Differences in DNA methylation, DNA structure and embryogenesis-related gene expression between embryogenic and non embryogenic lines of Pinus radiata D. don

2017 ◽  
Vol 130 (3) ◽  
pp. 521-529 ◽  
Author(s):  
Soraya Bravo ◽  
Ariana Bertín ◽  
Aileen Turner ◽  
Francisco Sepúlveda ◽  
Paz Jopia ◽  
...  
Genomics ◽  
2020 ◽  
Vol 112 (6) ◽  
pp. 5147-5156
Author(s):  
Min Zhou ◽  
Liang Zhang ◽  
Qiao Yang ◽  
Chaochao Yan ◽  
Peng Jiang ◽  
...  

2020 ◽  
Vol 124 (9) ◽  
pp. 903-911 ◽  
Author(s):  
Yufei Zhu ◽  
Shizhao Li ◽  
Yulan Duan ◽  
Zhouzheng Ren ◽  
Xin Yang ◽  
...  

AbstractThis study aimed to evaluate the effect of in ovo feeding (IOF) of vitamin C at embryonic age 11 (E11) on post-hatch performance, immune status and DNA methylation-related gene expression in broiler chickens. A total of 240 Arbor Acres breeder eggs (63 (sem 0·5) g) were randomly divided into two groups: normal saline and vitamin C (VC) groups. After incubation, newly hatched chicks from each group were randomly divided into six replicates with ten chicks per replicate. Hatchability, average daily feed intake (D21–42 and D1–42), and average daily gain and feed conversion ratio (D1–21) were improved by vitamin C treatment (P < 0·05). IOF of vitamin C increased vitamin C content (D1), total antioxidant capacity (D42), IgA (D1), IgM (D1 and D21), stimulation index for T lymphocyte (D35) and lysozyme activity (D21) in plasma (P < 0·05). On D21, vitamin C increased the splenic expression of IL-4 and DNMT1 and decreased IL-1β, Tet2, Tet3 and Gadd45β expression (P < 0·05). On D42, vitamin C increased the splenic expression of IL-4 and DNMT3A and decreased IFN-γ, Tet3, MBD4 and TDG expression (P < 0·05). In conclusion, the vitamin C via in ovo injection can be absorbed by broiler’s embryo and IOF of vitamin C at E11 improves the post-hatch performance and immune status and, to some extent, the antioxidant capacity of broiler chickens. The expression of enzyme-related DNA methylation and demethylation indicates that the level of DNA methylation may increase in spleen in the VC group and whether the fluctuating expression of pro- and anti-inflammatory cytokines is related to DNA methylation change remained to be further investigated.


2020 ◽  
Vol 21 (12) ◽  
pp. 4476
Author(s):  
Marcela A S Pinhel ◽  
Natália Y Noronha ◽  
Carolina F Nicoletti ◽  
Vanessa AB Pereira ◽  
Bruno AP de Oliveira ◽  
...  

Weight regulation and the magnitude of weight loss after a Roux-en-Y gastric bypass (RYGB) can be genetically determined. DNA methylation patterns and the expression of some genes can be altered after weight loss interventions, including RYGB. The present study aimed to evaluate how the gene expression and DNA methylation of PIK3R1, an obesity and insulin-related gene, change after RYGB. Blood samples were obtained from 13 women (35.9 ± 9.2 years) with severe obesity before and six months after surgical procedure. Whole blood transcriptome and epigenomic patterns were assessed by microarray-based, genome-wide technologies. A total of 1966 differentially expressed genes were identified in the pre- and postoperative periods of RYGB. From these, we observed that genes involved in obesity and insulin pathways were upregulated after surgery. Then, the PIK3R1 gene was selected for further RT-qPCR analysis and cytosine-guanine nucleotide (CpG) sites methylation evaluation. We observed that the PI3KR1 gene was upregulated, and six DNA methylation CpG sites were differently methylated after bariatric surgery. In conclusion, we found that RYGB upregulates genes involved in obesity and insulin pathways.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2497-2497
Author(s):  
Michael Trus ◽  
Ying Lin ◽  
Gurmit Singh ◽  
Mark D. Minden

