Artículo de publicación ISIRoot hypoxia in fruit trees affects growth, vegetative
development, and reproductive development, which
is reflected in low productivity, poor fruit quality, and
premature decay of trees. Using Illumina Hiseq2000, we performed transcriptome analysis of roots from two different
rootstocks, ‘Mariana 2624’ and ‘Mazzard F12/1,’
which are tolerant and sensitive to hypoxia, respectively.
Transcriptomes from control and hypoxia-stressed plants
(6, 24, and 72 h) were compared, using Prunus persica
(L.) as reference genome. Hypoxic conditions altered the
transcription in both genotypes. There were a high number
of common differentially expressed genes (DEG) between
the two genotypes for each sampling time, but also exclusive
DEG for each genotype, with a few DEG that presented
opposite modes of regulations during the hypoxia
treatment. An important group of DEGs exclusively upregulated
in the tolerant genotype are associated to enzymes
of posttranslational protein modifications, such as leucinerich
repeat (LRR), kinases and ubiquitin-protein ligases,
regulation of transcription, and process of oxide reduction.
Singular enrichment analysis of gene ontology (GO), detected
at least 115 GOs involved in the response to root
hypoxia in the sensitive and/or tolerant genotypes. At least
25 GOs were identified as part of the baseline differences
between the genotypes, most GO were disturbed in the
sensitive genotype. The contribution from the baseline
gene expression to the differential response between the
Prunus genotypes is evidence that the resistant genotype
is already Bprepared^ for a hypoxia event. An example are
GO BP:0042221 of response to chemical stimulus;
BP:0006979 of response to oxidative stress; MF:0016209
of antioxidant activity; MF:0016684 of oxidoreductase activity,
acting on peroxide as acceptor; and MF:0004601 of
peroxidase activity, which were disturbed only in the sensitive
genotype, but not in the tolerant.FONDECYT (No. 1121117) and CEAF_R08I100
IntroductionSystemic sclerosis (SSc) and primary biliary cirrhosis (PBC) are rare polygenic autoimmune diseases (AIDs) characterized by fibroblast dysfunction. Furthermore, both diseases share some genetic bases with other AIDs, as evidenced by autoimmune gene pleiotropism. The present study was undertaken to investigate whether single-nucleotide polymorphisms (SNPs) identified by a large genome-wide association study (GWAS) in PBC might contribute to SSc susceptibility.MethodsSixteen PBC susceptibility SNPs were genotyped in a total of 1,616 patients with SSc and 3,621 healthy controls from two European populations (France and Italy).ResultsWe observed an association between PLCL2 rs1372072 (odds ratio (OR) = 1.22, 95% confidence interval (CI) 1.12 to 1.33, Padj = 7.22 × 10−5), nuclear factor-kappa-B (NF-κB) rs7665090 (OR = 1.15, 95% CI 1.06 to 1.25, Padj = 0.01), and IRF8 rs11117432 (OR = 0.75, 95% CI 0.67 to 0.86, Padj = 2.49 × 10−4) with SSc susceptibility. Furthermore, phenotype stratification showed an association between rs1372072 and rs11117432 with the limited cutaneous subgroup (lcSSc) (Padj = 4.45 × 10−4 and Padj = 0.001), whereas rs7665090 was associated with the diffuse cutaneous subtype (dcSSc) (Padj = 0.003). Genotype-mRNA expression correlation analysis revealed that the IRF8 protective allele was associated with increased interferon-gamma (IFN-γ) expression (P = 0.03) in patients with SSc but decreased type I IFN (IFIT1) expression in patients and controls (P = 0.02). In addition, we found an epistatic interaction between NF-κB and IRF8 (OR = 0.56, 95% CI 0.00 to 0.74, P = 4 × 10−4) which in turn revealed that the IRF8 protective effect is dependent on the presence of the NF-κB susceptibility allele.ConclusionsAn analysis of pleiotropic genes identified two new susceptibility genes for SSc (NF-κB and PLCL2) and confirmed the IRF8 locus. Furthermore, the IRF8 variant influenced the IFN signature, and we found an interaction between IRF8 and NF-κB gene variants that might play a role in SSc susceptibility.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-015-0572-y) contains supplementary material, which is available to authorized users.
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