Project description:We used adult male Sprague-Dawley rats (280-329 g body weight). Controls were naïve rats. Ischemic rats were subjected to 1-hour occlusion of the right middle cerebral artery and 16h reperfusion. The goal was to identify the changes in the gene expression profile of PV after brain ischemia.
Project description:Analysis of embronic day 30.5 (E30.5) fetal rabbit left lung after creation of diapragmatic hernia (DH) at E25 and tracheal occlusion (TO) at E27. The fetuses of timed pregnant New Zealand rabbits were subjected to creation of a left diaphragmatic hernia at E25 with or without tracheal occlusion at E27. At E30.5, the fetuses were sacrificed with collection of the lateral aspect of the left upper lobe for NextGen mRNA sequencing.
Project description:Here, we employed single-cell RNA sequencing (scRNA-seq) to comprehensively map the cell populations in the mouse model of MCAO (middle cerebral artery occlusion).
Project description:Centromeres are essential to ensure proper chromosome segregation in eukaryotes. Their definition relies on the presence of a centromere-specific H3 histone variant CenH3, known as CENP-A in mammals. Its overexpression in aggressive cancers raises questions concerning its effect on chromatin dynamics and contribution to tumorigenesis. We find that CenH3 overexpression in human cells leads to ectopic enrichment at sites of active histone turnover. Furthermore, in over-expressing conditions, we see the formation of a novel heterotypic particle (CenH3-H4/H3.3-H4) that occludes CTCF binding, but this occlusion has only a minor effect on gene expression. Ectopic localization and CTCF occlusion depends on the H3.3 chaperone DAXX, rather than its dedicated chaperone HJURP. This DAXX-dependent occlusion also occurs in naturally overexpressing cancer cells. Furthermore, our cellular model reveals a DAXX-dependent survival advantage when challenged by DNA damage. Our findings illustrate how changes in histone variant levels can disrupt chromatin dynamics in disease and provides a possible mechanism for cell resistance to anti-cancer treatments. Examination of CenH3 ChIP-seq and RNA-seq transcriptional programs in two conditions - WT and CenH3 over-expressing.
