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In the current climate of cuts to science and research funding, the commitment of researchers to influencing science policy has resurfaced as an essential issue.
The primary cilium is proposed to restrain the level of canonical Wnt signalling, but it was unknown how the cilium achieves this. β-catenin, a component of the canonical Wnt signalling pathway, is now shown to be sequestered to the cilium by the Wnt signalling modulator Jouberin (Jbn) to restrain Wnt responses.
Aurora A kinase is a key regulator of cell division, whose functions were attributed to its ability to phosphorylate diverse substrates. Aurora A is now shown to have a kinase-independent role in the regulation of chromatin-mediated microtubule assembly.
Tissue remodelling events create gaps in the basement membrane and have been previously accounted for by the degradation or reduced synthesis of basement membrane components. Live-cell imaging shows that basement membrane sliding enlarges the opening of the uterus during Caenorhabditis elegans development and that integrins-based adhesion negatively regulates sliding.
In human embryonic stem cells, the histone demethylase LSD1 is found to occupy the promoters of a subset of developmental genes that bear methylation marks on the lysine residues 4 and 27 of histone 3, and are co-occupied by OCT4 and NANOG. LSD1 participates in the silencing of these genes by controlling the levels of methylation at their regulatory regions on lysine 4 of histone 3.
Live-cell imaging of the spatiotemporal kinetics of PKA activation during cell migration reveals that PKA regulates the protrusion and retraction cycle of the leading edge. Protrusion formation correlates with RhoA and PKA activation. PKA subsequently phosphorylates RhoA to increase its interaction with RhoGDI and terminate RhoA activity at the leading edge.
Very little is known about how chromatin-modifying enzymes are regulated in response to signalling cascades. A jmjc demethylase, PHF2, is found to be activated by PKA-mediated phosphorylation, which promotes its association with the DNA-binding protein ARID5B. PHF2 then induces demethylation of ARID5B, and the PHF2–ARID5B complex modifies histone at its target promoters.
Semaphorin 3A (Sema3A) is a key guidance cue for neuronal growth. Sema3A is now shown to facilitate the conversion of axons to dendrites by stimulating signalling through CaV2.3 calcium channels.
In zebrafish, angiogenic sprouts from the apposed dorsal aorta and vein emanate in opposite directions. Whereas growth from the dorsal aorta is modulated by VEGF signalling, BMP is shown to be a vein-specific angiogenic cue for vascular network formation during development.
The mechanisms governing the biosynthesis of multiple motile cilia in vertebrates remain largely elusive. miR-449 accumulates specifically in multiciliated cells of Xenopus skin and human lung to promote multicilia formation through modulation of Notch signalling.
Through the action of intraflagella transport, primary cilia are found to sequester Jouberin, a positive regulator of Wnt signalling, to limit β-catenin nuclear entry and to modulate Wnt responsiveness. Consequently, Wnt is exacerbated in cells without cilia but inhibited in cells with more than one cilium.
Assembly of mitotic spindle microtubules in Caenorhabditis elegans embryos requires the Aurora A kinase. Live-cell imaging and RNAi-based experiments now reveal that the kinase activity of Aurora A is dispensible for this function.
Internalization and endocytic recycling of the β2-adrenergic receptor (β2AR) is critical for its signalling activities and is known to depend on sorting nexin 27 (SNX27). SNX27 is now shown to link β2AR to the retromer complex to mediate recycling of the receptor.
Mechanical force causes stiffening, or reinforcement, of integrin-based cellular adhesions. This reinforcement is shown to be mediated by the recruitment of the LARG and GEF-H1 guanine nucleotide exchange factors, which activate distinct signalling pathways in response to integrin stimulation.
The lipid phosphatase and tumour suppressor PTEN is regulated by ubiquitylation. The E3 ligase WWP2/AIP-2 is found to mediate PTEN degradation and is suggested to function as an oncogene.
