Strain Tuning Self-Assembled Quantum Dots for Energy-Tunable Entangled-Photon Sources Using a Photolithographically Fabricated Microelectromechanical System

Self-assembled quantum dots (QDs) offer versatile sources of quantum light for photonic quantum technologies thanks to their atomic-like discrete energy levels for deterministic generation of single photons. Though, the unavoidable inhomogeneous broadening and the ubiquitous presence of the fine structure splitting (FSS) of the exciton states hamper their use as high-fidelity entangled-photon sources (EPSs) with well-defined energies, core elements in scalable networking quantum applications. To overcome these challenges, in this work, we propose and demonstrate a photolithographically fabricated microelectromechanical system (MEMS) to dynamically control the optical properties of QDs. The device features two orthogonal and independent uniaxial stresses that can tune the exciton energy and the FSS simultaneously, enabling demonstration of energy-tunable EPSs based on self-assembled QDs. The device can be processed by only employing standard photolithography techniques, which alleviates the use of sophisticated device design and fabrications, thus providing a viable route toward the realization of entanglement swapping with all-solid-state quantum emitters

Sculpting Nanoscale Functional Channels in Complex Oxides Using Energetic Ions and Electrons

The formation of metastable phases has attracted significant attention because of their unique properties and potential functionalities. In the present study, we demonstrate the phase conversion of energetic-ion-induced amorphous nanochannels/tracks into a metastable defect fluorite in A₂B₂O₇ structured complex oxides by electron irradiation. Through in situ electron irradiation experiments in a scanning transmission electron microscope, we observe electron-induced epitaxial crystallization of the amorphous nanochannels in Yb₂Ti₂O₇ into the defect fluorite. This energetic-electron-induced phase transformation is attributed to the coupled effect of ionization-induced electronic excitations and local heating, along with subthreshold elastic energy transfers. We also show the role of ionic radii of A-site cations (A = Yb, Gd, and Sm) and B-site cations (Ti and Zr) in facilitating the electron-beam-induced crystallization of the amorphous phase to the defect-fluorite structure. The formation of the defect-fluorite structure is eased by the decrease in the difference between ionic radii of A- and B-site cations in the lattice. Molecular dynamics simulations of thermal annealing of the amorphous phase nanochannels in A₂B₂O₇ draw parallels to the electron-irradiation-induced crystallization and confirm the role of ionic radii in lowering the barrier for crystallization. These results suggest that employing guided electron irradiation with atomic precision is a useful technique for selected area phase formation in nanoscale printed devices

Up-regulated CPSF6 expression is associated with poor survival of multiple cancers.

(A) Human CPSF6 expression levels in different tumor types from TCGA database were determined by TIMER (*P P P B-F) Kaplan-Meier analysis of overall survival and disease-free survival of ACC, KIRP, LUAD, MESO or PADD patients (data from GEPIA). (G) Human miR-377-3p expression levels in different tumor types from TCGA database were determined by CancerMIRNome (*P P P (TIF)</p

CPSF6 protein expression is decreased in virus-infected cells.

(A, B) Immunoblot analyses the CFIm complex expression in BMDMs infected with VSV-eGFP or HSV-1 (A) or stimulated with poly (I:C) or Poly (dA:dT) (B) at indicated time points. Data are representative of three independent experiments, with one representative shown in (A and B). (TIF)</p

Original scan images for Figs 1E–1H, 2A, 2D–2E, 2H, 2J, 6F–6I, S1A–S1B, S2G, S2I, S6E–S6I and S7N.

Original scan images for Figs 1E–1H, 2A, 2D–2E, 2H, 2J, 6F–6I, S1A–S1B, S2G, S2I, S6E–S6I and S7N.</p

CPSF6 deficiency promotes IFN-I signalling activation.

(A, B) The heatmap shows the mRNA abundance of IFNB and ISGs in WT, Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells infected with VSV-eGFP (A) or stimulated with poly (I:C) or Poly (dA:dT) (B) at indicated time points. (n = 3 replicates) (C-E) ELISA analyses of IFN-β secretion in cell supernatant from WT, Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells infected with VSV-eGFP (C) or stimulated with poly (I:C) (D) or Poly (dA:dT) (E) at indicated time points. (n = 3 replicates) (F, G) Immunoblot analyses of phosphorylated (p-) TBK1 and IRF3 in WT, Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells infected with VSV-eGFP at indicated time points. (H) Immunoblot analyses of the protein expression of ISGs in WT and CPSF6-/- A549 and L929 cells infected with VSV-eGFP at indicated time points. (I) Immunoblot analyses knocking-down efficiency of CPSF6 in BMDMs from Cpsf6+/+ and Cpsf6+/- mice. (J) qRT–PCR analyses of VSV mRNA abundance in Cpsf6+/+ and Cpsf6+/- BMDMs infected with VSV-eGFP at indicated time points. (n = 3 replicates) (K) Plaque assays of VSV titers in cell supernatants from Cpsf6+/+ and Cpsf6+/- BMDMs infected with VSV-eGFP for 12 h. (n = 4 replicates) (L) qRT–PCR analyses of Ifnb1 mRNA abundance in Cpsf6+/+ and Cpsf6+/- BMDMs infected with VSV-eGFP at indicated time points. (n = 4 replicates) (M) ELISA analyses of IFN-β secretion in cell supernatant from Cpsf6+/+ and Cpsf6+/- BMDMs infected with VSV-eGFP at indicated time points. (n = 4 replicates) (N-Q) qRT–PCR analyses of Ddx58 (N), Ifit2 (O), Ifit3 (P) and Isg15 (Q) mRNA abundance in Cpsf6+/+ and Cpsf6+/- BMDMs infected with VSV-eGFP at indicated time points. (n = 4 replicates) R, qRT–PCR analyses the ratio of longer 3’ UTR isoforms to total mRNA of tested genes Ddx58, Ddx3x, Ddx21, Ifit2 and Ifit3 mRNA abundance in Cpsf6+/+ and Cpsf6+/- BMDMs infected with VSV-eGFP at indicated time points. (n = 3 replicates). Data are representative of three independent experiments, with one representative shown in (F)-(I). The values represent mean ± SD with individual measurements overlaid as dots, statistical analysis was performed using a two-tailed Student’s t-test in (C)-(E) and (J)-(Q).</p

