Structure Of Er Research Articles

Visualizing ER-phagy and ER architecture in vivo

ER-phagy is an evolutionarily conserved mechanism crucial for maintaining cellular homeostasis. However, significant gaps persist in our understanding of how ER-phagy and the ER network vary across cell subtypes, tissues, and organs. Furthermore, the pathophysiological relevance of ER-phagy remains poorly elucidated. Addressing these questions requires developing quantifiable methods to visualize ER-phagy and ER architecture in vivo. We generated two transgenic mouse lines expressing an ER lumen–targeting tandem RFP-GFP (ER-TRG) tag, either constitutively or conditionally. This approach enables precise spatiotemporal measurements of ER-phagy and ER structure at single-cell resolution in vivo. Systemic analysis across diverse organs, tissues, and primary cultures derived from these ER-phagy reporter mice unveiled significant variations in basal ER-phagy, both in vivo and ex vivo. Furthermore, our investigation uncovered substantial remodeling of ER-phagy and the ER network in different tissues under stressed conditions such as starvation, oncogenic transformation, and tissue injury. In summary, both reporter models represent valuable resources with broad applications in fundamental research and translational studies.

Concentration effects on the local structures and electronic properties of Er x BaY2− x F8: a first-principles study

Er3+ doped barium yttrium fluoride (BaY2F8) crystal has gained long-term attention due to its great potential in laser and medical device applications. However, the local structures of Er3+ doped BaY2F8 system (Er:BYF) remain uncertain, and the effect of doping concentration on structures and properties is unknown. Therefore, in this study, the first-principles study of the structural evolution of Er x BaY2−x F8 (x = 0.125, 0.25) crystals was carried out. By means of density functional theory and particle swarm optimization algorithm, the stable structures of Er:BYF crystals with two different concentrations are shown as standard monoclinic structures with P2 symmetry for the first time. The impurity Er3+ ions successfully enter the main lattice, replacing the Y3+ ions, and forming a [ErF8]5− polyhedron with C 2 point group symmetry. By calculating the electronic properties, the band gap values of the two structures are significantly reduced compared with that of pure BaY2F8 crystal. However, the conduction band does not break through the Fermi level, and the crystals still maintain the insulation characteristic. According to the calculation of the electron local density function, we conclude that Er–F and Y–F in Er:BYF are connected by ionic bonds. These results fill a theoretical gap in the study of Er:BYF crystals and provide inspiration for structural evolution and material design at different doping concentrations.

Porcine epidemic diarrhea virus E protein induces formation of stress granules and attenuates protein translation through activation of the PERK/eIF2α signaling pathway

Porcine epidemic diarrhea virus (PEDV) envelope protein (E) has been characterized as an important structural protein that plays critical roles in the interplay with its host to affect the virus life cycle. Stress granules (SGs) are host translationally silent ribonucleoproteins, which are mainly induced by the phosphorylation of eIF2α in the PERK/eIF2α signaling pathway. Our previous study found that PEDV E protein caused endoplasmic reticulum stress response (ERS)-mediated suppression of antiviral proteins’ translation. However, the link and the underlying mechanism by which PEDV induces SGs formation and suppresses host translation remain elusive. In this study, our results showed that PEDV E protein significantly elevated the expression of GRP78, CANX, and phosphorylation of PERK and eIF2α, indicating that the PERK/eIF2α branch of ERS was activated. PEDV E protein localized to the ER and aggregated into puncta to reconstruct ER structure, and further induced SGs formation, which has been caused through upregulating the G3BP1 expression level. In addition, a significant global translational stall and endogenous protein translation attenuation were detected in the presence of E protein overexpression, but the global mRNA transcriptional level remained unchanged, suggesting that the shutoff of protein translation was associated with the translation, not with the transcription process. Collectively, this study demonstrates that PERK/eIF2α activation is required for SGs formation and protein translation stall. This study is beneficial for us to better understand the mechanism by which PEDV E suppresses host protein synthesis, and provides us a new insight into the host translation regulation during virus infection.

