Volume 14 Issue 8, August 2013

A vesicle-based mechanism to regulate the dynamics and density of intracellular actin networks.

Cell migration through tight spaces becomes restricted by nuclear deformation.

The timing of SHC1 phosphorylation events regulates the output of EGF signalling.

BRD4 inhibits the propagation of the DDR by recruiting a chromatin-condensing complex to acetylated histones.

MBNL proteins regulate alternative splicing events that affect pluripotency and reprogramming.

Different cell types engage in a 'chase-and-run' behaviour to drive collective cell migration.

The discovery that GSK3β is a target of lithium.

The extracellular matrix (ECM) is a key component of the stem cell niche and is now emerging as more than just an inert scaffold. Indeed, new technologies have provided mechanistic insights into the effects of the ECM on stem cell fate choice.

The mechanisms that regulate miRNA stability and the generation of distinct miRNA isoforms are beginning to be elucidated. Better understanding of how such miRNAs mediate gene expression control will require quantitative analyses that dissect different models of miRNA function.

Lineage-tracing and genetic labelling technologies, combined with statistical analyses of cell proliferation and clonal fate, provide powerful tools to study the mechanisms and dynamics of stem and progenitor cell fate determination in development and disease.

The ability of integrins to link the extracellular environment to intracellular networks enables cells to respond to chemical and physical cues. Insight has been gained into how talins and kindlins, two families of FERM-domain proteins that bind the cytoplasmic tail of integrins, mediate integrin activation and the cellular processes that depend on this.

Recent work revealed new insights into the temporal regulation of G1–S cell cycle transcription, during proliferation and in response to activation of the DNA replication checkpoint. This has established the importance of G1–S transcription for both cell cycle progression and the maintenance of genome stability.

The adult mammalian heart has limited potential for regeneration and repair. Progress has been made in elucidating the cellular processes and regulatory mechanisms involved in heart growth and development, and this can be exploited to restore function in the injured adult heart.