Abstract Abstract 2497 Background. High cure rates seen in acute promyelocytic leukemia (APL) result from adding the retinoid all trans retinoic acid (ATRA) to chemotherapy. The addition of ATRA to chemotherapy has not consistently improved survival for other acute myelogenous leukemia (AML) subtypes. This likely reflects differences in the degree ATRA overcomes transcriptional repression imposed by the epigenetic mechanisms of histone acetylation and DNA methylation between AML and APL. Purpose To determine if differences in induction of retinoic acid receptor (RAR) β2 accounts for variations in ATRA-responses between APL and AML cells and to determine the effects epigenetic modifying agents have on the expression of RARβ2 and related gene sets in AML cells. Methods Primary AML samples, NB-4 (APL), and OCI/AML-2 (AML) cell lines were cultured in standard conditions. Treatments included ATRA 1μM, valproic acid (VPA) 0.6 mM, and 5-aza-2`-deoxycytidine (5-aza-2CDR) 400 ng/mL. Gene expression was measured by real-time PCR. Histone-acetylation was measured by chromatin immunoprecipitation (ChIP) and DNA methylation by EpiTYPER. Gene expression profiles were analyzed with Affymetrix U133A arrays followed by Gene Set Enrichment Analysis (GSEA) to identify RARβ2 related gene sets. Results Treatment of APL (NB-4 and primary samples) with ATRA induced expression of RARβ2 and expression remained attenuated in similarly treated AML (OCI/AML-2 and primary samples) cells. Histone deacetylase inhibitors (HDACi) and DNA methyltransferase inhibitors (DNMTi) can potentially reverse epigenetic-mediated transcriptional repression. Treatment of OCI/AML-2 cells with the HDACi VPA and/or the DNMTi 5-aza-2CDR and treatment of primary AML samples with VPA restored ATRA-inducible RARβ2 expression. In accordance, DNA methylation and predominantly deacetylated histones were seen at the OCI/AML-2 RARβ promoter. Treatment of OCI/AML-2 cells with ATRA and VPA (HDACi) in the absence of 5-aza-2CDR (DNMTi) had little effect on DNA methylation at the RARβ promoter, however, 5-aza-2CDR treatments markedly decreased DNA methylation. An unexpected finding was VPA further reduced DNA methylation when added to 5-aza-2CDR treatment. Histone acetylation increased minimally at the RARβ promoter in ATRA-treated OCI/AML-2 cells. However, combining ATRA with VPA (HDACi) and/or 5-aza-2CDR (DNMTi) markedly increased histone acetylation that correlated with gene-induction. The greatest change in histone acetylation and DNA methylation was seen in OCI/AML-2 cells treated with the combination of ATRA + VPA + 5-aza-2CDR that correlated with the largest induction of RARβ2. Heterogeneous levels of DNA methylation were seen at the RARβ promoter in 26 primary AML samples compared to 4 normal bone marrow (NBM) samples. Levels of DNA methylation were similar to NBM in 13 AML samples (50%), decreased in 5 (19%), both increased and decreased in the same sample in 2 (8%), and increased in 6 (23%) primary AML samples. Next, we used Affymetrix gene arrays and GSEA to delineate differences in ATRA-mediated gene regulation between NB-4 (APL) and OCI/AML-2 (AML) cells and to determine whether treatment with VPA (HDACi) and 5-aza-2CDR (DNMTi) restored expression of gene sets that included RARβ2 signaling. ATRA-treatment induced twelve such gene sets in NB-4 cells and six gene sets in OCI/AML-2 cells. Treatment of OCI/AML-2 cells with VPA alone did not induce expression of RARβ2 associated gene sets, whereas treatment of OCI/AML-2 cells with 5-AZA-2CDR modulated expression of a further five gene sets that were modulated in ATRA-treated NB-4 (APL) cells. Treatment of OCI/AML-2 cells with all three agents ATRA + VPA + 5-aza-2CDR was the only treatment combination that modulated the ligand_dependent_nuclear_receptor_activity gene set. This gene set includes many genes regulating retinoid signaling and are engaged as early as 3 hours after ATRA treatment in NB-4 cells. Conclusions RARβ2 is a frequent target for transcriptional repression by epigenetic mechanisms in AML cells. Combinations of HDACi and DNMTi increase ATRA-mediated induction of RARβ2 and epigenetic modifications that favor transcription over individual treatments. This includes a possible demethylating effect of the HDACi VPA. These treatment combinations also restore modulation of a number of RARβ2 related gene sets in AML cells that are similarly regulated in ATRA-treated APL cells. Disclosures: No relevant conflicts of interest to declare.


2020 ◽  
Author(s):  
Anouschka S. Ramsteijn ◽  
Rikst Nynke Verkaik-Schakel ◽  
Danielle J. Houwing ◽  
Torsten Plösch ◽  
Jocelien D.A. Olivier

AbstractMany pregnant women experience symptoms of depression, and are often treated with selective serotonin reuptake inhibitor (SSRI) antidepressants, such as fluoxetine. In utero exposure to SSRIs and maternal depressive symptoms is associated with sex-specific effects on the brain and behavior. However, knowledge about the neurobiological mechanisms underlying these sex differences is limited. In addition, most animal research into developmental SSRI exposure neglects the influence of maternal adversity. Therefore, we used a rat model relevant to depression to investigate the molecular effects of perinatal fluoxetine exposure in male and female juvenile offspring. We performed RNA sequencing and targeted DNA methylation analyses on the prefrontal cortex and basolateral amygdala; key regions of the corticolimbic circuit. Perinatal fluoxetine enhanced myelin-related gene expression in the prefrontal cortex, while inhibiting it in the basolateral amygdala. SSRI exposure and maternal adversity interacted to affect expression of genes such as myelin−associated glycoprotein (Mag) and myelin basic protein (Mbp). We speculate that altered myelination reflects altered brain maturation. In addition, these effects are stronger in males than in females, resembling known behavioral outcomes. Finally, Mag and Mbp expression correlated with DNA methylation, highlighting epigenetic regulation as a potential mechanism for developmental fluoxetine-induced changes in myelination.


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