Phenotypical, genotypical and pathological characterization of the moonwalker mouse, a model of ataxia

We performed a comprehensive study of the morphological, functional, and genetic features of moonwalker (MWK) mice, a mouse model of spinocerebellar ataxia caused by a gain of function of the TRPC3 channel. These mice show numerous behavioral symptoms including tremor, altered gait, circling behavior, impaired motor coordination, impaired motor learning and decreased limb strength. Cerebellar pathology is characterized by early and almost complete loss of unipolar brush cells as well as slowly progressive, moderate loss of Purkinje cell (PCs). Structural damage also includes loss of synaptic contacts from parallel fibers, swollen ER structures, and degenerating axons. Interestingly, no obvious correlation was observed between PC loss and severity of the symptoms, as the phenotype stabilizes around 2 months of age, while the cerebellar pathology is progressive. This is probably due to the fact that PC function is severely impaired much earlier than the appearance of PC loss. Indeed, PC firing is already impaired in 3 weeks old mice. An interesting feature of the MWK pathology that still remains to be explained consists in a strong lobule selectivity of the PC loss, which is puzzling considering that TRPC is expressed in every PC. Intriguingly, genetic analysis of MWK cerebella shows, among other alterations, changes in the expression of both apoptosis inducing and resistance factors possibly suggesting that damaged PCs initiate specific cellular pathways that protect them from overt cell loss.

Heat treatment and fiber drawing effect on the matrix structure and fluorescence lifetime of Er- and Tm-doped silica optical fibers

We investigate the influence of the optical fiber fabrication process on the fluorescence lifetime of Er3+ and Tm3+ ions. Optical fiber preforms were prepared using the MCVD method combined with Al2O3 nanoparticle doping. The preforms were subjected to various fabrication processes, such as preform elongation, fiber drawing, and heat treatment. The matrix structure of the preforms and fibers was studied by XRD and TEM. The fluorescence lifetime was measured. The fabrication processes caused the dissolution of the doped Al2O3 nanoparticles and a significant decrease of fluorescence lifetime of Tm3+ ions, from 875 µs in the preform down to 610 µs in the fiber, whereas no significant effect was observed for Er3+ ions, with fluorescence lifetime in the 9.6–10.2 ms range.

A node-based SIRS epidemic model on two-layer interconnected networks: Dynamical analysis of interplay between layers

From the micro-level perspective of individuals, this paper proposes a node-based SIRS epidemic model on two-layer networks, and investigates the stability of the equilibrium in the model as well as the influence of network structures and infected or recovered rate on disease propagation. By using the stability theory, we give the accurate sufficient condition for the stability as well as the threshold of disease prevalence, showing the threshold of such two-layer network is less than that of isolated single-layer network. Also, an easy-to-use approximate criterion for stability of disease-free equilibrium is provided for the two-layer network with general intra-layer structures when the infected rate across layers is far less than that within layers. Further, extensive numerical simulations on several classical network structure models verify the theoretical results, and show some new interesting results: (1) for the duplex network with equivalent number of connections each layer, the infected rate across layers has more significant effect on epidemic spreading than that within layers; (2) when fixing the whole network edge density, the same number of connections each layer always be the most conductive to propagate of the disease for the duplex network of ER structures, but it is the most/worst conductive to propagate at large/small infected rate for the duplex network of small-world structures.

Enhanced photocatalytic activity of Er doped ZnO nanospindles and nanorods for degradation of organic pollutants

Rare earth doping in ZnO is an efficient way to improve the photocatalytic performance. In the present work, Er doped ZnO nanospindles and nanorods were prepared through a simple cost effective wet chemical approach and were thoroughly characterized by FESEM, XRD, Raman spectroscopy, UV–vis-DRS, UV–vis absorption and PL spectroscopy. Nanospindle and nanorod-like morphologies of the fabricated samples were revealed by FESEM. XRD analyses revealed hexagonal wurtzite structure of Er doped ZnO nanostructures and confirmed Er doping into ZnO. PL studies showed increased defect concentration in ZnO nanostructures doped with Er ions. The photodegradation ability of nanostructures was investigated using cationic and anionic dyes and photodecomposition rate of 0.042 min−1 was achieved for MB decolorization using 0.5 % Er doped ZnO sample upon 32 min of solar light illumination. The probable photodecomposition mechanism supported by in-situ radical trapping experiments and repeatability test have also been discussed and results suggest that Er doped ZnO photocatalyst exhibit potential for use as commercial solar-active photocatalysts.

