Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The function of 53BP1 in DNA double-strand break repair is multifaceted, and includes mediator and effector roles. New appreciation of how it is recruited to damaged chromatin, and how it exerts control on pathway choice, has cemented the central role of 53BP1 in genome stability maintenance.
Renewal and repair of the intestinal epithelium depend on small populations of intestinal stem cells. Specific markers for these stem cells have recently been discovered. This advance, together with the development of new technologies to track endogenous stem cell activity and to generate new epitheliaex vivo, is shedding light on the mechanisms underlying intestinal stem cell-driven homeostasis and regeneration.
The mechanisms that drive cell intercalation and thereby cell rearrangements during morphogenesis vary in different developmental contexts and species. Comparison of the key control steps in each case has improved our understanding of the specific parts played by adhesion and cytoskeletal changes, as well as planar cell polarity signalling.
Interactions on the mitochondrial outer membrane between members of the three subgroups of the BCL-2 protein family set the apoptotic threshold. Recent structural insights into the molecular mechanisms of this commitment to apoptosis are guiding the development of new therapeutics for cancer, and potentially also autoimmune and infectious diseases.
Autophagy was thought to be a purely cytosolic event. However, recent data highlight a role for the nucleus in autophagy regulation, showing that a complex network of histone modifications, microRNAs and transcription factors also control this process.