Project description:Mouse ES-cells with different sex chromosome compliment were differentiated into EpiSC, samples were taken every 4-12 hours for 84 hours in total. The original data for the XX-cells is also available as GSE34243, but normalisation of these differs.
Project description:RNA-seq of bovine genital ridges from male and female fetuses at three different time points corresponding to sex determination and early differentiation of the gonads
Project description:Transcription profiling of mouse spinal cord from mock-infected and Theilers murine encephalomyelitis (TME)-virus infected animals - time series
Project description:Transcription profiling of murine J1 embryonic stem cells undergoing a differentiation time course to study changes in transcription during stem cell differentiation
Project description:Abdominal aortic aneurysms (AAAs) are a prevalent and deadly human pathology with strong sexual dimorphism. Research demonstrates that sex hormones influence, but do not fully explain, male versus female AAA pathology. In addition to sex hormones, the X and Y sex chromosomes, and their unique complements of genes, may contribute to sexually dimorphic AAA pathology. Here, for the first time, we defined the effect of female (XX) versus male (XY) chromosome complement on AAA formation and rupture in phenotypically female mice using an established murine model. Abdominal aortas from female mice bearing the XY chromosome selectively expressed Y chromosome genes, while genes known to escape X-inactivation were higher in XX females. The majority of gene differences in XY females fell within inflammatory pathways. When XY females were infused with AngII, AAA incidences doubled and aneurysms ruptured. AAAs from XY females exhibited significant inflammation. Moreover, infusion of AngII to XY females augmented aortic activity of matrix metalloproteinases. Finally, testosterone exposure applied chronically, or as a single bolus at postnatal day 1, markedly worsened AAA outcomes in XY compared to XX females. These results demonstrate that an XY sex chromosome complement profoundly influences aortic gene expression profiles and promotes AAA severity.