Higher-order assembly enables and links pathogen recognition and downstream steps in the TRIM5-mediated anti-HIV response.

To protect mammals against retroviral infections, TRIM5 restriction factors recognize viral capsids by forming complementary hexagonal nets that can adapt to the patterns of capsid protein subunits on the viral capsid surface.

Mutations in the TRIM5α retrovirus-binding interface frequently improve but rarely disrupt retroviral restriction.

Combining in vitro and in vivo assays demonstrates that the cytidine deaminase APOBEC3A can inhibit LINE-1 retrotransposition by deaminating transiently exposed single-strand DNA that arises during the process of LINE-1 integration.

The specification of a very small number of progenitor cells with competence to adapt their neurogenic output to different probabilistic rules underlies the generation of distinct cortical cytoarchitectures.

Genomes take advantage of the gene-duplicating ability of retroelements to birth novel innate immune defense genes.

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.

The human leukemia virus HTLV-1 causes abnormal chromatin looping in tens of thousands of infected T cell clones in each host, and abnormal host transcription both flanking the integrated provirus and at distant loci in cis.

The integration of signals via the pleiotropic NF-kappaB (NF-κB) system enables microenvironmental cues to tune cellular responses to pathogenic substances.

A panel of chimpanzee induced pluripotent stem cells (iPSCs) will help realise the potential of iPSCs in primate studies, and in combination with genomic technologies, transform studies of comparative evolution.