Correlation between the methylation of the FUT1 promoter region and FUT1 expression in the duodenum of piglets from newborn to weaning

Dai, Chaohui; Sun, Li; Xia, Riwei; Sun, Shengyuan; Zhu, Guoqiang; Wu, Shenglong; Bao, Wenbin

doi:10.1007/s13205-017-0880-9

Cited by 8 publications

(6 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Methylation sequencing revealed that the 13 CpG sites in the sequencing region were methylated to varying degrees, and one of the CpG sites (mC-7) had a significant difference in methylation level between the E. coli F18-infected and -uninfected IPEC-J2 cells. Studies have confirmed that the DNA methylation of FUT1 and FUT2 promoters controls their expression, which in turn controls weaned piglets' resistance to the ETEC F18 pathogen [35,36]. Additionally, there are also studies indicating that ETEC F4ab/ac infection can trigger variation in DNA methylation and alter the expression of genes associated with immune responses [37].…”

Section: Discussionmentioning

confidence: 88%

Identification of a 5-Methylcytosine Site (mC-7) That May Inhibit CXCL11 Expression and Regulate E. coli F18 Susceptibility in IPEC-J2 Cells

Shi

Huang

et al. 2022

Veterinary Sciences

Self Cite

View full text Add to dashboard Cite

The primary pathogen causing post-weaning diarrhea in piglets is Escherichia coli F18 (E. coli F18), hence it is essential to investigate the mechanism governing E. coli F18 resistance in native pig breeds. Based on the previous RNA-seq results of the duodenum from E. coli F18-resistant and -susceptible Meishan piglets, CXCL11, an important functional gene, was preliminarily screened. In this investigation, in order to further examine the expression regulation mechanism of E. coli F18 in intestinal porcine epithelial cells (IPEC-J2) against E. coli F18 infection, CXCL11 gene expression on IPEC-J2 cells infected by E. coli F18 was detected, which was significantly downregulated (p < 0.01). Secondly, the overexpression on the IPEC-J2 cell line was successfully structured, and a relative quantification method of the PILIN, bacteria enumeration, and immunofluorescence assay indicated that the CXCL11 overexpression significantly reduced the ability of E. coli F18 to interact with IPEC-J2 in vitro. The promoter region of the CXCL11 gene was predicted to contain a CpG island (−619 ~ −380 bp) of which 13 CpG sites in the sequencing region were methylated to varying degrees, and the methylation level of one CPG site (mC-7) positively linked negatively with the expression of the CXCL11 gene (p < 0.05). Meanwhile, a dual luciferase assay detected the mutation of the mC-7 site that significantly inhibited the luciferase activity of the CXCL11 gene promoter (p < 0.01). Transcription factor prediction and expression verification indicated that mC-7 is located in the OSR1-binding domain, and that its expression level is related to E. coli F18 susceptibility. We speculated that methylation modification of the mC-7 site of the CpG island in the promoter region of the CXCL11 gene might inhibit the binding of transcription factor OSR1 with the mC-7 site, and then affect its expression level to regulate the susceptibility to E. coli F18.

show abstract

Section: Discussionmentioning

confidence: 88%

Identification of a 5-Methylcytosine Site (mC-7) That May Inhibit CXCL11 Expression and Regulate E. coli F18 Susceptibility in IPEC-J2 Cells

Shi

Huang

et al. 2022

Veterinary Sciences

Self Cite

View full text Add to dashboard Cite

show abstract

“…Research has reported that bacterial endotoxins have profound impacts on gene expression in intestinal epithelial cells through DNA methylation modifications. The expressions of FUT1 (Dai et al, 2017) and FUT2 (Wu et al, 2018) were epigenetically modulated by DNA methylation of their promoters, regulating ETEC F18 resistance in weanling piglets. Other studies also addressed the impact of infection and LPS on the DNA methylation status of immune cells.…”

