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The planar cell polarity effector Fuz regulates membrane trafficking to cilia in Xenopus (the image shows a scanning electron micrograph of wild-type epidermis) and in mouse.letter p1225
A supplement contextualizes key advances in light microscopy over 400 years, while the Tara expedition sets sail to explore oceanic ecosystems at the microscopic level.
Various microbes harness the actin polymerization machinery through their surface proteins to allow intracellular motility within host cells, but other virulence factors regulate dissemination. The cortical actin tension of polarized cells may represent a physical barrier that hinders the formation of microbial protrusions during cell-to-cell spreading.
Progerin, a mutated form of lamin A, causes the premature ageing disease Hutchinson-Gilford progeria syndrome and is also involved in normal ageing. Progerin accumulation leads to distinct chromatin-related defects and the NURD complex appears to affect ageing-related chromatin defects.
To fulfil its lipid phosphatase function, PTEN must be in close proximity to the plasma membrane where its substrates reside. PTEN translocation to the plasma membrane is an active process that is mediated by the myosin-based transport machinery. MyosinV controls PTEN membrane association and thus, PTEN-mediated cell growth in neurons.
The transcriptional regulators that couple keratinocyte proliferation arrest with commitment to differentiation are yet to be identified. C/EBPs are shown to couple mice basal keratinocyte cell-cycle exit with commitment to differentiation through, respectively, E2F repression and DNA binding.
Inactivation of the tumour suppressor PTEN leads to enlarged neuronal soma. The actin-based motor myosin Va is shown to control soma size by transporting PTEN in a manner dependent on PTEN phosphorylation by CK2 and/or GSK3.
BBF2H7, a transcription factor activated by ER stress, is shown to be essential for chondrogenesis. Mice lacking BBF2H7 show severe chondrodysplasia and null chondrocytes have defects in secreting cartilage matrix proteins. BBF2H7 induces the expression of Sec23a, which is required for ER to Golgi transport, and rescues the secretion of cartilage matrix proteins in null cells.
The transcription factor OASIS was previously implicated in the ER stress response. BMP2 signalling, which is required for bone formation, induces OASIS expression and activation. Mice lacking OASIS show severe defects in bone formation and in response to BMP2 signalling. OASIS directly induces expression of Col1a1, a component of type 1 collagen.
Listeria monocytogenes spreads by membrane protrusions produced by actin 'comet tails'. The secreted Listeria protein InclC binds the mammalian adaptor protein Tuba to prevent activation of the actin regulator N-WASP2, which causes disruption of apical junctions and protrusion formation.
Fluid flow towards the leading edge has been suggested to have a role in cell motility, but the existence of fluid flow had not been demonstrated directly. Insertion of quantum dots into the lamellipodia of fish keratinocytes now reveals a forward-directed fluid flow that is dependent on myosin II activity.
The planar cell polarity (PCP) effector Fuz had not been studied in mice. Due to disrupted ciliogenesis, Fuz mutant mice show neural tube and skeletal defects. Fuz regulates trafficking of membrane cargoes to cilia through its interaction with a GTPase of the Rab family.
Autophagy degrades invading bacteria in the cytoplasm, however, Listeria monocytogenes can efficiently escape autophagy. The Listeria protein ActA recruits the actin-regulators Arp2/3 and Ena/VASP to disguise it from autophagic recognition. Tagging PolyQ-containing, aggregate-prone proteins or a Golgi-membrane protein with ActA also prevents their autophagy-mediated degradation.
The function of oxidation of specific proteins during apoptosis has been unclear. Oxidation of the actin-binding protein cofilin induces its translocation to the mitochondria, where it triggers the opening of the permeability transition pore independently of the BH3-only apoptotic factor Bax, and is required for oxidant-induced apoptosis.
Inhibition of the CDC25A phosphatase is critical for activation of the DNA damage-induced G2/M checkpoint. The DNA damage-activated kinase CHK1 phosphorylates the NIMA-related kinase NEK11, which in turn phosphorylates CDC25A to induce its degradation.
The brassinosteroid (BR) signalling pathway results in the activation of BZR transcription factors to control plant development. The complete pathway is established here, by showing that BR induces the BSU1 phosphatase-dependent inactivation of the GSK3-like kinase BIN2, thereby leading to accumulation of unphosphorylated BZR factors in the nucleus.
Cells undergoing normal or premature ageing show several global defects in chromatin. Components of the NURD chromatin remodelling complex, such as histone chaperones, are now shown to be lost in cells from patients with a premature aging disorder and in normally aged cells. Conversely, depleting NURD subunits and Hdac1 recapitulates the chromatin defects seen in aged cells.
Vault particles, containing three proteins and non-coding vault RNAs (vRNAs), regulate multidrug resistance. Human vRNAs are found to be processed into several small RNAs (svRNAs), one of which associates with Argonaute proteins to downregulate the expression of CYP3A4, an enzyme involved in drug metabolism.