Project description:Dosage compensation in D. melanogaster males is achieved via targeting of the MSL complex to X chromosomal genes. This is proposed to involve initial sequence-specific recognition of the X at ~150-300 chromatin entry sites, and subsequent spreading to nearby active genes. Here we test a model in which the spreading step requires transcription and is sequence-independent. We ask whether, in the native context of the X chromosome, MSL complex will target genes of autosomal origin. We find that MSL complex does bind such genes, but only if transcriptionally active. Targeting is accompanied by acetylation of the histone H4K16 residue and two-fold transcriptional up-regulation. We conclude that the presence of a long-sought specific DNA sequence within X-linked genes is not obligatory for MSL complex binding. Instead, physical linkage and transcription play the pivotal roles in the identification of MSL targets irrespective of their origin and DNA sequence. Keywords: Epigenetics ChIP-seq measurements of MSL complex binding and input control. Chromatin was prepared from third instar male larvae of a genotype y w TrojanElephant; MSL3-TAP; msl3. TrojanElephant is a mini-white- and yellow-marked transposition of genomic region spanning 65 kb from cg13773 to snRNP70K. MSL3-TAP is a mini-white-marked TAP-tagged genomic msl3 transgene. IgG beads were used for pull-down.
Project description:This is a post-marketing, single-arm, prospective study investigating the use of GI Genius CADx device in the real-time characterization of colorectal polyps (i.e. prediction of their histology during the colonoscopy). Patients enrolled will undergo a standard white-light colonoscopy with the support of the latest version of the CE-marked GI Genius CADx device. Colonoscopy will be performed according to the standard practice.
Project description:Transcriptional effectors of white adipocyte-selective gene expression have not been described. TLE3 is a white-selective cofactor that acts reciprocally with the brown-selective cofactor Prdm16 to specify lipid storage and thermogenic gene programs. When expressed at elevated levels in brown fat, TLE3 counters Prdm16, suppressing brown-selective genes and inducing white-selective genes, resulting in impaired fatty acid oxidation and thermogenesis. To further test the functional consequences of the changes in BAT phenotype in aP2-TLE3 Tg mice, we challenged them with cold exposure at 4C. aP2-TLE3 Tg mice had an impaired ability to respond to cold exposure compared to littermate control mice, as evidenced by a marked drop in core body temperature.