Post-translational regulation of retrotransposons plays a key role in preventing retrotransposon mobilization in the epigenetically dynamic mouse germline.

The expression of human L1 retrotransposons is highly locus-specific and variable between different cell types.

Retrotransposon-derived messenger RNA plays a critical role in rice root development via sequestration of miR171, which suggests a novel trans-acting regulation by transposable elements.

The mechanisms by which a retrotransposon called LINE-1 duplicates itself and spreads through the human genome are becoming clearer.

The reanalysis of data from a recent study that claimed retrotransposon mutations are ubiquitous in the human brain outlines a general framework for the design and analysis of single-cell genomics studies.

The range of molecular forms adopted by L1 retrotransposons reflect a tapestry of lifecycle-permissive and -restrictive host-parasite interactions occurring within cells.

The maternally provided histone demethylase LSD1/KDM1A has an instrumental role at the beginning of life, shaping the histone methylation landscape and the transcriptional repertoire of the early mouse embryo.

A combination of functional, biochemical and imaging studies show that LINE-1/L1 proteins and mRNA enter the nucleus through mitotic nuclear membrane breakdown, interact with components of the DNA replication fork and mediate retrotransposition during S phase.

Research into genomic imprinting has provided a foundation for the study of epigenetic mechanisms, especially during development, and has also shed light on a range of rare genetic disorders and common diseases.

Soon after fertilisation, a critical portion of the embryonic genome is switched on through the actions of maternally inherited Stella, in part through controlling the activation of transposable elements.