scholarly journals Estrogen signaling, through estrogen receptor β, regulates DNA methylation and its machinery in male germ line in adult rats

Epigenetics ◽  
2017 ◽  
Vol 12 (6) ◽  
pp. 476-483 ◽  
Author(s):  
Kushaan Dumasia ◽  
Anita Kumar ◽  
Sharvari Deshpande ◽  
Nafisa H. Balasinor
Keyword(s):  
Dna Methylation ◽  
Estrogen Receptor ◽  
Germ Line ◽  
Estrogen Receptor Β ◽  
Estrogen Signaling ◽  
Male Germ Line ◽  
Adult Rats

scholarly journals De Novo DNA Methylation in the Male Germ Line Occurs by Default but Is Excluded at Sites of H3K4 Methylation

Cell Reports ◽  
2013 ◽  
Vol 4 (1) ◽  
pp. 205-219 ◽  
Author(s):  
Purnima Singh ◽  
Arthur X. Li ◽  
Diana A. Tran ◽  
Nathan Oates ◽  
Eun-Rim Kang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
De Novo ◽  
Germ Line ◽  
H3k4 Methylation ◽  
Male Germ Line

scholarly journals Δ9-Tetrahydrocannabinol Disrupts Estrogen-Signaling through Up-Regulation of Estrogen Receptor β (ERβ)

2013 ◽  
Vol 26 (7) ◽  
pp. 1073-1079 ◽  
Author(s):  
Shuso Takeda ◽  
Kazutaka Yoshida ◽  
Hajime Nishimura ◽  
Mari Harada ◽  
Shunsuke Okajima ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Estrogen Signaling

scholarly journals Estrogen receptor β acts as a dominant regulator of estrogen signaling

Oncogene ◽  
2000 ◽  
Vol 19 (43) ◽  
pp. 4970-4978 ◽  
Author(s):  
Katarina Pettersson ◽  
Franck Delaunay ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Estrogen Signaling

scholarly journals Timing and Sequence Requirements Defined for Embryonic Maintenance of Imprinted DNA Methylation at Rasgrf1

2006 ◽  
Vol 26 (24) ◽  
pp. 9564-9570 ◽  
Author(s):  
Rebecca Holmes ◽  
Yanjie Chang ◽  
Paul D. Soloway
Keyword(s):  
Dna Methylation ◽  
Germ Line ◽  
Direct Repeat ◽  
Repeat Sequence ◽  
Paternal Allele ◽  
Imprinted Genes ◽  
Male Germ Line ◽  
Specific Expression ◽  
Morula Stage ◽  
Allele Specific

ABSTRACT Epigenetic programming is critical for normal development of mammalian embryos. Errors cause misexpression of genes and aberrant development (E. Li, C. Beard, and R. Jaenisch, Nature 366:362-365, 1993). Imprinted genes are important targets of epigenetic regulation, but little is known about how the epigenetic patterns are established in the parental germ lines and maintained in the embryo. Paternal allele-specific expression at the imprinted Rasgrf1 locus in mice is controlled by paternal allele-specific methylation at a differentially methylated domain (DMD). DMD methylation is in turn controlled by a direct repeat sequence immediately downstream of the DMD which is required for establishing Rasgrf1 methylation in the male germ line (B. J. Yoon et al., Nat. Genet. 30:92-96, 2002). To determine if these repeats have a role in methylation maintenance, we developed a conditional deletion of the repeat sequence in mice and showed that the repeats are also required during a narrow interval to maintain paternal methylation of Rasgrf1 in developing embryos. Removing the repeats upon fertilization caused a total loss of methylation by the morula stage, but by the epiblast stage, the repeats were completely dispensable for methylation maintenance. This developmental interval coincides with genome-wide demethylation and remethylation in mice which most imprinted genes resist. Our data show that the Rasgrf1 repeats serve at least two functions: first, to establish Rasgrf1 DNA methylation in the male germ line, and second, to resist global demethylation in the preimplantation embryo.

scholarly journals Estrogen Signaling via Estrogen Receptor β

2010 ◽  
Vol 285 (51) ◽  
pp. 39575-39579 ◽  
Author(s):  
Chunyan Zhao ◽  
Karin Dahlman-Wright ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Estrogen Signaling

302 IMPRINTED microRNA ARE DIFFERENTIALLY EXPRESSED IN ADULT MOUSE TESTES-DERIVED MALE GERM-LINE STEM CELLS

2011 ◽  
Vol 23 (1) ◽  
pp. 248
Author(s):  
J. Y. Shin ◽  
Y. H. Jung ◽  
M. K. Gupta ◽  
S. J. Uhm ◽  
S. T. Shin ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Stem Cells ◽  
Germ Line ◽  
Es Cells ◽  
Embryonic Stem ◽  
Culture Conditions ◽  
Male Germ Line ◽  
Comparison Results ◽  
Differentiation Stage

Testis-derived male germ-line stem (GS) cells, the in vitro counterpart of spermatogonial stem cells, can acquire multipotency under appropriate culture conditions to become multipotent adult germ-line stem (maGS) cells, which, upon testicular transplantation, produce teratomas instead of initiating spermatogenesis. This study evaluated the DNA methylation and expression of imprinted microRNA (miRNA) in mouse GS and maGS cells. The GS and maGS cell lines were established essentially as described earlier (Jung et al. 2010 Mol. Hum. Reprod. PMID: 20610616) and were quantified for maternally (miR-296-3p, miR-296-5p, miR-483) and paternally (miR-127, miR-127-5p) imprinted miRNA by real-time TaqMan® MicroRNA assay and for DNA methylation at imprinting control regions of respective miRNA (Gnas-Nespas DMR, Igf2-H19 ICR, and Dlk1-Dio3 IG-DMR) by bisulfite genomic sequencing. Sperm and embryonic stem (ES) cells were used as controls for comparison. Results showed that, similar to sperm, expression of maternally imprinted miRNA was consistently higher (P < 0.001), whereas that of paternally imprinted miRNA was consistently lower (P < 0.001) in GS cells than in control ES cells. The DNA methylation analyses further confirmed that imprinted miRNA were androgenetic in GS cells. On the other hand, DNA methylation of maGS cells resembled that of ES cells, but the expression pattern of imprinted miRNA was intermediate between that of GS cells and ES cells. The expression of imprinted miRNA in GS and maGS cells was also altered during their in vitro differentiation but varied with both the differentiation stage and the miRNA. In conclusion, our data suggest that GS cells have androgenetic DNA methylation and expression of imprinted miRNA which changes to an ES cell-like pattern upon their conversion to maGS cells and, therefore, may serve as an epigenetic miRNA signature or molecular marker to distinguish GS cells from maGS cells. This work was supported by a grant (Code #200901FHT010305191) from BioGreen 21 Program, RDA, Republic of Korea.

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