-
The Sirt1 protein suppressed transcription of Dnmt3l.
-
The Dnmt3l mutation greatly reduced DNA methylation levels at most retrotransposons, but its impact on their RNA abundance was limited in prospermatogonia. In Pld6 mutant germ cells, although only a few retrotransposons exhibited reduced DNA methylation, many showed increased expression at the RNA level.
-
Dnmt3l-KO donor cells may offer a more permissive epigenetic state that is beneficial for Nuclear transfer reprogramming
-
By interacting with TRIM28, DNMT3L can attract various enzymes to form a DNMT3L-induced repressive complex to remove active marks and add repressive marks to histone proteins.
-
Hypomethylation of highly methylated CpG islands was caused by the downregulation of Dnmt3L and Dnmt3a due to hepatitis B X-protein bound to their promoters.
-
DNMT3L is required to delicately balance the cycling and quiescence of spermatogonial progenitor cells
-
Study demonstrates that Dnmt3L interacts with the Polycomb PRC2 complex in competition with the DNA methyltransferases Dnmt3a and Dnmt3b to maintain low methylation levels at the Histone 3 H3K27me3 regions.
-
Data indicate that expression of Dnmt3a, Dnmt3b, Dnmt3L as well as maintenance Dnmt1o in oocytes and zygotes was not disrupted.
-
Reduced expression of DNMT3L in male germ cells, associated with haploinsufficiency of the paternal-effect gene Dnmt3L, results in abnormal hypomethylation of prenatal germline progenitor cells.
-
The maternal store of Dnmt3L is not involved in embryonic de novo methylation.
-
Dnmt3l is one of the key players in de novo DNA methylation of imprinting control elements and retrotransposons, which occurs after genome-wide epigenetic erasure during germ cell development. (Review)
-
We observe evidence for a context-dependent contribution of Dnmt3l to set and maintain CpG and non-CpG methylation at distinct classes of repetitive elements and selected single copy genes
-
Data show in DNMT3L-deficient germ cells at 16.5 dpc, average DNA methylation levels were about 30% of wildtype levels; however, by postnatal day 6, about half of the DNMT3L deficiency-specific hypomethylated loci had acquired normal methylation levels.
-
Reduced dosage of the modifiers of epigenetic reprogramming Dnmt1, Dnmt3L, SmcHD1 and Foxo3a has no detectable effect on mouse telomere length in vivo.
-
show that both Dnmt3L(s) and Dnmt3L(o) produce full-length proteins but that the Dnmt3L(at) transcripts are not translated
-
The data demonstrate previously unrecognised roles for DNMT3L in late meiosis and in the transcriptional regulation of meiotic and post-meiotic germ cells.
-
CG dinucleotide recognized by the Dnmt3a and Dnmt3L complex are distinctive at retroelements and imprinted domains.
-
likely to function not directly as a DNA methyltransferase but as a regulator of methylation at imprinted loci
-
Dnmt3L is required for the establishment of methylation imprints in oocyte. Dnmt3L is required for spermatogenesis.
-
Loss of Dnmt3L from early germ cells caused meiotic failure in spermatocytes, which do not express Dnmt3L
