IGF2R, KCNQ1, PLAGL1, and SNRPN DNA methylation is completed in bovine by the early antral follicle stage

Imprinted genes are inherited with different DNA methylation patterns depending on the maternal or paternal origin of the allele. In cattle (Bos taurus), abnormal methylation of these genes is linked to the large offspring syndrome, a neonatal overgrowth phenotype analogous to the human Beckwith–Wie...

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Bibliographic Details
Published in:Molecular reproduction and development 2022-07, Vol.89 (7), p.290-297
Main Authors: Lafontaine, Simon, Sirard, Marc‐André
Format: Article
Language:English
Subjects:
Bos taurus
bovine
DNA methylation
DNA methylation
Embryos
Follicles
Folliculogenesis
imprinting
Insulin-like growth factor II receptors
KCNQ1 protein
Neonates
oocyte
Oocytes
Phenotypes
Potassium channels (voltage-gated)
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Summary:Imprinted genes are inherited with different DNA methylation patterns depending on the maternal or paternal origin of the allele. In cattle (Bos taurus), abnormal methylation of these genes is linked to the large offspring syndrome, a neonatal overgrowth phenotype analogous to the human Beckwith–Wiedemann syndrome. We hypothesized that in bovine oocytes, some of the methylation patterns on maternally imprinted genes are acquired in the last phase of folliculogenesis. The pyrosequencing analysis of IGF2R, KCNQ1, PLAGL1, and SNRPN imprinted genes showed no clear progression of methylation in oocytes from follicles 1–2 mm (late pre antral/early antral) and up. Instead, these oocytes displayed complete methylation at the imprinted differentially methylated regions (>80%). Other mechanisms related to imprint maintenance should be investigated to explain the hypomethylation at IGF2R, KCNQ1, PLAGL1, and SNRPN maternally imprinted sites observed in some bovine embryos. Hypothesis 1: “Late imprinting.” Late onset of methylation of imprinted genes could mean that an incomplete methylation pattern is transmitted to the embryo (invalidated). Hypothesis 2: “Early imprinting.” Imprinted genes are methylated early during follicular development. Abnormal embryo methylation is a result of imprint maintenance failure.
ISSN:1040-452X
1098-2795
DOI:10.1002/mrd.23621