Topic: ChIP-seq

Study gene regulation by processing and integrating RNA-seq, ATAC-seq, MNase-seq, ChIP-seq and Hi-C measurements. The five workshop days cover expression analysis, chromatin accessibility, chromatin composition, three-dimensional genome interactions and multi-omics integration. Practical work includes quality control, alignment, differential expression, peak and motif analysis, and visualisation of genomic contacts. Reproducible Linux and R notebooks connect assay design to biological interpretation. Live online, 22–26 February, 13:00–19:00 Europe/Berlin (CET). Fee €480. Participants need a b

In vivo, the human genome folds into a characteristic ensemble of 3D structures. The mechanism driving the folding process remains unknown. A theoretical model for chromatin (the minimal chromatin model) explains the folding of interphase chromosomes and generates chromosome conformations consistent with experimental data is presented. The energy landscape of the model was derived by using the maximum entropy principle and relies on two experimentally derived inputs: a classification of loci into chromatin types and a catalog of the positions of chromatin loops. This model was generalized by u

Silencing of FMR1 and loss of its gene product, FMRP, results in fragile X syndrome (FXS). FMRP binds brain mRNAs and inhibits polypeptide elongation. Using ribosome profiling of the hippocampus, we find that ribosome footprint levels in Fmr1-deficient tissue mostly reflect changes in RNA abundance. Profiling over a time course of ribosome runoff in wild-type tissue reveals a wide range of ribosome translocation rates; on many mRNAs, the ribosomes are stalled. Sucrose gradient ultracentrifugation of hippocampal slices after ribosome runoff reveals that FMRP co-sediments with stalled ribosomes,