Project description:The bark represents the outer protective layer of trees. It contains high concentrations of antimicrobial extractives, in addition to regular wood polymers. It represents a huge underutilized side stream in forestry, but biotechnological valorization is hampered by a lack of knowledge on microbial bark degradation. Many fungi are efficient lignocellulose degraders, and here, spruce bark degradation by five species, Dichomitus squalens, Rhodonia placenta, Penicillium crustosum, Trichoderma sp. B1, and Trichoderma reesei, was mapped, by continuously analyzing chemical changes in the bark over six months. The study reveals how fungi from different phyla degrade bark using diverse strategies, regarding both wood polymers and extractives, where toxic resin acids were degraded by Basidiomycetes but unmodified/tolerated by Ascomycetes. Proteome analyses of the white-rot D. squalens revealed several proteins, with both known and unknown functions, that were specifically upregulated during growth on bark. This knowledge can accelerate improved utilization of an abundant renewable resource.
Project description:Induced pluripotent stem cells (iPSC) were prepared from multiple subjects with Ataxia-telangiectasia (A-T). iPSC were prepared from activated T-cells using commercial Sendai virus to deliver reprogramming factors. ATM protein-expressing and non-expressing cultures would found in multiple sub-lines (sub-lines are generated from distinct founder colonies of cells) from a single subject (Q3). Genetic analysis determined that all sub-lines originated from the same subject and were likely the product of spontaneous reversion by gene correction. To compare gene expression profiles, three iPSC samples were assayed: (1) A reverted ATM+/- subline from subject Q3, (2) An ATM-/- subline from subject Q3, and (3) An iPSC line from an unrelated ATM-/- subject, Q1. Analysis reveals that the majority of significantly-different genes between the unrelated ATM-/- line (Q1SA) and the reverted ATM+/- line (Q3SC) was due to genetic variation between individuals. A more focused set of contrasting genes could be identified between the isogenic Q3-derived lines (Q3SA, ATM-/-, vs. Q3SC, ATM+/-). The 206 transcripts that are significantly different point to a differential regulation of p53-associated pathways.
Project description:Induced pluripotent stem cells (iPSC) were prepared from multiple subjects with Ataxia-telangiectasia (A-T). iPSC were prepared from activated T-cells using commercial Sendai virus to deliver reprogramming factors. ATM protein-expressing and non-expressing cultures would found in multiple sub-lines (sub-lines are generated from distinct founder colonies of cells) from a single subject (Q3). Genetic analysis determined that all sub-lines originated from the same subject and were likely the product of spontaneous reversion by gene correction. To compare gene expression profiles, three iPSC samples were assayed: (1) A reverted ATM+/- subline from subject Q3, (2) An ATM-/- subline from subject Q3, and (3) An iPSC line from an unrelated ATM-/- subject, Q1. Analysis reveals that the majority of significantly-different genes between the unrelated ATM-/- line (Q1SA) and the reverted ATM+/- line (Q3SC) was due to genetic variation between individuals. A more focused set of contrasting genes could be identified between the isogenic Q3-derived lines (Q3SA, ATM-/-, vs. Q3SC, ATM+/-). The 206 transcripts that are significantly different point to a differential regulation of p53-associated pathways. Total cellular RNA was prepared from each iPSC culture. Different passage numbers or sister cultures were used as replicates (n=2).
Project description:Penicillium digitatum is the pathogen of Green mold in Postharvest citrus. After inoculating Penicillium digitatum into the wound of citrus to infect it, transcriptome sequencing was carried out and compared with the results of transcriptome sequencing of Penicillium digitatum before inoculation in order to screen the differentially expressed genes and reveal its infection mechanism.