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The molecular mechanisms that regulate the transition from totipotency into divergent cellular states are unclear. Two new studies show that the transcription factors TFAP2C, NR5A2 and TEAD4 (TNT) support the formation of a transient bipotent state by activating early pluripotency and trophectoderm genes and modulating HIPPO signaling.
The commander complex was recently shown through interactomic screens to be a ubiquitous and conserved protein complex with fundamental biological roles. Two recent reports together revealed the structure of the complete commander assembly and explored its functional implications.
Branch point selection is required for pre-mRNA splicing, and its mis-regulation is associated with many diseases. Two structural studies provide insights into the dynamics of active site formation and the spliceosomal proteins that may contribute to activation of the correct branch point in eukaryotic introns.
Stabilization of a branch structure would intuitively suggest a direct connection between trunk and bough, but in actin filament networks, cortactin clamps the branching Arp2/3 complex to the daughter filament. This has fundamental consequences for mechanistic understanding of actin branch turnover and cortactin biology.
ADP-ribosylation regulates the activity of numerous proteins involved in the DNA damage response and repair. A new study shows that telomeric DNA can be ADP-ribosylated by PARP1, and prompt removal of the ADP-ribose by TARG1 is essential to preserve telomere integrity, unveiling DNA–ADP-ribosylation as a novel player in telomere stability.
The human cytoskeleton consists of three major classes of filaments: microfilaments, microtubules and intermediate filaments. Here, we summarize recent progress in deciphering the structure and function of intermediate filaments and their implications for human disease.
Spliceosome biogenesis and recycling remains a largely unexplored area. Two papers now reveal how protein chaperones remodel the 20S U5 snRNP, leading to formation of the U4/U6.U5 tri-snRNP.
Pregnancy loss is common in humans, but maternal genetic factors modulating its incidence are largely unknown. In a meta-analysis of genome-wide association studies, researchers identified a genetic variant that seems to increase risk of pregnancy loss by dysregulating meiotic recombination between homologous chromosomes during egg formation.