Quantitation of ER Morphology and Dynamics.

The plant endoplasmic reticulum forms a network of tubules connected by three-way junctions or sheet-like cisternae. Although the network is three-dimensional, in many plant cells, it is constrained to thin volume sandwiched between the vacuole and plasma membrane, effectively restricting it to a 2-D planar network. The structure of the network, and the morphology of the tubules and cisternae can be automatically extracted following intensity-independent edge-enhancement and various segmentation techniques to give an initial pixel-based skeleton, which is then converted to a graph representation. ER dynamics can be determined using optical flow techniques from computer vision or persistency analysis. Collectively, this approach yields a wealth of quantitative metrics for ER structure and can be used to describe the effects of pharmacological treatments or genetic manipulation. The software is publicly available.

Magnetocaloric, magnetostrictive and 57Fe Mössbauer studies of the multicomponent (Er,Y,Sm)Fe[formula omitted] compounds

The effect of substitutional 4f-elements on the magnetism of rare-earth compounds RFe2-type with the Laves phase structure is studied to find new multifunctional materials, as well as to define the macro- and microscopic parameters of multicomponent magnets. The crystal structure of (Er,Y,Sm)Fe2 compounds is investigated by X-ray powder diffraction. Detailed information on the magnetic properties of the iron sublattice for multicomponent compounds with three different rare-earth elements is obtained for the first time by means of the 57Fe Mössbauer spectroscopy. The main regularities in the magnitude variation of magnetocaloric effect and magnetostriction (linear, anisotropic and volume) in varying composition of the (Er,Y,Sm)Fe2 compounds are determined.

Inhibiting the compensatory elevation of xCT collaborates with disulfiram/copper-induced GSH consumption for cascade ferroptosis and cuproptosis

Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors and the fourth leading cause of cancer-related death globally, which is characterized by complicated pathophysiology, high recurrence rate, and poor prognosis. Our previous study has demonstrated that disulfiram (DSF)/Cu could be repurposed for the treatment of HCC by inducing ferroptosis. However, the effectiveness of DSF/Cu may be compromised by compensatory mechanisms that weaken its sensitivity. The mechanisms underlying these compensatory responses are currently unknown. Herein, we found DSF/Cu induces endoplasmic reticulum stress with disrupted ER structures, increased Ca2+ level and activated expression of ATF4. Further studies verified that DSF/Cu induces both ferroptosis and cuproptosis, accompanied by the depletion of GSH, elevation of lipid peroxides, and compensatory increase of xCT. Comparing ferroptosis and cuproptosis, it is interesting to note that GSH acts at the crossing point of the regulation network and therefore, we hypothesized that compensatory elevation of xCT may be a key aspect of the therapeutic target. Mechanically, knockdown of ATF4 facilitated the DSF/Cu-induced cell death and exacerbated the generation of lipid peroxides under the challenge of DSF/Cu. However, ATF4 knockdown was unable to block the compensatory elevation of xCT and the GSH reduction. Notably, we found that DSF/Cu induced the accumulation of ubiquitinated proteins, promoted the half-life of xCT protein, and dramatically dampened the ubiquitination–proteasome mediated degradation of xCT. Moreover, both pharmacologically and genetically suppressing xCT exacerbated DSF/Cu-induced cell death. In conclusion, the current work provides an in-depth study of the mechanism of DSF/Cu-induced cell death and describes a framework for the further understanding of the crosstalk between ferroptosis and cuproptosis. Inhibiting the compensatory increase of xCT renders HCC cells more susceptible to DSF/Cu, which may provide a promising synergistic strategy to sensitize tumor therapy and overcome drug resistance, as it activates different programmed cell death.

