and all co-circulated with Chinese non S-INDEL strains. Of 29 identified <i>S1</i> genes, the SS2 epitope (Y⁷⁴⁸SNIGVCK⁷⁵⁵) was highly conserved, while the SS6 epitope (L⁷⁶⁴QDGQVKI⁷⁷¹) and pAPN receptor-binding region (aa 490–615) exhibited amino substitutions. Nine possible recombination events were identified between the 29 identifed <i>S1</i> genes and the 3 <i>S1</i> reference genes from early Chinese PEDV strains. The complete <i>S</i> genes of selected Chinese PEDV field strains (2011–2015) showed 5.18%–6.07% nucleotide divergence, which is far higher than the divergence observed in early Chinese PEDV strains (3.1%) (<i>P</i><0.05). Our data provide evidence that PEDV non S-INDEL strains with genetic diversities and potential recombination circulate in seven regions of China in 2015; Chinese PEDV S-INDEL strains exhibit genetic diversity and co-circulate with non S-INDEL strains.</p></div

Phylogenetic analysis of the identified PEDV strains on the basis of <i>S1</i> gene sequences.

<p><i>Note</i>. The “CV777” S-INDEL strain, North American (NA) prototype strain USA/Colorado/2013 (non S-INDEL), US S-INDEL strain OH851, Chinese S-INDEL strains (LZC, JS2008, and CH/S), Japanese S-INDEL strain ZK-O, South Korea S-INDEL strains (SM98 and virulent DR13), European S-INDEL strains (FR/001/2014, 15V010/BEL/2015, and GER/L00721/2014), Chinese PEDV field strains, and other countries non S-INDEL strains were choose for genotyping and phylogenetic analysis of the 29 <i>S1</i> genes identified in our study. Light purple dot represents PEDV strains identified in North China; red dot represents PEDV strains identified in East China; pink dot represents PEDV strains identified in Northeast China; grey dot represents PEDV strains identified in Northwest China; green dot represents PEDV strains identified in South China; yellow dot represents PEDV strains identified in Central China; blue green dot represents PEDV strains identified in Southwest China.</p

Potential recombination analysis between the 29 identified <i>S1</i> genes and the 3 <i>S1</i> genes from early Chinese PEDV strains.

<p>Potential recombination analysis between the 29 identified <i>S1</i> genes and the 3 <i>S1</i> genes from early Chinese PEDV strains.</p

Divergence analysis of complete <i>S</i> gene of the selected Chinese PEDV strains.

<p><i>Note</i>. The values (red) represent “average value ± standard deviation” of the nucleotide divergence (%) of each group; the different letters represent statistically significantly difference (<i>P</i><0.05) among six groups, and the same letters (one or more) represent no significant difference (<i>P</i>>0.05) among six groups.</p

Multiple Autoimmune-Associated Variants Confer Decreased IL-2R Signaling in CD4⁺CD25^hi T Cells of Type 1 Diabetic and Multiple Sclerosis Patients

<div><p>IL-2 receptor (IL-2R) signaling is essential for optimal stability and function of CD4⁺CD25^hiFOXP3⁺ regulatory T cells (Treg); a cell type that plays an integral role in maintaining tolerance. Thus, we hypothesized that decreased response to IL-2 may be a common phenotype of subjects who have autoimmune diseases associated with variants in the <i>IL2RA</i> locus, including T1D and MS, particularly in cells expressing the high affinity IL-2R alpha chain (IL-2RA or CD25). To examine this question we used phosphorylation of STAT5 (pSTAT5) as a downstream measure of IL-2R signaling, and found a decreased response to IL-2 in CD4⁺CD25^hi T cells of T1D and MS, but not SLE patients. Since the <i>IL2RA</i>rs2104286 haplotype is associated with T1D and MS, we measured pSTAT5 in controls carrying the rs2104286 risk haplotype to test whether this variant contributed to reduced IL-2 responsiveness. Consistent with this, we found decreased pSTAT5 in subjects carrying the rs2104286 risk haplotype. Reduced IL-2R signaling did not result from lower CD25 expression on CD25^hi cells; instead we detected increased CD25 expression on naive Treg from controls carrying the rs2104286 risk haplotype, and subjects with T1D and MS. However the rs2104286 risk haplotype correlated with increased soluble IL-2RA levels, suggesting that shedding of the IL-2R may account in part for the reduced IL-2R signaling associated with the rs2104286 risk haplotype. In addition to risk variants in <i>IL2RA,</i> we found that the T1D-associated risk variant of <i>PTPN2</i>rs1893217 independently contributed to diminished IL-2R signaling. However, even when holding genotype constant at <i>IL2RA</i> and <i>PTPN2</i>, we still observed a significant signaling defect in T1D and MS patients. Together, these data suggest that multiple mechanisms converge in disease leading to decreased response to IL-2, a phenotype that may eventually lead to loss of tolerance and autoimmunity.</p></div