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The formation of a coalition government led by David Cameron has ended the uncertainty following the general election in the United Kingdom. Although the challenges facing a coalition government are immense, securing the future of UK science must remain a priority.
The balance of cohesion and remodelling is essential for the integrity and morphogenesis of epithelia. This requires adhesion and transmission of actomyosin tension, both of which are mediated by E-cadherin. The finding that actomyosin tension reinforces mechanical coupling of actin to E-cadherin through α-catenin reveals similarities with integrin regulation.
Innovations in live-cell microscopy and single-molecule analysis have allowed a new direct view of nuclear messenger RNA dynamics. A new study extends previous analyses of mRNA-protein intranuclear transport and links this critical step to the kinetics of moving through nuclear pore complexes. Seeing nuclear mRNA on the move will impact future work on pore translocation and nuclear organization.
The distribution of secreted morphogens in a developing organ determines its form by instructing size, shape and pattern. Pentagone has been identified as a secreted factor that controls the distribution of the morphogen Decapentaplegic (Dpp) in the Drosophila melanogaster wing.
α-Catenin can respond to myosinII-mediated forces in cell–cell junctions through a force-dependent interaction with vinculin that regulates adherens junction development.
Real-time visualization of single mRNA-protein complexes reveals messenger ribonucleotide protein transport dynamics in the nucleoplasm and determines the translocation time through the pore to be 500 ms. The presence of introns does not affect movement through the nucleoplasm but increases export efficiency.
BH3-only protein tBID induces mitochondrial outer membrane permeabilization in response to death receptor activation. The mitochondrial carrier homologue 2 (MTCH2) protein acts as the tBID receptor on the mitochondria and is required for fas-induced cell death in mouse liver.
Cyclin-dependent kinase 5 phosphorylates Ape1, a regulator of base excision repair, to reduce its endonuclease activity and increase neuronal death following treatment with neurotoxins. Interestingly, increase in Ape1 phosphorylation is also observed in patients with neurodegenerative diseases.
Hair follicle stem cells have increased resistance to DNA damage-induced cell death. This is due to higher expression of Bcl2 and to a faster non-homologous end-joining (NHEJ) DNA repair activity, which attenuates p53 activation.
The microtubule plus end protein CLIP-170 has been shown to be an AMP activated protein kinase (AMPK) substrate. AMPK-mediated phosphorylation of CLIP-170 regulates microtubule polarization and directional cell migration.
A photoactivatable Rac construct reveals that localized Rac activation in one Drosophila border cell is sufficient to induce protrusion in that cell, with concomitant JNK-dependent retraction in neighbouring cells.
Focal adhesion proteins promote cell adhesion and migration in both two-dimensional and three-dimensional environments. When cells are embedded in a 3D matrix, focal adhesion proteins modulate the speed and persistence of migration by regulating protrusion activity.
In humans, immune cell transmigration requires the Rap1 GTPase. A new model of transmigration is characterized in Drosophila, where haemocytes require the GTPase RhoL to trigger Rap1 localization to the leading edge and cell invasion.
Morphogens direct cell fates across tissues through concentration gradients. Pentagone, a secreted protein and a newly identified target of the Drosophila bone morphogenetic protein decapentaplegic (Dpp), is shown to promote long-range distribution of the Dpp ligand in the wing through its binding to the heparan-sulphate proteoglycan Dally.
Fisher and colleagues find that Jarid2 is a subunit of PRC2 (Polycomb Repressor Complex 2) that recruits PRC1 complex and Ser 5-phosphorylated RNA Polymerase II to developmental regulators in embryonic stem (ES) cells. Jarid2-deficient ES cells do not efficiently differentiate to mesoderm or neural lineages in vitro.