Expression of CPSF6 target genes may be regulated by miRNAs.

(A) The number of miRNAs binding to immune-related gene 3’ UTRs was predicted by a miRNA target prediction program (TargetScan). (B and C) Binding diagram of specific microRNAs in the 3’ UTR region of Ccl2 (B) and Fos (C) transcripts. (TIF)</p

CPSF6 deficiency inhibits virus replication.

(A) Immunoblot analyses knocking-out efficiency of CPSF6 in A549 and L929 cells. (B) qRT–PCR analyses of VSV mRNA abundance in WT and CPSF6-/- A549 and L929 cells infected with VSV-eGFP at indicated time points. (n = 3 replicates) (C) FACS analyses of VSV replication in WT and CPSF6-/- A549 and L929 cells infected with VSV-eGFP for 12 h. (n = 3 replicates) (D, E) Immunoblot analyses of VSVG protein expression in WT and CPSF6-/- L929 (D) or A549 (E) cells infected with VSV-eGFP at indicated time points. (F) Plaque assays of VSV titers in cell supernatants from WT and Cpsf6-/- L929 cells infected with VSV-eGFP for 12 h. (n = 3 replicates) (G) Fluorescence microscope analyses of GFP intensity in WT and Cpsf6-/- L929 cells infected with VSV-eGFP for 16 or 24 h. Scale bar, 100 μm. (H) Immunoblot analyses the expression of CPSF6 in WT, Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells. (I) qRT–PCR analyses of VSV mRNA abundance in WT, Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells infected with VSV-eGFP at indicated time points. (n = 3 replicates) (J) Immunoblot analyses of VSVG protein expression in Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells infected with VSV-eGFP at indicated time points. (K-M) Fluorescence microscope (K), FACS (L) and plaque assays (M) analyses of VSV expression in Cpsf6-/-L929PLVX and Cpsf6-/- L929CPSF6 L929 cells infected with VSV-eGFP at indicated time points. Scale bar, 100 μm. (n = 3 replicates). Data are representative of three independent experiments, with one representative shown in (A), (D), (E), (H) and (J). The values represent mean ± SD with individual measurements overlaid as dots, statistical analysis was performed using a two-tailed Student’s t-test in (B), (C), (F), (I), (L) and (M).</p

Global 3’ UTR shortening caused by CPSF6 deficiency orchestrates the cellular antiviral capacity.

(A) Notched box plot of the weighted mean of the 3’ UTR length. For each gene with UTR-APA, the length of each 3′ UTR isoform was normalized to the longest 3’ UTR, and the weighted mean of 3’ UTR length was calculated. (B) The number of poly (A) site-switched genes in L929 cells at rest. (C), Venn diagram showing the overlap of genes from (B). (D) KEGG enrichment analysis of the overlapped transcripts presented in (C). (E) The number of differentially expressed genes (DEGs) in L929 cells upon VSV-eGFP infection. (F) Venn diagram showing the overlap of genes from CPSF6 target genes and up-regulated genes after the deletion of CPSF6. (G) GO analysis of the overlapped transcripts presented in (F). (H) The heatmap shows the mRNA abundance of immune-related genes from IVT-SAPAS data.</p

CPSF6 protein expression is decreased in virus-infected cells.

(A-D) Mouse BMDMs were challenged with VSV (A), HSV-1 (B) poly (I:C) (C) or HSV60 (D) for 12h, and the mRNA levels of core 3’ processing factors were analyzed by qRT–PCR. (n = 3 replicates) (E, F) Immunoblot analyses of CFIm complex expression in A549 (E) and L929 (F) cells infected with VSV or SeV at indicated time points. (G, H) Immunoblot analyses of CFIm complex expression in A549 (G) and L929 (H) cells stimulated with poly (I:C) or Poly (dA:dT) at indicated time points. The expression of RIG-I indicates that viral infection or analogue stimulation has successfully activated the antiviral signaling of cells. (I-L) The relative mRNA expression of CPSF6 in whole blood (I), PBMCs (J), monocytes and DCs (K) from patients with COVID-19 or in peripheral blood cells (L) from patients with influenza are shown. (M-P) The relative mRNA expression of CPSF6 in RV-A16-infected AECs (M), HCV-infected Huh7 cells (N), S. aureus-infected hMDMs (O) and helminth-infected mouse lung tissues (P) are shown. Data are representative of three independent experiments, with one representative shown in (E-H). The values represent mean ± SD with individual measurements overlaid as dots, statistical analysis was performed using a two-tailed Student’s t-test or Mann–Whitney U test in (A-D) and (I-P).</p