Abstract 17218: CES1 Deficiency is Associated With Metabolic Reprograming and Endothelial Dysfunction in Pulmonary Arterial Hypertension

Introduction: PAH is associated with loss of pulmonary microvessels & vascular remodeling. Metabolic reprogramming(MR) characterized by high glycolysis & reduced FAO is hallmark feature of PAH linked to oxidative stress, endothelial cell(EC) dysfunction & reduced angiogenesis. BMPR2 gene mutations promote MR; however, due to low penetrance, alterations in other genes are likely necessary for PAH development. We found Carboxylesterase 1 (CES1) is an ER enzyme involved in lipid metabolism & cellular detoxification with a potentially important role in MR & EC dysfunction in PAH. Hypothesis: Loss of CES1 leads to EC dysfunction through MR, lipotoxicity & oxidative stress & serves as a genetic modifier of BMPR2 in ECs Methods: Healthy/PAH ECs & lung tissues were obtained from transplants and commercial sources. Healthy ECs were transfected with siRNA/plasmid to knockdown/overexpress CES1. Mitochondrial & ER structure & function was assessed by confocal microscopy & proteomic assays. Metabolic flux in ECs was analyzed using the SeahorseXF. CES1 HET KO mice exposed to normoxia and hypoxia were studied & lungs were processed for scRNA-seq. Results: CES1 mRNA/protein expression was reduced in PAH ECs & lung vascular lesions. Compared to controls, siCES1 ECs have high apoptosis,reduced angiogenesis,increased ROS,mitochondrial fragmentation & ER stress. Lipid staining of siCES1 PMVECs demonstrates cytoplasmic lipid droplet accumulation correlating with reduced FAO and switch to glycolysis. Restoring CES1 expression reverses MR, reduces ROS & improves functional status of siCES1/PAH ECs. CES1 is a downstream target of BMPR2 under NRF2 transcriptional regulation & its loss exacerbates MR & dysfunction associated with BMPR2 loss that improves via CES1 restoration. Hemodynamic & scRNA-seq studies show that hypoxic CES1 HETKO mice develop more severe PH & demonstrate dysregulation of genes in key metabolic & angiogenic pathways. Conclusions: CES1 is essential for maintenance & repair of the pulmonary endothelium & acts as a key modifier of BMPR2 signaling. Limitations of current therapies to reverse EC dysfunction and prevent small vessel loss warrant therapeutic interventions that can restore CES1 expression and serve as a novel treatment approach for PAH.

Cholesterol induction in CD8+ T cell exhaustion in colorectal cancer via the regulation of endoplasmic reticulum-mitochondria contact sites.

