Project description:This experiment studies the effect of knocking out the transcriptional regulator SIR2 in 3D7 parasites. RNA was harvested from ring-stage parasites at 8 hours post-infection. Keywords = SIR2 Keywords = epigenetic regulation Keywords = antigenic variation Keywords = var Keywords = Plasmodium falciparum Keywords: other
Project description:All Rap1, Sir2, Sir3, Sir4, and mock immunoprecipitation experiments associated with Lieb et al. Nature Genetics, August 2001, Volume 28, Issue 4 Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
Project description:Telomere chromatin structure is pivotal for maintaining genome stability by regulating the binding of telomere-associated proteins and inhibition of a DNA damage response. In yeast, the silent information regulator (Sir) proteins bind to terminal telomeric repeats and to subtelomeric X-elements resulting in histone deacetylation and transcriptional silencing. Herein, we show that sir2 mutant strains display a very specific loss of a nucleosome residing in the X-element. Most yeast telomeres contain an X-element and the nucleosome occupancy defect in sir2 mutants is remarkably consistent between different telomeres.
Project description:Although SIRT1 plays a central role in maintaining metabolic homeostasis, the molecular mechanisms remain unclear. Here we show that loss of the Drosophila SIRT1 homolog sir2 leads to the progressive onset of diabetic phenotypes, similar to studies of SIRT1 in mice. Sir2 function is both necessary and sufficient in the fat body to maintain peripheral insulin sensitivity. This activity is mediated by the Drosophila HNF4 nuclear receptor, which is deacetylated and stabilized through protein interactions with Sir2. This study demonstrates that the key metabolic activities of SIRT1 have been conserved through evolution and establishes HNF4 as a critical downstream target. 4 sir2 mutant, 4 control samples, independent biological replicates
Project description:O-acetyl-ADP-ribose (AAR) is a small metabolic molecule that is generated during NAD-dependent deacetylation by Sir2. Sir2 regulates gene expression, DNA repair, and genome stability. chromatin affinity-precipitation (ChAP) method was used to detect the chromatin fragments at which small molecules interact with binding partners. Chromatin immunoprecipitation of Sir3 and of Sir2, respectively, applied with tilling array chip (ChIP on chip of Sir3 and of Sir2, respectively) and Chromatin affinity-precipitation of AAR applied with tilling array chip (ChAP on chip of AAR ) analysis demonstrated that an extended spreading of Sir3 and of AAR, but not Sir2 in Saccharomyces cerevisiae Ysa1 deleted cells compared with those in wild type cells
Project description:Sir2-family of NAD-dependent histone deacetylases are involved in gene transcription repression in yeast. The C. glabrata genes encoding members of this family are SIR2 (CAGL0K01463g), HST1 (CAGL0C05357g), HST2 (CAGL0L08668g), HST3 (CAGL0H08239g) and HST4 (CAGL0F05621g). SIR4 (CAGL0K11396g) encodes a factor that forms a functional complex with Sir2. In this experiment, the transcription profile of C. glabrata HST1 null, HST2 null, SIR2 null or SIR4 null strain individually comparing with that of wild type strain was determined. All strains were grown in YPD liquid medium in Log phase at 30 C. Keywords: transcriptional profiling by microarray
Project description:Although SIRT1 plays a central role in maintaining metabolic homeostasis, the molecular mechanisms remain unclear. Here we show that loss of the Drosophila SIRT1 homolog sir2 leads to the progressive onset of diabetic phenotypes, similar to studies of SIRT1 in mice. Sir2 function is both necessary and sufficient in the fat body to maintain peripheral insulin sensitivity. This activity is mediated by the Drosophila HNF4 nuclear receptor, which is deacetylated and stabilized through protein interactions with Sir2. This study demonstrates that the key metabolic activities of SIRT1 have been conserved through evolution and establishes HNF4 as a critical downstream target.