Natasha Zamudio

TL;DR: It is shown that DNMT3C is the enzyme responsible for methylating the promoters of evolutionarily young retrotransposons in the male germ line and that this specialized activity is required for mouse fertility, revealing the plasticity of the mammalian DNA methylation system and expanding the scope of the mechanisms involved in the epigenetic control of retro transposons.

TL;DR: Paternal effects of this type have not been reported previously in mammals and suggest that the untransmitted genotype of male parents can influence the phenotype of their offspring.

TL;DR: Biochemical and structural studies demonstrate that these compounds are reversible competitors of acetyl coenzyme A and inhibit MYST-catalysed histone acetylation, induce cell cycle exit and cellular senescence without causing DNA damage, and arrest lymphoma progression in mouse models.

TL;DR: Recent insights are reviewed that have provided a detailed picture of the defense mechanisms that concur toward retrotransposon silencing in mammalian genomes, and in particular in the germline.

TL;DR: It is demonstrated that DNA methylation restrains transposons from adopting chromatin characteristics amenable to meiotic recombination, which is proposed prevents the occurrence of erratic chromosomal events.