Hypercholesterolemia is one of the risk factors for colorectal cancer (CRC). Cholesterol can participate in the regulation of human T cell function and affect the occurrence and development of CRC. To elucidate the pathogenesis of CRC immune escape mediated by CD8+ T cell exhaustion induced by cholesterol. CRC samples (n = 217) and healthy individuals (n = 98) were recruited to analyze the relationship between peripheral blood cholesterol levels and the clinical features of CRC. An animal model of CRC with hypercholesterolemia was established. Intraperitoneal intervention with endoplasmic reticulum stress (ERS) inhibitors in hypercholesterolemic CRC mice was performed. CD69, PD1, TIM-3, and CTLA-4 on CD8+ T cells of spleens from C57BL/6J mice were detected by flow cytometry. CD8+ T cells were cocultured with MC38 cells (mouse colon cancer cell line). The proliferation, apoptosis, migration and invasive ability of MC38 cells were detected by CCK-8 assay, Annexin-V APC/7-AAD double staining, scratch assay and transwell assay, respectively. Transmission electron microscopy was used to observe the ER structure of CD8+ T cells. Western blotting was used to detect the expression of ERS and mitophagy-related proteins. Mitochondrial function and energy metabolism were measured. Immunoprecipitation was used to detect the interaction of endoplasmic reticulum-mitochondria contact site (ERMC) proteins. Immunofluorescence colocalization was used to detect the expression and intracellular localization of ERMC-related molecules. Peripheral blood cholesterol-related indices, including Tc, low density lipoproteins (LDL) and Apo(a), were all increased, and high density lipoprotein (HDL) was decreased in CRCs. The proliferation, migration and invasion abilities of MC38 cells were enhanced, and the proportion of tumor cell apoptosis was decreased in the high cholesterol group. The expression of IL-2 and TNF-α was decreased, while IFN-γ was increased in the high cholesterol group. It indicated high cholesterol could induce exhaustion of CD8+ T cells, leading to CRC immune escape. Hypercholesterolemia damaged the ER structure of CD8+ T cells and increased the expression of ER stress molecules (CHOP and GRP78), lead to CD8+ T cell exhaustion. The expression of mitophagy-related proteins (BNIP3, PINK and Parkin) in exhausted CD8+ T cells increased at high cholesterol levels, causing mitochondrial energy disturbance. High cholesterol enhanced the colocalization of Fis1/Bap31, MFN2/cox4/HSP90B1, VAPB/PTPIP51, VDAC1/IPR3/GRP75 in ERMCs, indicated that high cholesterol promoted the intermolecular interaction between ER and mitochondrial membranes in CD8+ T cells. High cholesterol regulated the ERS-ERMC-mitophagy axis to induce the exhaustion of CD8+ T cells in CRC.

Atl (atlastin) regulates mTor signaling and autophagy in Drosophila muscle through alteration of the lysosomal network

ABSTRACT The hereditary spastic paraplegias (HSPs) represent a family of genetic disorders comprising at least 72 different genes with the common pathology of progressive locomotor deficits and spasticity. ATL1/SPG3A (atlastin GTPase 1) encodes an ER fusion protein that controls ER morphology, which implicates ER structure as a causal factor in HSP. Here we use Drosophila to study effects of decreased atl (atlastin) on properties of the larval body wall muscle. We found that muscle atl loss causes accumulation of aggregates containing polyubiquitin (polyUB), mostly bound to the autophagy receptor ref(2)P/SQSTM1/p62. Muscle atl loss also decreased volume and complexity of the endolysosomal network and decreased lysosome number. To determine effects of these lysosomal deficits on progression through the basal autophagy pathway, we expressed Atg8a tagged with both GFP and mCherry in a wild-type and atl mutant background. We found numerous structures containing mCherry but not GFP fluorescence in wild type, indicating that Atg8a was found mostly in mature autolysosomes. In contrast, muscles lacking atl exhibited significant amounts of GFP signal, indicating failure of autophagosome maturation with acidic lysosomes. Many of these GFP-positive puncta contained the late-endosome marker Rab7 but not Lamp1, indicating that some autophagy cargo was accumulating within amphisomes. We also found that this autophagy block was accompanied by an inability to activate the mTor kinase. Our results provide mechanistic insights into the role of atl in maintaining proper function of the autophagy pathway and suggests that certain pathologies in patients with mutations in ATL1/SPG3A might result from altered MTOR signaling. Abbreviations atl atlastin; ALR autophagic lysosome reformation; ER endoplasmic reticulum; GFP green fluorescent protein; HSP hereditary spastic paraplegia; Lamp1 lysosomal associated membrane protein 1 PolyUB polyubiquitin; RFP red fluorescent protein; spin spinster; mTor mechanistic Target of rapamycin; VCP valosin containing protein

Calculation of the hyperfine structure of Er and Fm

Calculation of the hyperfine structure of Er and Fm

The nanoscale organization of reticulon 4 shapes local endoplasmic reticulum structure in situ.

