Tissue-specific laminin expression facilitates integrin-dependent association of the embryonic wing disc with the trachea in Drosophila

AbstractThe interaction of heterologous tissues involves cell adhesion mediated by the extracellular matrix and its receptor integrins. The Drosophila wing disc is an ectodermal invagination that contacts specific tracheal branches at the basolateral cell surface. We show that an α subunit of laminin, encoded by wing blister (wb), is essential for the establishment of the interaction between the wing and trachea. During embryogenesis, wing disc cells present Wb at their basolateral surface and extend posteriorly, expanding their association to more posteriorly located tracheal branches. These migratory processes are impaired in the absence of the trachea, Wb, or integrins. Time-lapse and transmission electron microscopy analyses suggest that Wb facilitates integrin-dependent contact over a large surface and controls the cellular behavior of the wing cells, including their exploratory filopodial activity. Our data identify Wb laminin as an extracellular matrix ligand that is essential for integrin-dependent cellular migration in Drosophila

Chiral Soliton Lattice Formation in Monoaxial Helimagnet Yb(Ni1−x_{1-x}Cux_x)3_3Al9_9

Helical magnetic structures and its responses to external magnetic fields in Yb(Ni$_x$Cu$_{1-x}$)$_3$Al$_9$, with a chiral crystal structure of the space group $R32$, have been investigated by resonant X-ray diffraction. It is shown that the crystal chirality is reflected to the helicity of the magnetic structure by a one to one relationship, indicating that there exists an antisymmetric exchange interaction mediated via the conduction electrons. When a magnetic field is applied perpendicular to the helical axis ($c$ axis), the second harmonic peak of $(0, 0, 2q)$ develops with increasing the field. The third harmonic peak of $(0, 0, 3q)$ has also been observed for the $x$=0.06 sample. This result provides a strong evidence for the formation of a chiral magnetic soliton lattice state, a periodic array of the chiral twist of spins, which has been suggested by the characteristic magnetization curve. The helical ordering of magnetic octupole moments, accompanying with the magnetic dipole order, has also been detected.Comment: 13 pages, 18 figures, accepted for publication in J. Phys. Soc. Jp

Activation of cytosolic phospholipase A2 in dorsal root ganglion neurons by Ca2+/calmodulin-dependent protein kinase II after peripheral nerve injury

<p>Abstract</p> <p>Background</p> <p>Peripheral nerve injury leads to a persistent neuropathic pain state in which innocuous stimulation elicits pain behavior (tactile allodynia), but the underlying mechanisms have remained largely unknown. We have previously shown that spinal nerve injury induces the activation of cytosolic phospholipase A₂(cPLA₂) in injured dorsal root ganglion (DRG) neurons that contribute to tactile allodynia. However, little is known about the signaling pathway that activates cPLA₂after nerve injury. In the present study, we sought to determine the mechanisms underlying cPLA₂activation in injured DRG neurons in an animal model of neuropathic pain, focusing on mitogen-activated protein kinases (MAPKs) and Ca²⁺/calmodulin-dependent protein kinase II (CaMKII).</p> <p>Results</p> <p>Pharmacological inhibition of either p38 or extracellular signal-regulated kinase (ERK) in the injured DRG, which led to suppression of the development of tactile allodynia, did not affect cPLA₂phosphorylation and translocation after nerve injury. By contrast, a CaMKII inhibitor prevented the development and expression of nerve injury-induced tactile allodynia and reduced both the level of cPLA₂phosphorylation and the number of DRG neurons showing translocated cPLA₂in response to nerve injury. Applying ATP to cultured DRG neurons increased the level of both phosphorylated cPLA₂and CaMKII in the vicinity of the plasma membrane and caused physical association of these two proteins. In addition, ATP-stimulated cPLA₂and CaMKII phosphorylation were inhibited by both a selective P2X₃R/P2X₂₊₃R antagonist and a nonselective voltage-dependent Ca²⁺channel (VDCC) blocker.</p> <p>Conclusion</p> <p>These results suggest that CaMKII, but not MAPKs, has an important role in cPLA₂activation following peripheral nerve injury, probably through P2X₃R/P2X₂₊₃R and VDCCs in primary afferent neurons.</p

Trion confinement in monolayer MoSe2 by carbon nanotube local gating

We have successfully confined trions into a one-dimensional restricted space of a MoSe2 device with CNT gate electrodes. The dry transfer process, including deterministic dry transfer of aligned CNTs, has led to an hBN-encapsulated MoSe2 device with CNT back gate electrodes. In contrast to a location without CNT gate electrodes, applying voltage via CNT gate electrodes significantly alters PL spectra at a location with CNT gate electrodes. PL imaging has revealed that image contrast from trions is linear along the CNT electrode underneath, consistent with 1D confinement of trions in response to the CNT local gating. The confinement width obtained from the PL image is 5.5 x 10^2 nm, consistent with nanoscale 1D confined trions with the diffraction limit broadening. This work has demonstrated electrical control of excitonic states at the nanoscale, leading to novel optoelectronic properties and exciton devices in the future