News & Comment

Many eukaryotic proteins, including key transcription regulators, contain intrinsically disordered regions (IDRs), which serve as flexible interaction platforms. The molecular understanding of IDR-based interactions is now emerging, providing new insights into how IDRs promote protein compartmentalization and/or phase separation and how these processes regulate gene expression.

Two independent studies now show that polymerization of branched actin at DNA double-strand breaks (DSBs) mediates chromatin dynamics associated with homology-directed repair and is required for a robust and error-free DSB repair process.

The inner nuclear membrane is metabolically active and generates lipid droplets.

MicroRNAs derived from a virus and teratocytes of a parasitic wasp are expressed in a host moth and delay its development by inhibiting the ecdysone receptor.

Increased shortening of RNA 3′ untranslated regions associated with tumorigenic transformation interferes with competing endogenous RNA (ceRNA) networks, which results in trans-repression of tumour suppressors through microRNA-mediated silencing.

Muscle stem cells produce collagen V, which becomes a component of the niche that promotes their quiescence.

The spindle checkpoint complex BUB3–BUB1 facilitates telomere replication through recruitment of the helicase BLM, and the telomere capping protein TRF2 promotes replication at pericentromeres by recruiting the helicase RTEL1; both helicases resolve G-quadruplex structures.

EpiTOF characterized the epigenetic landscape of various types of single immune cells and revealed that their heterogeneity increases with age.

Loss of the ribosome rescue factor Pelota causes epidermal defects in mice, indicating a link between translation and tissue homeostasis.

Shieldin is a newly characterized protein complex that functions downstream of 53BP1 in promoting NHEJ

The microRNA-induced silencing complex undergoes phase separation, which promotes the sequestration and deadenylation of target mRNAs.

The lysosomal degradation of protein aggregates declines with ageing in mammalian neural stem cells, reducing their capacity to transition from a quiescent to an active state.

Ultraviolet radiation induces p38–MK2-dependent phosphorylation of NELFE, which causes its dissociation from chromatin and promotes transcription of damage-response genes.

This study describes the molecular mechanisms underlying epigenetic reprogramming in primordial germ cells.

Kindlin-2 controls mesenchymal stem cell differentiation in response to matrix stiffness by regulating the levels and activity of YAP and TAZ.

The decondensed, permissive chromatin state of pluripotent stem cells is sensitive to translation, creating a positive feedback loop whereby hypertranscription depends on the high output of translation it produces.

Oncogenes induce firing of replication origins at transcribed genes; this promotes transcription–replication conflicts and genome instability.

The polyploidy of mammalian cardiomyocytes is a barrier to heart regeneration, but modification of the cardiomyocyte cell cycle can boost their regenerative potential.

Myosin VI is recruited to ubiquitylated mitochondria and drives their encapsulation into actin cages to sequester them for mitophagy.

Fatty acid oxidation and increased acetyl-CoA levels act to suppress endothelial–mesenchymal transition.