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The formation of subnuclear domains, such as the paraspeckles where hyperdited mRNAs are stored, is not well understood. The transcription of the paraspeckle non-coding RNA MEN ɛ/β initiates the recruitment of other components to assemble this nuclear body.
In the developing mouse embryo, a region of the dorsal aorta endothelium generates haematopoietic cells, but how the switch to endothelium or haematopoiesis is controlled has been unclear. HoxA3 induces endothelial differentiation through repression of key haematopoietic transcription factors, including Runx1, and is downregulated during haematopoietic differentiation.
Deletion of the E3 ubiquitin ligase Wwp2 in mice is shown to induce malformations in the craniofacial regions. Wwp2 mono-ubiquitylates Goosecoid, a modification found to be essential for Goosecoid effects on the transcription of the cartilage regulatory protein Sox6.
Apoptotic cell corpses are engulfed and removed through an evolutionarily conserved pathway. In Caenorhabditis elegans, inhibition of the Rac GAP SRGP-1 permits sick or dying cells to escape clearance by this pathway.
The genetic locus encompassing TSPYL5 is frequently amplified in breast cancer. TSPYL5 is now shown to repress p53 accumulation by interacting with and inhibiting the p53 de-ubiquitylating enzyme USP7.
The four transcription factors Oct4, Sox2, Klf4 and c-myc induce somatic cells to reprogramme to an early embryonic stem cell state. When expressed in somatic cells under culture conditions that are normally used for stem cells derived from mouse epiblast tissue of post-implantation embryos (EpiSCs), these factors drive reprogramming to a state that closely resembles EpiSCs, highlighting the importance of culture environment in determining the outcome of reprogramming.
The Polycomb group protein EZH2 promotes trimethylation of histone H3K27 and gene silencing. Cdk1 is found to phosphorylate EZH2 to inhibit its methyltransferase activity, affecting EZH2-target genes involved in osteogenic differentiation.
Calcineurin signalling or pressure overload is shown to lead to cardiac hypertrophy through NFAT-mediated increase in miR-199. miR-199 inhibits the Dyrk1a kinase, which leads to further activation of NFAT. Inhibition of miR-199 reverses hypertrophy and fibrosis in mouse models of cardiac failure.
Cyclic AMP is known to affect RAF–MEK–ERK signalling, but the precise mechanism has remained unknown. An interaction between AKAP-Lbc and the scaffolding protein KSR1 is now shown to tie cAMP production to ERK pathway regulation.
Legs-at-odd-angles (Loa) mutations in cytoplasmic dynein tail have been linked to neurodegeneration in mice although how they affect dynein function has remained unclear. Biochemical, live-cell imaging and modelling techniques now show that loa mutations affect the motor run-length in vitro and in vivo as well as altering motor domain coordination.
EFA-6, originally identified as a suppressor of defects associated with dynein muations in early Caenorhabditis elegans embryos, regulates microtubule growth at the embryo cortex through a conserved amino-terminal motif but independently of its ARF6 GTP exchange factor activity.
The transcriptional regulation of haematopoietic stem cell quiescence is only starting to be understood. The nuclear transcription factor Nurr1 drives early haematopoietic progenitors into quiescence through the upregulation of the quiescence factor p18/INK4C.
The Rickettsia protein Sca2 was previously implicated in actin ‘comet tail’ formation and bacterial cell motility. Sca2 is now found to possess formin-like properties and assembles long, unbranched actin filaments.
The mTOR pathway is a well-known regulator of cell size, and deregulation of mTOR has been observed in cilia-related diseases. Cilia modulate cell size by restricting LKB-1-mediated activation of AMPK to the basal body, which subsequently affects mTOR signalling.
The activity of myriad nuclear proteins is regulated by S-nitrosylation, but a nuclear nitrosylase has remained elusive. GAPDH is now shown to be nitrosylated in the cytoplasm, which promotes its import into the nucleus, where it then transnitrosylates nuclear proteins.
The methyltransferase PR-Set7 catalyses the methylation of Histone H4 on Lys 20. This methylation mark is now found to correlate with replication-origin licensing. Expression of a non-degradable PR-Set7 mutant leads to retention of this mark and repeated DNA replication at origins.
The iron binding protein melanotransferrin (MTf) is found to localize to Drosophila septate junctions. During epithelial maturation, the assembly of septate junctions depends on endocytosis and recycling of iron-bound MTf.
Fish retinal regeneration starts with the dedifferentiation of glia cells into progenitors. Following injury, the proneural transcription factor, Ascl1a, upregulates the pluripotency factor Lin-28, which in turn prevents let-7 microRNA-mediated inhibition of regeneration-associated genes.
In interphase plant cells, microtubule nucleation occurs at the cell cortex. By examining the localization and dynamics of γ-tubulin nucleating complexes in Arabidopsis, the microtubule-severing protein katanin is shown to be involved in the release of daughter microtubules.
The SUMO E3 ligase PIAS3 is shown to promote Rac1 SUMOylation. This modification stimulates Rac1 activity and regulates its ability to drive lamellipodium formation.