Parental epigenetic asymmetry in mammals

Area of Science:

• Developmental Biology
• Epigenetics
• Genomics

Background:

• Early mammalian embryos exhibit genome-wide epigenetic asymmetries inherited from sperm and oocytes.
• These parental epigenetic programs are essential for embryonic development; uniparental embryos are non-viable.
• Most parental epigenetic marks are erased as the embryonic genome establishes its own chromatin signature.

Purpose of the Study:

• To review the inheritance, modification, and developmental influence of parental epigenetic asymmetries.
• To highlight the selective erasure and persistence of these asymmetries throughout embryonic development.
• To explore the implications of nongenetic germline contributions for inheritance and genomic incompatibilities.

Main Methods:

• Review of existing literature on parental epigenetic asymmetries in early mammalian embryos.
• Analysis of mechanisms for elimination, reinforcement, and protection of epigenetic marks.
• Discussion of the role of imprinted loci in maintaining parent-of-origin information.

Main Results:

• Parental epigenetic asymmetries are inherited and amplified shortly after fertilization.
• The majority of these asymmetries are lost during development, except at specific imprinted loci.
• Imprinted loci retain distinct parent-of-origin chromatin and transcriptional states throughout life.

Conclusions:

• Understanding parental epigenetic contributions is vital for insights into non-Mendelian inheritance and phenotypic variation.
• The selective maintenance of epigenetic information at imprinted loci influences development and potentially inter-parental genomic interactions.
• Further research into germline epigenetic contributions can illuminate origins of inherited traits and reproductive incompatibilities.