The Role of Epigenetics in Addiction: Clinical Overview and Recent Updates.

Addiction is an international public health problem. It is a polygenic disorder best understood by accounting for the interplay between genetic and environmental factors. A recent way of perceiving this interaction is through epigenetics, which help grasp the neurobiological changes that occur in addiction and explain its relapsing-remitting nature.

Mouse REC114 is essential for meiotic DNA double-strand break formation and forms a complex with MEI4.

Programmed formation of DNA double-strand breaks (DSBs) initiates the meiotic homologous recombination pathway. This pathway is essential for proper chromosome segregation at the first meiotic division and fertility. Meiotic DSBs are catalyzed by Spo11.

paralogs are new members of the piRNA pathway controlling retrotransposon suppression.

genes are mammalian specific and duplicated to give and in some species, such as the mouse and rat. It has been demonstrated that mutant males display a variable degree of infertility whereas they all upregulate MMERVK10C transposons in their germ line. In order to study the function of both paralogs in the mouse, we generated and studied double knockout (DKO) mutant mice.

Tex19 and Sectm1 concordant molecular phylogenies support co-evolution of both eutherian-specific genes.

Background: Transposable elements (TE) have attracted much attention since they shape the genome and contribute to species evolution. Organisms have evolved mechanisms to control TE activity. Testis expressed 19 (Tex19) represses TE expression in mouse testis and placenta.

The mammalian-specific Tex19.1 gene plays an essential role in spermatogenesis and placenta-supported development.

Study Question: What is the consequence of Tex19.1 gene deletion in mice?

Summary Answer: The Tex19.1 gene is important in spermatogenesis and placenta-supported development.

TRIM28 repression of retrotransposon-based enhancers is necessary to preserve transcriptional dynamics in embryonic stem cells.

TRIM28 is critical for the silencing of endogenous retroviruses (ERVs) in embryonic stem (ES) cells. Here, we reveal that an essential impact of this process is the protection of cellular gene expression in early embryos from perturbation by cis-acting activators contained within these retroelements. In TRIM28-depleted ES cells, repressive chromatin marks at ERVs are replaced by histone modifications typical of active enhancers, stimulating transcription of nearby cellular genes, notably those harboring bivalent promoters.