Project description:A hallmark of aging-related disease such as neurodegeneration, metabolic disorders, and cancer is the inability of differentiated cells to maintain their identity. In a search for identity regulators, we found that transcription factor Hey supervises the identity of differentiated enterocytes (ECs) in the adult Drosophila midgut. Lineage tracing of ECs established that Hey-deficient ECs lose differentiated identity, are unable to maintain their unique nuclear organization, and exhibit pathological reprograming. Orchestrating this organization, Hey specifies and maintains enhancer activity and nuclear lamins expression, remodeling nuclear architecture from a stem-cell configuration into a differentiated one. Moreover, maintaining this configuration of nuclear lamins is key for cell identity, and lamin misexpression overrides cell identities. At the tissue level, loss of Hey or expression of stem cell-related lamin (LamDm0) in ECs resulted in mis-differentiation, impaired epithelial integrity, and reduced organismal survival. Thus, a single transcription factor concomitantly supervises chromatin and nuclear organization, safeguarding cell identity
Project description:We over-expressed biotinylated-thyroid hormone receptor beta 1 (TRb1) in mouse liver using an adenovirus in order to perform ChIP-seq experiments. These microarrays were performed to determine gene expression changes in response to tri-iodothyronine (thyroid hormone; T3) stimulation. A control GFP adenovirus was used and gene expression from these livers was also done as a comparison. We performed microarrays from Ad-GFP-infected propylthiouracil (PTU)-fed livers injected with either saline or T3 and Ad-TRb1-GFP infected livers injected with either saline or T3. RNA was extracted from livers of biotin ligase (BirA)-expressing mice that had been infected with either Ad-GFP or Ad-TRb1, fed with PTU for 3 weeks followed by saline or T3 injections for 4 consecutive days.
Project description:We over-expressed biotinylated-thyroid hormone receptor beta 1 (TRb1) in mouse liver using an adenovirus in order to perform ChIP-seq experiments. These microarrays were performed to determine gene expression changes in response to tri-iodothyronine (thyroid hormone; T3) stimulation. A control GFP adenovirus was used and gene expression from these livers was also done as a comparison. We performed microarrays from Ad-GFP-infected propylthiouracil (PTU)-fed livers injected with either saline or T3 and Ad-TRb1-GFP infected livers injected with either saline or T3.
Project description:We used RNA-seq to examine transcriptional proflies of midguts with suppression of Imd in progenitors (e_* samples) or enterocytes (M_* samples) . We found significant differences between the contributions of enterocyte IMD and progenitor IMD to intestinal homeostasis.
Project description:To gain an overview of the cellular impact of Guanabenz analogues, we analyzed the gene expression changes in PC12 cells expressing GFP-mHtt-74Q utilizing Affimatrix rat genome microarrays. Following exposure of PC12 cells expressing GFP-mHtt-74Q to Compound 6 for 48 hrs, we noted the enhanced expression of over 46 genes and the reduced expression of 8 genes compared to DMSO
Project description:Bulk RNAseq from whole Drosophila melanogaster guts expressing either mCherry-RNAi (control) or RNAi against nicotinic acetylcholine receptor subunits β1 and β3 (nAchRβ1 and nAchRβ3) under control of a enterocyte-specific driver to assess their role in barrier function.
Project description:ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice to assess the effects of a CKIαΔgut knock-out in the jejunum and a CKIαΔgut/p53 double knock-out. In addition, enterocytes expressing a mutant p53 (R172H) in combination with CKIαΔgut knockout were analyzed.