Opinion

Both microRNAs (miRNAs) and other small non-coding RNAs (ncRNAs) are induced by DNA breaks and have been linked to the DNA damage response. This interplay between ncRNAs and repair factors may help to ensure efficient DNA repair and maintenance of genome stability.

Myofilament length is a crucial parameter for efficient skeletal muscle contraction. Thin actin filament specification can be explained by a novel 'two-segment' model, whereby the filament consists of two concatenated segments that are of either constant or variable length. This model implicates that actin dynamics are subject to position-specific microregulation.

An increasing number of proteins have been discovered that evade turnover and instead are maintained over a cell's lifetime. Accumulation of damage in these long-lived proteins may contribute to the ageing process.

Three surveillance pathways specialize in the degradation of mRNA molecules trapped in stalled translation complexes: the non-stop decay (NSD), the no-go decay (NGD) and the 18S-rRNA decay (18S-NRD) pathways. These quality control mechanisms degrade faulty mRNAs and contribute to maintaining the production of functional proteins.

Research on the cadherin–junctional actin interaction has focused on how the two physically interact. However, the actin cytoskeleton is dynamic, regulated by a network of proteins, so a broader perspective that takes this into account may provide new insights on cadherin cell–cell contacts and on the role of cadherins in disease.

Forces transmitted through cell–cell and cell–extracellular matrix adhesions control cell fate decisions. But how are mechanical cues translated into gene expression programmes? The transcriptional regulators YAP and TAZ have arisen as convergence points of mechanical and biochemical signals.

Membrane trafficking relies on changes in membrane identity, which are determined by RAB GTPases and phosphoinositides. Coordinated regulation of RABs and phosphoinositides, which is achieved by direct physical and functional interactions between their regulatory enzymes, is emerging as a central mechanism to ensure membrane trafficking fidelity.

Metabolic signalling pathways and telomere shortening are both thought to, independently, have crucial roles in driving the ageing process. But links between these two processes suggest that they may converge on mitochondria to compromise energy maintenance, thereby driving ageing.

Increasing evidence suggests that cell-to-cell communication in mammals can occur through the exchange of genetic information, mainly in the form of microRNAs (miRNAs). This exchange can be mediated by extracellular vesicles such as exosomes through intimate membrane contacts between donor and acceptor cells, or a combination of both.

Endocytic recycling, for some time considered to occur by default, is now emerging as an active sorting process. These studies are increasing our understanding of the physiological events that require recycling.

Signalling is known to regulate metabolism, and it is becoming clear that this regulation is reciprocal, with signalling pathways being regulated by the availability of nutrient-sensitive modifications, such as acetylation and glycosylation. This tight link between signalling and metabolism allows cells to modulate their activities according to metabolic status.

Satellite cells are a heterogeneous population of stem and progenitor cells with crucial roles in muscle repair and regeneration. Although paired-box 7 (PAX7) is necessary to maintain the undifferentiated stem cell state, a requirement for PAX7 in adult satellite cells was recently challenged and remains controversial.

Although the multivesicular body (MVB) is classically defined as an intermediate that delivers material for lysosomal degradation, its role in the sequestration of glycogen synthase kinase 3 during WNT signalling has revealed a positive influence of this organelle in signalling control. This Opinion article proposes that this function of MVBs as a signalling organelle is physiologically relevant during development and may be common to diverse signalling pathways.

Caspase 8 initiates apoptosis but also has non-apoptotic roles during embryonic development and for immune cell proliferation. Recent findings indicate that the non-apoptotic functions of caspase 8 are defined by the suppression of receptor-interacting protein kinase 3 (RIPK3), a kinase that triggers programmed necrosis.

The phosphodiesterase autotaxin (ATX) produces the lipid mediator lysophosphatidic acid (LPA) to regulate diverse processes, including cell migration and proliferation. Studies of the structure of ATX may shed new light on how ATX recognizes its substrates and associates with the cell surface to promote specificity in LPA signalling.

Differentiated cells can become pluripotent through reprogramming by nuclear transfer, cell fusion and induced pluripotent stem cell technology. The characteristics of reprogramming by nuclear transfer and cell fusion suggest that they occur in a deterministic, rather than a stochastic, manner.

The production of mature and export-competent messenger ribonucleoproteins (mRNPs) is a multistep process that is regulated in a spatial and temporal manner. Recent studies suggest that post-translational modifications play a part in coordinating the co-transcriptional assembly, remodelling and export of mRNP complexes through nuclear pores.

Alan Turing showed that spatial patterns can be generated when two morphogens diffuse and react. Although he realized the importance of mechanics, it has only recently become clear that mechanical processes (forces and flows generated by motors) can also contribute to patterning when coupled to chemical reactions.

The improper distribution of chromosomes during mitosis can contribute to malignant transformation. Higher eukaryotes have developed strategies for eliminating mitosis-incompetent cells, one of which is mitotic catastrophe. From a functional perspective, mitotic catastrophe can be defined as an oncosuppressive mechanism that precedes (and is distinct from) apoptosis, necrosis or senescence.

The p53 family of transcription factors have diverse roles during development and in cancer. However, there is increasing evidence that their ancestral function may have been to regulate unique aspects of maternal fertility.