Germ free (GF) and conventionalized (CONV-D) wild-type C57Bl/6 male mice in the CARB-fed, 24h fasted, and 30d trained states; plus GF and CONV-D CARB-fed Ppara-/- mice. CARB-fed indicates a standard polysaccharide-rich mouse chow diet.
Regulation of myocardial ketone body metabolism by the gut microbiota during nutrient deprivation.
Sex, Specimen part
View SamplesDNA methylation is critical for normal development and plays important roles in genome organization and transcriptional regulation. Although DNA methyltransferases have been identified, the factors that establish and contribute to genome-wide methylation patterns remain elusive. Here, we report a high-resolution cytosine methylation map of the murine genome modulated by Lsh, a chromatin remodeling family member that has previously been shown to regulate CpG methylation at repetitive sequences. We provide evidence that Lsh also controls genome-wide cytosine methylation at nonrepeat sequences and relate those changes to alterations in H4K4me3 modification and gene expression. Deletion of Lsh alters the allocation of cytosine methylation in chromosomal regions of 50 kb to 2 Mb and, in addition, leads to changes in the methylation profile at the 5 end of genes. Furthermore, we demonstrate that loss of Lsh promotesas well as preventscytosine methylation. Our data indicate that Lsh is an epigenetic modulator that is critical for normal distribution of cytosine methylation throughout the murine genome.
Lsh, chromatin remodeling family member, modulates genome-wide cytosine methylation patterns at nonrepeat sequences.
Specimen part
View SamplesDNA methylation is critical for normal development and plays important roles in genome organization and transcriptional regulation. Although DNA methyltransferases have been identified, the factors that establish and contribute to genome-wide methylation patterns remain elusive. Here, we report a high-resolution cytosine methylation map of the murine genome modulated by Lsh, a chromatin remodeling family member that has previously been shown to regulate CpG methylation at repetitive sequences. We provide evidence that Lsh also controls genome-wide cytosine methylation at nonrepeat sequences and relate those changes to alterations in H4K4me3 modification and gene expression. Deletion of Lsh alters the allocation of cytosine methylation in chromosomal regions of 50 kb to 2 Mb and, in addition, leads to changes in the methylation profile at the 5 end of genes. Furthermore, we demonstrate that loss of Lsh promotesas well as preventscytosine methylation. Our data indicate that Lsh is an epigenetic modulator that is critical for normal distribution of cytosine methylation throughout the murine genome.
Lsh, chromatin remodeling family member, modulates genome-wide cytosine methylation patterns at nonrepeat sequences.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
General detoxification and stress responses are mediated by oxidized lipids through TGA transcription factors in Arabidopsis.
No sample metadata fields
View Samples12-oxo-phytodienoic acid (OPDA) and phytoprostane A1 (PPA1) are cyclopentenone oxylipins that are formed via the enzymatic
General detoxification and stress responses are mediated by oxidized lipids through TGA transcription factors in Arabidopsis.
No sample metadata fields
View Samples12-Oxo-phytodienoic acid (OPDA) and several phytoprostanes are structurally related cyclopentenone oxylipins that can be formed via the enzymatic jasmonate pathway and a non-enzymatic, free radical-catalyzed pathway, respectively. To elucidate the biological activities of phytoprostanes in comparison to OPDA as well as the metabolism we performed genome-wide expression analysis.
General detoxification and stress responses are mediated by oxidized lipids through TGA transcription factors in Arabidopsis.
No sample metadata fields
View SamplesNonsyndromic clefts of the palate and/or lip are common birth defects arising in about 1/700 live births worldwide. They are caused by multiple genetic and environmental factors, can only be corrected surgically and require complex post-operative care that imposes significant burdens on individuals and society. Our understanding of the molecular networks that control palatogenesis has advanced through studies on mouse genetic models of cleft palate. In particular, the transcription factor Pax9 regulates palatogenesis through the Bmp, Fgf and Shh pathways in mice. But there is still much to learn about Pax9's relationship with other signaling pathways in this process. Expression analyses and unbiased gene expression profiling studies offer a molecular explanation for the resolution of palatal defects by showing that Wnt and Eda/Edar-related genes are expressed in normal palatal tissues and that the Wnt and Eda/Edar signaling pathway is downstream of Pax9 in palatogenesis. Overall design: E13.5 mouse embryos palate were micro-dissceted, control and mutant samples were seperated and individually lyzed for the RNA extraction.
Small-molecule Wnt agonists correct cleft palates in <i>Pax9</i> mutant mice <i>in utero</i>.
Specimen part, Cell line, Treatment, Subject
View SamplesNonsyndromic clefts of the palate and/or lip are common birth defects arising in about 1/700 live births worldwide. They are caused by multiple genetic and environmental factors, can only be corrected surgically and require complex post-operative care that imposes significant burdens on individuals and society. Our understanding of the molecular networks that control palatogenesis has advanced through studies on mouse genetic models of cleft palate. In particular, the transcription factor Pax9 regulates palatogenesis through the Bmp, Fgf and Shh pathways in mice. But there is still much to learn about Pax9''s relationship with other signaling pathways in this process. Here we show alterations of Wnt expression and decreased Wnt activity in Pax9-/- palatal shelves are a likely result of Pax9''s ability to directly bind and repress the promoters of Dkk1 and Dkk2, proteins that antagonize Wnt signaling. We exploited this relationship by delivering small-molecule Dkk inhibitors into the tail-veins of pregnant Pax9+/- females from E10.5 to E14.5. Such therapies restored Wnt signaling, promoted cell proliferation, bone formation and fusion of palatal shelves in Pax9-/- embryos. These data uncover a connection between the roles of Pax9 and Wnt genes in palatogenesis and offer a new approach for treating human cleft palates. Overall design: E14 embryos of Pax9-/- and control littermates with or without WAY-262611 treatment, mouse embryos palate were micro-dissected, control and mutant samples were separated and individually lysed for the RNA extraction.
Small-molecule Wnt agonists correct cleft palates in <i>Pax9</i> mutant mice <i>in utero</i>.
Specimen part, Cell line, Treatment, Subject
View SamplesLoss of Syk in normal breast cells in vivo and in vitro: gene expression and phenotypic switch to stem-cell like with induction of invadopodia
Tumor suppressor function of Syk in human MCF10A in vitro and normal mouse mammary epithelium in vivo.
Cell line
View SamplesEngineering of genetically encoded calcium indicators predominantly focused on optimizing fluorescence changes, but effects of indicator expression on host organisms have largely not been addressed. Here, we report biocompatibility and wide-spread functional expression of the genetically encoded calcium indicator TN-XXL in a transgenic mouse model. To validate the model and to characterize potential effects of indicator expression we assessed both indicator function and a variety of host parameters such as anatomy, physiology, behavior and gene expression profiles in these mice. We also demonstrate the usefulness of primary cell types and organ explants prepared from these mice for imaging applications. While we do find mild signatures of indicator expression that may guide further indicator development the green indicator mice generated provide a well characterized resource of primary cells and tissues for in vitro and in vivo calcium imaging applications.
Biocompatibility of a genetically encoded calcium indicator in a transgenic mouse model.
Specimen part
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