The maize gene maternal depression of r1 (mdr1) encodes a DNA glycosylase with maternal and paternal fertility functions

2021 ◽  
Author(s):  
Jonathan I. Gent ◽  
Kyle W. Swentowsky ◽  
Kaitlin M. Higgins ◽  
Fang-Fang Fu ◽  
Yibing Zeng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Repetitive Dna ◽  
Double Mutant ◽  
Dna Demethylation ◽  
Dna Glycosylase ◽  
Imprinted Genes ◽  
Main Function ◽  
Maize Endosperm ◽  
Maize Gene ◽  
Close Homolog

Demethylation of transposons can activate expression of nearby genes and cause imprinted gene expression in endosperm, and it is hypothesized to lead to expression of transposon siRNAs that reinforce silencing in the next generation through transfer either into egg or embryo. Here we describe maternal derepression of R1 (mdr1), a DNA glycosylase with homology to Arabidopsis DEMETER that is partially responsible for demethylation of thousands of regions in endosperm. Maternally-expressed imprinted genes were enriched strongly enriched for overlap with demethylated regions, but the majority of genes that overlapped demethylated regions were not imprinted. Demethylated regions were depleted from the majority of repetitive DNA in the genome but enriched in a set of transposon families accounting for about a tenth of the total demethylated regions. Demethylated regions produced few siRNAs and were not associated with excess CHH methylation in endosperm or other tissues. mdr1 and its close homolog dng102 are essential factors in maternal and paternal fertility in maize, as neither double mutant microgametophytes nor megagametophytes gave rise to seeds. These data establish DNA demethylation by glycosylases as essential in maize endosperm and pollen and suggest that neither transposon regulation nor genomic imprinting are its main function.

DNA Demethylation Regulates Anabolic and Catabolic Gene Expression in Intervertebral Disc Cells

2014 ◽  
Vol 4 (1_suppl) ◽  
pp. s-0034-1376587-s-0034-1376587
Author(s):  
N. Chutkan ◽  
R. Sangani ◽  
H. Zhou ◽  
S. Fulzele
Keyword(s):  
Gene Expression ◽  
Intervertebral Disc ◽  
Dna Demethylation ◽  
Catabolic Gene ◽  
Disc Cells

Reparação óssea no implante dental

2020 ◽  
Vol 12 (45) ◽  
pp. 63-66
Author(s):  
Halim Nagem Filho ◽  
Reinaldo Francisco Maia ◽  
Reinaldo Missaka ◽  
Nasser Hussein Fares
Keyword(s):  
Gene Expression ◽  
Titanium Surface ◽  
Close Contact ◽  
The Other ◽  
Main Function ◽  
Indirect Interaction ◽  
M2 Macrophages ◽  
Activated Macrophages ◽  
M1 Macrophages ◽  
High Production

The osseointegration is the stable and functional union between the bone and a titanium surface. A new bone can be found on the surface of the implant about 1 week after its installation; the bone remodeling begins between 6 and 12 weeks and continues throughout life. After the implant insertion, depending on the energy of the surface, the plasma fluid immediately adheres, in close contact with the surface, promoting the adsorption of proteins and inducing the indirect interaction of the cells with the material. Macrophages are cells found in the tissues and originated from bone marrow monocytes. The M1 macrophages orchestrate the phagocytic phase in the inflammatory region and also produce inflammatory cytokines involved with the chronic inflammation and the cleaning of the wound and damaged tissues from bacteria. On the other hand, alternative-activated macrophages (M2) are activated by IL-10, the immune complex. Its main function consists on regulating negatively the inflammation through the secretion of the immunosuppressant IL-10. The M2 macrophages present involvement with the immunosuppression, besides having a low capacity for presenting antigens and high production of cytokines; these can be further divided into M2a, M2b, and M2c, based on the gene expression profile.

scholarly journals Maternal prenatal depression is associated with decreased placental expression of the imprinted gene PEG3

2016 ◽  
Vol 46 (14) ◽  
pp. 2999-3011 ◽  
Author(s):  
A. B. Janssen ◽  
L. E. Capron ◽  
K. O'Donnell ◽  
S. J. Tunster ◽  
P. G. Ramchandani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Maternal Depression ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Prenatal Depression ◽  
Placental Lactogen ◽  
Maternal Behaviour ◽  
Imprinted Genes ◽  
Neurodevelopmental Outcomes