Section: Introductionmentioning

confidence: 99%

Combined Analysis of RRBS DNA Methylome and Transcriptome Reveal Novel Candidate Genes Related to Porcine Clostridium perfringens Type C-Induced Diarrhea

et al. 2022

View full text Add to dashboard Cite

Clostridium perfringens type C (Cp) is one of the principal microorganisms responsible for bacterial diarrhea in neonatal and pre-weaning piglets. To better understand the molecular effects of Cp infection, we performed a genome-wide comparison of the changes in DNA methylation and gene expression in Cp infected resistant and susceptible piglets. We characterized the pattern of changes in methylation and found 6485, 5968, and 6472 differentially methylated regions (DMRs) of piglets infected with Cp in IR vs. IC, IS vs. IC, and IS vs. IR groups, respectively. These methylation changes for genes mainly involved in immune and inflammatory responses, cell adhesion, and activation of transcription factors. Gene ontology and KEGG pathway analyses showed that the differentially methylated genes (DMGs) were associated with negative regulation of transcription, apoptotic processes, protein binding, and kinase activity. In addition, they were enriched in immunity-related pathways, such as MAPK signaling pathway, Toll-like receptor signaling pathway, and NF-kappa B signaling pathway. Integrative analysis identified 168, 198, and 7 mRNAs showing inverse correlations between methylation and expression with Cp infection. Altered DNA methylation and expression of various genes suggested their roles and potential functional interactions upon Cp infection, 14 immune-associated mRNAs with differential methylation and transcriptional repression were identified in IS vs. IR, commonly revealing that the differentially expressed genes (DEGs) LBP, TBX21, and LCN2 were likely involved in the piglets against Cp infection. The present results provide further insight into the DNA methylation epigenetic alterations of C. perfringens type C infected piglet ileum tissues, and may advance the identification of biomarkers and drug targets for predicting susceptibility to and controlling C. perfringens type C-induced piglet diarrhea.

show abstract

“…It has been reported that DNA methylation plays a crucial role in maintaining cell function, regulating individual development and disease [2][3][4]. DNA methylation is considered to be a significant research hotspot in the current field of pig genetics and breeding, relevant studies mainly focus on tissue-specific expression [5,6], cell apoptosis [7], variety differences [8], growth and development [9][10][11], immune response [12,13]. However, DNA methylation has been rarely reported in expression regulation of pig resistance to pathogenic microorganism infection.…”

Section: Introductionmentioning

confidence: 99%

DNA Methylation of Pig FUT3 Promoter Alters mRNA Expression to Regulate E. coli F18 Susceptibility

Shi

Jin

et al. 2021

Genes

Self Cite

View full text Add to dashboard Cite

Post-weaning diarrhea (PWD) is frequently associated with E. coli F18 infections in piglets. However, the underlying molecular mechanism concerning the resistance of E. coli F18 in local weaned piglets in China is not clearly understood. In the present study, by a comparative analysis of the transcriptome, a-1,3-fucosyltransferase (FUT3) was evaluated as a key candidate correlated with resistance to E. coli F18 in Sutai and Meishan piglets. Functional analysis demonstrated that FUT3 acts as a key positive regulator of E. coli F18 susceptibility in newly food accustomed piglets. However, the core promoter of FUT3 was present at −500–(−206) bp (chr.2: g.73171117–g.73171616), comprising of 9 methylated CpG sites. Among these, the methylation levels of the two CpG sites (mC-3, mC-5) located in HIF1A and Sp1 transcription factor (TF) considerably associated with mRNA expression of FUT3 (p < 0.05). Our findings indicated that the methylation of mC-3 and mC-5 sites has certain inhibitory effect on FUT3 expression and promotes the resistance of E. coli F18 in piglets. The underlined study may explore FUT3 as a new candidate target in E. coli F18 infection in Chinese local weaned piglets.

show abstract

Correlation between the methylation of the FUT1 promoter region and FUT1 expression in the duodenum of piglets from newborn to weaning

Cited by 8 publications

References 36 publications

Identification of a 5-Methylcytosine Site (mC-7) That May Inhibit CXCL11 Expression and Regulate E. coli F18 Susceptibility in IPEC-J2 Cells

Identification of a 5-Methylcytosine Site (mC-7) That May Inhibit CXCL11 Expression and Regulate E. coli F18 Susceptibility in IPEC-J2 Cells

Combined Analysis of RRBS DNA Methylome and Transcriptome Reveal Novel Candidate Genes Related to Porcine Clostridium perfringens Type C-Induced Diarrhea

DNA Methylation of Pig FUT3 Promoter Alters mRNA Expression to Regulate E. coli F18 Susceptibility

Contact Info

Product

Resources

About