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Loss of DNA methylation disrupts syncytiotrophoblast development: Proposed consequences of aberrant germline gene activation

Lea, Georgia ; Hanna, Courtney W.

BioEssays, 2024-01, Vol.46 (1), p.e2300140-n/a [Revista revisada por pares]

United States: Wiley Subscription Services, Inc

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Loss of DNA methylation disrupts syncytiotrophoblast development: Proposed consequences of aberrant germline gene activation
Autor: Lea, Georgia ; Hanna, Courtney W.
Materias: Ablation ; Animal models ; Animals ; Deoxyribonucleic acid ; DNA ; DNA (Cytosine-5-)-Methyltransferases - genetics ; DNA (Cytosine-5-)-Methyltransferases - metabolism ; DNA methylation ; DNA Methylation - genetics ; DNA methyltransferase ; Epigenetics ; Female ; Gametogenesis ; Gene regulation ; Gene silencing ; Genes ; Germ Cells ; germline genes ; Lethality ; Meiosis ; Mice ; Mice, Transgenic ; Molecular modelling ; Phenotypes ; piRNA ; placenta ; Placenta - metabolism ; Pregnancy ; Transcription ; Transcriptional Activation ; Transgenic mice ; trophoblast ; Trophoblasts - metabolism
Es parte de: BioEssays, 2024-01, Vol.46 (1), p.e2300140-n/a
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descripción: DNA methylation is a repressive epigenetic modification that is essential for development and its disruption is widely implicated in disease. Yet, remarkably, ablation of DNA methylation in transgenic mouse models has limited impact on transcriptional states. Across multiple tissues and developmental contexts, the predominant transcriptional signature upon loss of DNA methylation is the de‐repression of a subset of germline genes, normally expressed in gametogenesis. We recently reported loss of de novo DNA methyltransferase DNMT3B resulted in up‐regulation of germline genes and impaired syncytiotrophoblast formation in the murine placenta. This defect led to embryonic lethality. We hypothesize that de‐repression of germline genes in the Dnmt3b knockout underpins aspects of the placental phenotype by interfering with normal developmental processes. Specifically, we discuss molecular mechanisms by which aberrant expression of the piRNA pathway, meiotic proteins or germline transcriptional regulators may disrupt syncytiotrophoblast development. DNA methyltransferase 3B (Dnmt3b) knockout conceptuses show embryonic lethality due to impaired placental formation. These placental cells exhibit aberrant DNA methylation and de‐repression of germline genes. We propose that germline gene expression disrupts normal placental development through altered transcript regulation, disrupted cell division, and spurious piRNA silencing of endogenous retroviruses.
Editor: United States: Wiley Subscription Services, Inc
Idioma: Inglés

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Loss of DNA methylation disrupts syncytiotrophoblast development: Proposed consequences of aberrant germline gene activation

Lea, Georgia ; Hanna, Courtney W.

United States: Wiley Subscription Services, Inc

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