gene expression was measured in control and heat resistance selected adult female flies before and at 8 time points after heat stress for 1h @ 36 degrees

Full genome gene expression analysis of the heat stress response in Drosophila melanogaster.

Drosophila heat stress response time series analysis

gene expression was measured in five independent heat resistance selected replicate lines and five control lines.

Differential expression in heat resistance selected adult female Drosophila melanogaster

We compared transcriptional profiles of CD4+ and CD8+ T lymphocytes from HIV infected individuals before and 1 year after interruption of antiretroviral therapy (ART).

Effect of analytical treatment interruption and reinitiation of antiretroviral therapy on HIV reservoirs and immunologic parameters in infected individuals.

Effect of Analytic Treatment Interruption of Antiretroviral Therapy on HIV Reservoirs and Immunological Parameters

Postnatal neural progenitors of the enteric nervous system are a potential source for future cell replacement therapies of developmental dysplasia like Hirschsprung's disease. However, little is known about the molecular mechanisms driving the homeostasis and differentiation of this cell pool. In this work, we conducted Affymetrix gene chip experiments to identify differences in gene regulation between proliferation and early differentiation of enteric neural progenitors. We detected a total of 1333 regulated genes that were linked to different groups of cellular mechanisms involved in cell cycle, apoptosis, neural proliferation, and differentiation. As expected, we found a strong inhibition of cell cycle progression as well as an enhanced expression of neuronal and glial markers. We further found a marked inactivation of the canonical Wnt pathway during the beginning of cellular differentiation. Taken together, this data illustrated the various mechanisms taking place during the proliferation and early differentiation of enteric neural progenitor cells.

Comparative Microarray Analysis of Proliferating and Differentiating Murine ENS Progenitor Cells.

Expression data of proliferating and differentiating ENS progenitor cells

These arrays contain data from hypthalamus tissue of nestin-Pex5 -/- male mice

Peroxisome deficiency but not the defect in ether lipid synthesis causes activation of the innate immune system and axonal loss in the central nervous system.

Hypothalamus

Differentiation assays with neural progenitor cells of the enteric nervous system (ENS) showed elongated neurite outgrowth under influence of 3,5,3'-Triiodothyronine (concentrations 50 nm and 100 nm). For analysis, neural cells were stained with TUJ1 (beta-Tubulin III). Microarray analysis should enlighten these results on a genetical basis and give hints about the regulation pathways.

Molecular and cell biological effects of 3,5,3'-triiodothyronine on progenitor cells of the enteric nervous system in vitro.

Influence of 3,5,3'-Triiodothyronine (T3) on differentiating progenitor cells of the enteric nervous system (ENS)

The hearts rhythm is initiated and regulated by a group of specialized cells in the sinoatrial node (SAN), the primary pacemaker of the heart. Abnormalities in the development of the SAN can result in irregular heart rates (arrhythmias). Although several of the critical genes important for SAN formation have been identified, our understanding of the transcriptional network controlling SAN development remains at a relatively early stage. The homeodomain transcription factor Shox2 plays an essential early role in the specification and patterning of the SAN.

Islet1 is a direct transcriptional target of the homeodomain transcription factor Shox2 and rescues the Shox2-mediated bradycardia.

Expression data from Shox2 knockout and wildtype right atria of E11.5 mouse hearts

Primary liver tumours include hepatocellular carcinomas (HCC), cholangiocarcinomas  (CC) and a group of rare tumours exhibiting biliary and hepatocytic differentiation called combined hepatocholangiocarcinomas (cHCC-CC). To better define this latter group, we take advantage of a series of these tumours based on their morphological characteristics and we performed transcriptional analysis allowing thereafter global comparison with published data. We show that most cHCC-CCs express progenitor cell traits, are committed to biliary lineage and are mainly associated to the activation of Wnt/beta-catenin and TGFbeta signalling pathways. Wnt/beta-catenin pathway activation in cHCC-CC is evidenced by the expression of both its direct targets such as LEF1 and EPCAM. In addition, extracellular matrix (ECM) genes and ECM-remodelling genes which are upon the control of TGF profibrotic program were found up-regulated in cHCC-CC. Interestingly, we show that CC and  most cHCC-CC share characteristics associated to a subtype of poorly differentiated HCC suggesting that these tumours could originate from a stem/progenitor cell. The plasticity of these cells may explain the phenotypical heterogeneity of these tumors with the maintenance of some hepatocellular differentiation features such as albumin expression. Interestingly, this is shared by at least one third of CC, raising the hypothesis of a potential continuum between CC, cHCC-CC and poorly differentiated HCC.

Combined hepatocellular-cholangiocarcinomas exhibit progenitor features and activation of Wnt and TGFβ signaling pathways.

Combined hepatocellular-cholangiocarcinomas exhibit progenitor features and activation of Wnt and TGFbeta signaling pathways

Physiologically, Notch signal transduction plays a pivotal role in differentiation; pathologically, Notch signaling contributes to the development of cancer. Transcriptional activation of Notch target genes involves cleavage of the Notch receptor in response to ligand binding, production of the Notch intracellular domain (NICD), and NICD migration into the nucleus and assembly of a coactivator complex. Posttranslational modifications of the NICD are important for its transcriptional activity and protein turnover. Deregulation of Notch signaling and stabilizing mutations of Notch1 have been linked to leukemia development. We found that the methyltransferase CARM1 (coactivator-associated arginine methyltransferase 1; also known as PRMT4) methylated NICD at five conserved arginine residues within the C-terminal transactivation domain. CARM1 physically and functionally interacted with the NICD-coactivator complex and was found at gene enhancers in a Notch-dependent manner. Although a methylation-defective NICD mutant was biochemically more stable, this mutant was biologically less active as measured with Notch assays in embryos of Xenopus laevis and Danio rerio. Mathematical modeling indicated that full but short and transient Notch signaling required methylation of NICD.

Site-specific methylation of Notch1 controls the amplitude and duration of the Notch1 response.

Site-specific methylation of Notch1 controls the amplitude and duration of the Notch1 response

We used adult male Sprague-Dawley rats (280-329 g body weight). Controls were nave rats. Ischemic rats were subjected to 1-hour occlusion of the right middle cerebral artery and 16h reperfusion.