A growing body of evidence indicates that epigenetic mechanisms, particularly DNA methylation, play key regulatory roles in plant-nematode interactions. Nevertheless, the transcriptional activity of key genes mediating DNA methylation and active demethylation in the nematode feeding sites remains largely unknown. Here, we profiled the promoter activity of 12 genes involved in maintenance and establishment of DNA methylation and active demethylation in the syncytia and galls induced respectively by the cyst nematode and the root-knot nematode in Arabidopsis roots. The promoter activity assays revealed that expression of the CG-context is restricted to feeding site formation and development stages. C (), , and and () and , which mediate non-CG methylation, showed similar and distinct expression patterns in the syncytia and galls at various time points. Notably, the promoters of various DNA demethylases were more active in galls as compared with the syncytia, particularly during the early stage of infection. Mutants impaired in CG or CHH methylation similarly enhanced plant susceptibility to and , whereas mutants impaired in CHG methylation reduced plant susceptibility only to Interestingly, hypermethylated mutants defective in active DNA demethylation exhibited contrasting responses to infection by and , a finding most likely associated with differential regulation of defense-related genes in these mutants upon nematode infection. Our results point to methylation-dependent mechanisms regulating plant responses to infection by cyst and root-knot nematodes.
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http://dx.doi.org/10.3389/fpls.2022.1111623 | DOI Listing |
Zh Nevrol Psikhiatr Im S S Korsakova
December 2024
Mental Health Research Center, Moscow, Russia.
Mental disorders are complex illnesses with multifactorial etiologies involving genetic and environmental components. This review focuses on cellular models derived from the olfactory epithelium as a promising tool to study the molecular mechanisms of some neuropsychiatric diseases. The authors consider cell lines allowing the identification of potential biomarkers and pathogenetic mechanisms of schizophrenia, bipolar disorder, and Alzheimer's disease.
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December 2024
Department of Ecology, Evolution, and Marine Biology, Department of Molecular, Cellular, and Cell Biology, Neuroscience Research Institute, University of California, Santa Barbara, CA, 93106, USA.
Significant links between aging and DNA methylation are emerging from recent studies. On the one hand, DNA methylation undergoes changes with age, a process termed as epigenetic drift. On the other hand, DNA methylation serves as a readily accessible and accurate biomarker for aging.
View Article and Find Full Text PDFSci Rep
December 2024
Translational Oncogenomics and Bioinformatics Lab, Center for Medical Biotechnology, VIB-UGent & CRIG, Technologiepark-Zwijnaarde 75, 9052, Ghent, Belgium.
Esophageal adenocarcinoma (EAC) is an aggressive cancer characterized by a high risk of relapse post-surgery. Current follow-up methods (serum carcinoembryonic antigen detection and PET-CT) lack sensitivity and reliability, necessitating a novel approach. Analyzing cell-free DNA (cfDNA) from blood plasma emerges as a promising avenue.
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December 2024
Department Gynecological Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, No. 55, Section 4, South People's Road, Chengdu, 610041, China.
MYD88 is an IL-6 primary response gene and, its upregulation of expression has been shown to be a poor prognostic factor in epithelial ovarian cancer (EOC). We investigated the effects of CpG methylation at the proximal promoter/5'UTR and IL-6/SP1/IRF1 signaling on upregulation of MYD88 and prognosis in EOC. We assessed CpG methylation at the proximal promoter/5'UTR of MYD88 using bisulfite sequencing/PCR in 103 EOC patients, 28 normal ovarian tissues and two EOC cell lines with differential expression of MYD88 and identified the impact of the level of CpG methylation on MYD88 upregulation by SP1/IRF1 with knockdown or blockade of IL-6.
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December 2024
Department of Colorectal Surgery, The First Affiliated Hospital of Zhengzhou University, No.1 Eastern Jianshe Road, Zhengzhou, 450052, Henan, China.
Solute transport family 7A member 7 (SLC7A7) mutations contribute to lysinuric protein intolerance (LPI), which is the mechanism of action that has been extensively studied. In colorectal cancer (CRC), SLC7A7 appears to play a role, but the features and mechanisms are not yet well understood. Survival was analyzed using the Kaplan-Meier analysis.
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