Volume 15 Issue 1, January 2014

Der1 ensures transit of misfolded substrates for ER-associated degradation.

FtsA has a dual role in FtsZ network assembly and rearrangement.

YTHDF2 is a 'reader' protein that recognizes m⁶A-containing mRNAs and targets them for degradation.

Lin28aenhances tissue repair by increasing oxidative metabolism.

RZZ interacts with NDC-80 to inhibit the formation of end-coupled microtubule attachments.

Three-dimensional trajectories of chromatin have been visualized by Hi-C.

The role of E2F transcription factors in apoptosis depends on effects on mitochondrial function, as well as the transcription of pro-apoptotic genes.

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.