Project description:The tomato cultivars Querubín FCA (Q) and Gema FCA (G) as parental genotypes and the hybrids Q x G and G x Q were selected to perform and investigation of the gene actions involved in gene expression profile. In this work, we aimed to study the differences between parental lines and the presence of heterosis and reciprocal effects in the reciprocal hybrids.
Project description:Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high throughput mass spectrometry to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at post-natal day 90. Pathway Analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Behavioral testing of pID rats demonstrated social impairment and poor performance during novelty-induced exploration in pID animals in line with a abnormal neurodevelopmental phenotype. Considering the link between prenatal iron deficiency and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of prenatal iron deficiency.
Project description:The Arabidopsis RNA-binding proteins FCA and FPA were initially identified based on their suppression of the flowering time regulator FLC. Recently, however, they have been found to influence expression of a wide range of targets in the Arabidopsis genome. Here, we use whole-genome tiling arrays to determine the extent of their targets at two stages of seedling development. A wide range of genes and transposable elements were mis-expressed in the fcafpa double mutant with a significant bias for mis-regulated genomic segments mapping to the 3’ region of genes. A large number of previously unannotated (UA) genomic segments, which mapped to intergenic regions, were also mis-expressed in the fcafpa double mutant. We characterized a subset of these UA segments in detail and established them as strand-specific and direct targets of FCA and FPA, with a complex interplay between their functions. Only a few of the UA segments also showed regulation by a histone demethylase previously linked to FCA FPA function; however, others were associated with siRNA production and DNA methylation. Our data suggest that FCA/FPA play important roles in terminating transcription at many loci, often via promotion of proximal polyadenylation, and that in their absence, ectopic transcription and/or extensive read-through transcription occurs. These transcriptional products have the potential to interfere with overlapping transcripts and flanking genes and appear to form the basis for how modulation of FCA FPA function triggers RNA-mediated chromatin silencing mechanisms at a variety of loci in the Arabidopsis genome.
Project description:We performed mRNA 3'end sequencing experiments on three biological replicates of HeLa cells depleted of MATR3, PTBP1/2, controls, or combined depletion of MATR3/PTBP1/2. Cells were fractionated into cytoplasmic and nuclear RNAn and only the nuclear RNA was used. Library preparation was done with the QuantSeq library kit (Lexogen) according to manufacturer’s recommendations. Replicates 1 and 2 were prepared with the QuantSeq forward library kit, replicates 3 and 4 with the QuantSeq reverse library kit. All libraries were sequenced on Illumina HiSeq2 machines in a single-end manner with a read length of 100 nt.
Project description:Quantitative variation in expression of the Arabidopsis floral repressor FLC influences whether plants overwinter before flowering or have a rapid cycling habit, enabling multiple generations a year. Genetic analysis has identified activators and repressors of FLC expression, but how they interact to set expression level is poorly understood. Here, we show that antagonistic functions of the FLC activator FRIGIDA (FRI), and the repressor FCA, at a specific stage of embryo development, determines FLC expression and flowering. FRI antagonizes an FCA-induced proximal polyadenylation to increase FLC expression and delay flowering. Sector analysis shows that FRI activity during the early heart stage of embryo development maximally delays flowering. Opposing functions of co-transcriptional regulators during an early embryonic developmental window thus set FLC expression levels and determine flowering time.