Nutrição mineral de bovinos de corte no Pantanal Mato-grossense. IV. Levantamento de micronutrientes no baixo Piquiri

Cu, Fe, Mn and Zn were analysed in samples of soil, forages and lactating zebu cows' liver from the lower Piqui, in the Brazilian Pantanal. Soils and forages were collected in "campo cerrado" or savanna grassland, "campo limpo" or open grassland, "cerrado"/woodland forest, in August and November 1981, and liver in these occasions plus March and May 1952. Average levels of Cu, Fe, Mn and Zn in Soil were 2 ppm, 496 ppm, 33 ppm and 3 ppm, respectively; and in forages, 5.9 ppm, 130 ppm, 224 ppm and 14 ppm respectively. Liver Fe levels varied from 516 ppm in August to 733 ppm in May, Cu from 129 ppm in November to 278 ppm in February; Mn from 29 ppm in November to 43 ppm in May, and Zn from 75 ppm in August to 153 ppm in November. In August, 65% of liver samples presented less than 80 ppm of Zn and in Novembor 37% less than 100 ppm of Cu. The results suggest the possibility of ocurrence of Zn deficiencies, mainly in the dry season, and Cu deficiencies, especially in the early rainy season.Foram analisados Cu, Fe, Mn e Zn em amostras de solo, plantas forrageiras e fígado de vacas neloradas em lactação da zona do baixo Piquiri, no Pantanal Mato-grossense. Solos e forrageiras foram coletados em campo cerrado, campo limpo e cerrado/mata, em agosto e novembro/81, e fígado, nestas épocas e em março e maio/82. Os teores médios de Cu, Pc, Mn e Zn no solo foram: 2 ppm, 496 ppm, 33 ppm e 3 ppm, respectivamente; e nas forrageiras, 5,9 ppm, 130 ppm, 224 ppm e 14 ppm, respectivamente. Os teores hepáticos de Fe variaram de 516 ppm em agosto de 733 ppm em maio; de Cu, de 129 ppm em novembro a 278 ppm em fevereiro; de Mn, de 29 ppm em novembro a 43 ppm em maio; e de Zn, de 75 ppm em agosto a 153 ppm em novembro. Em agosto, 65% das amostras de fígado apresentaram menos de 80 ppm de Zn e em novembro 37%, menos de 100 ppm de Cu. Os resultados sugerem a possibilidade de ocorrência de deficiência de deficiências de Zn, sobretudo no período seco, e de Cu, especialmente no inicio do período chuvoso

Q&A: ChIP-seq technologies and the study of gene regulation

10.1186/1741-7007-8-56BMC Biology85

De-Novo Identification of PPARγ/RXR Binding Sites and Direct Targets during Adipogenesis

BACKGROUND: The pathophysiology of obesity and type 2 diabetes mellitus is associated with abnormalities in endocrine signaling in adipose tissue and one of the key signaling affectors operative in these disorders is the nuclear hormone transcription factor peroxisome proliferator-activated receptor-gamma (PPARgamma). PPARgamma has pleiotropic functions affecting a wide range of fundamental biological processes including the regulation of genes that modulate insulin sensitivity, adipocyte differentiation, inflammation and atherosclerosis. To date, only a limited number of direct targets for PPARgamma have been identified through research using the well established pre-adipogenic cell line, 3T3-L1. In order to obtain a genome-wide view of PPARgamma binding sites, we applied the pair end-tagging technology (ChIP-PET) to map PPARgamma binding sites in 3T3-L1 preadipocyte cells. METHODOLOGY/PRINCIPAL FINDINGS: Coupling gene expression profile analysis with ChIP-PET, we identified in a genome-wide manner over 7700 DNA binding sites of the transcription factor PPARgamma and its heterodimeric partner RXR during the course of adipocyte differentiation. Our validation studies prove that the identified sites are bona fide binding sites for both PPARgamma and RXR and that they are functionally capable of driving PPARgamma specific transcription. Our results strongly indicate that PPARgamma is the predominant heterodimerization partner for RXR during late stages of adipocyte differentiation. Additionally, we find that PPARgamma/RXR association is enriched within the proximity of the 5' region of the transcription start site and this association is significantly associated with transcriptional up-regulation of genes involved in fatty acid and lipid metabolism confirming the role of PPARgamma as the master transcriptional regulator of adipogenesis. Evolutionary conservation analysis of these binding sites is greater when adjacent to up-regulated genes than down-regulated genes, suggesting the primordial function of PPARgamma/RXR is in the induction of genes. Our functional validations resulted in identifying novel PPARgamma direct targets that have not been previously reported to promote adipogenic differentiation. CONCLUSIONS/SIGNIFICANCE: We have identified in a genome-wide manner the binding sites of PPARgamma and RXR during the course of adipogenic differentiation in 3T3L1 cells, and provide an important resource for the study of PPARgamma function in the context of adipocyte differentiation