BackgroundMaternal prenatal stress during pregnancy is associated with fetal growth restriction and adverse neurodevelopmental outcomes, which may be mediated by impaired placental function. Imprinted genes control fetal growth, placental development, adult behaviour (including maternal behaviour) and placental lactogen production. This study examined whether maternal prenatal depression was associated with aberrant placental expression of the imprinted genes paternally expressed gene 3 (PEG3), paternally expressed gene 10 (PEG10), pleckstrin homology-like domain family a member 2 (PHLDA2) and cyclin-dependent kinase inhibitor 1C (CDKN1C), and resulting impaired placental human placental lactogen (hPL) expression.MethodA diagnosis of depression during pregnancy was recorded from Manchester cohort participants’ medical notes (n = 75). Queen Charlotte's (n = 40) and My Baby and Me study (MBAM) (n = 81) cohort participants completed the Edinburgh Postnatal Depression Scale self-rating psychometric questionnaire. Villous trophoblast tissue samples were analysed for gene expression.ResultsIn a pilot study, diagnosed depression during pregnancy was associated with a significant reduction in placental PEG3 expression (41%, p = 0.02). In two further independent cohorts, the Queen Charlotte's and MBAM cohorts, placental PEG3 expression was also inversely associated with maternal depression scores, an association that was significant in male but not female placentas. Finally, hPL expression was significantly decreased in women with clinically diagnosed depression (44%, p < 0.05) and in those with high depression scores (31% and 21%, respectively).ConclusionsThis study provides the first evidence that maternal prenatal depression is associated with changes in the placental expression of PEG3, co-incident with decreased expression of hPL. This aberrant placental gene expression could provide a possible mechanistic explanation for the co-occurrence of maternal depression, fetal growth restriction, impaired maternal behaviour and poorer offspring outcomes.

scholarly journals ROS1 5-methylcytosine DNA glycosylase is a slow-turnover catalyst that initiates DNA demethylation in a distributive fashion

2009 ◽  
Vol 37 (13) ◽  
pp. 4264-4274 ◽  
Author(s):  
María Isabel Ponferrada-Marín ◽  
Teresa Roldán-Arjona ◽  
Rafael R. Ariza
Keyword(s):  
Dna Demethylation ◽  
Dna Glycosylase ◽  
Slow Turnover

scholarly journals TET2 coactivates gene expression through demethylation of enhancers

2018 ◽  
Vol 4 (11) ◽  
pp. eaau6986 ◽  
Author(s):  
Lu Wang ◽  
Patrick A. Ozark ◽  
Edwin R. Smith ◽  
Zibo Zhao ◽  
Stacy A. Marshall ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Regulation Of Gene Expression ◽  
Estrogen Receptor Α ◽  
Dna Demethylation ◽  
Estrogen Response ◽  
Dna Base ◽  
Modified Dna ◽  
Global Increase ◽  
Methylation Patterns

The tet methylcytosine dioxygenase 2 (TET2) enzyme catalyzes the conversion of the modified DNA base 5-methylcytosine to 5-hydroxymethylcytosine. TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. Here, using newly developed TET2-specific antibodies and the estrogen response as a model system for studying the regulation of gene expression, we demonstrate that endogenous TET2 occupies active enhancers and facilitates the proper recruitment of estrogen receptor α (ERα). Knockout of TET2 by CRISPR-CAS9 leads to a global increase of DNA methylation at enhancers, resulting in attenuation of the estrogen response. We further identified a positive feedback loop between TET2 and ERα, which further requires MLL3 COMPASS at these enhancers. Together, this study reveals an epigenetic axis coordinating a transcriptional program through enhancer activation via DNA demethylation.

scholarly journals High-throughput analysis of candidate imprinted genes and allele-specific gene expression in the human term placenta

BMC Genetics ◽  
2010 ◽  
Vol 11 (1) ◽  
pp. 25 ◽  
Author(s):  
Caroline Daelemans ◽  
Matthew E Ritchie ◽  
Guillaume Smits ◽  
Sayeda Abu-Amero ◽  
Ian M Sudbery ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Throughput ◽  
Specific Gene ◽  
Imprinted Genes ◽  
High Throughput Analysis ◽  
Human Term Placenta ◽  
Throughput Analysis ◽  
Term Placenta ◽  
Specific Gene Expression ◽  
Allele Specific

scholarly journals Genomic imprinting and its role in ethiology of human hereditary diseases

2004 ◽  
Vol 3 (3) ◽  
pp. 8-17
Author(s):  
S. A. Nazarenko
Keyword(s):  
Gene Expression ◽  
Genomic Imprinting ◽  
Special Class ◽  
Growth And Development ◽  
Epigenetic Inheritance ◽  
Hereditary Diseases ◽  
Parental Origin ◽  
Imprinted Genes ◽  
Methylation Of Dna ◽  
Differential Gene

Genomic imprinting is a form of non-Mendelian epigenetic inheritance that is defined by differential gene expression depending on its parental origin — maternal or paternal. It is known about 60 imprinted genes many of which effect significantly on the fetus growth and development. Methylation of DNA cytosine bases that defines the interaction of DNA and proteins identifying the modified bases and controls the gene expression through chromatin compacting-decompacting mechanism, is a main epigenetic genom modifier. Disturbances in monoallelic gene expression lead to the development of a special class of human hereditary diseases — genomic imprinting diseases.

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