The endoplasmic reticulum's (ER's) structure is directly linked to the many functions of the ER, but its formation is not fully understood. We investigate how the ER-membrane curving protein reticulon 4 (Rtn4) localizes to and organizes in the membrane and how that affects the local ER structure. We show a strong correlation between the local Rtn4 density and the local ER membrane curvature. Our data further reveal that the typical ER tubule possesses an elliptical cross-section with Rtn4 enriched at either end of the major axis. Rtn4 oligomers are linear shaped, contain about five copies of the protein, and preferentially orient parallel to the tubule axis. Our observations support a mechanism in which oligomerization leads to an increase of the local Rtn4 concentration with each molecule, increasing membrane curvature through a hairpin wedging mechanism. This quantitative analysis of Rtn4 and its effects on the ER membrane result in a new model of tubule shape as it relates to Rtn4.

Growth, structure and spectroscopic properties of Er:YSr3(PO4)3 disordered crystal for mid-infrared laser applications

Mid-infrared lasers in the ⁓ 3 µm region activated by Er3+ ion has attracted considerable attention due to their important applications. Herein, a heavy concentration (30 mol%) Er3+ ion doped YSr3(PO4)3 (Er:YSP) single crystal with a high crystalline quality was grown through the Czochralski pulling method. The structure of single crystal was ascertained to be cubic system with the point group 4¯3m using the powder X−ray diffraction and Rietveld structural refinement methods. Furthermore, the band structure and density of states of the crystal were analyzed by the first principal calculations. The absorption and fluorescence spectra were also investigated. An intense absorption band located at 974 nm with a full width half-maximum of 18 nm, where the absorption cross section was obtained to be 3.72 × 10−21 cm2. The full width half-maximum value of emission band centered at about 3090 nm is up to be 140 nm, which is very suitable for realizing ultrashort pulses and tunable lasers. In addition, the fluorescence lifetime of the upper 4I11/2 and lower 4I13/2 levels were obtained to be 0.65 ms and 5.37 ms, respectively. All the results show that the disordered structure crystal Er:YSP could potentially serve as a laser medium for the ⁓ 3µm region.

Study of novel androgen receptor V770 variant in androgen insensitivity syndrome patients reveals the transitional state of the androgen receptor ligand binding domain homodimer.

We report the discovery of the androgen receptor missense mutation V770D, that was found in two sisters suffering from complete androgen insensitivity. Experimental validation of AR V770 variants demonstrated that AR V770D was transcriptionally inactive due to the inability to dimerize and a reduced ligand binding affinity. The more conservative AR V770A variant showed a dimerization defect at low levels of DHT with a partial recovery of the transcriptional activity and of the receptor's ability to dimerize when increasing the DHT levels. With V770 located outside of the proposed LBD dimerization interface of the AR LBD homodimer crystal structure, the effects of the V770A mutation on AR dimerization were unexpected. We therefore explored whether the AR LBD dimerization interface would be better described by an alternative dimerization mode based on available human homodimeric LBD crystal structures of other nuclear receptors. Superposition of the monomeric AR LBD in the homodimeric crystal structures of GR, PR, ER, CAR, TRβ, and HNF-4α showed that the GR-like LBD dimer model was energetically the most stable. Moreover, V770 was a key energy residue in the GR-like LBD dimer while it was not involved in the stabilization of the AR LBD homodimer according to the crystal structure. Additionally, the observation that 4 AIS mutations impacted the stability of the AR LBD dimer while 16 mutations affected the GR-like LBD dimer, suggested that the AR LBD dimer crystal is a snapshot of a breathing AR LBD homodimer that can transition into the GR-like LBD dimer model.

Synthesis, crystal structure and NMR-study new mononuclear paramagnetic Er (III) complex based on imine derivatives of thiacalix[4]arene

The synthesis, crystal structure and NMR-study of new paramagnetic Er (III) complex based on imine derivatives of thiacalix[4]arene was carried out. Temperature dependences of the 1H NMR spectra of complex Er(III) and calix[4]arene with N-contained substituents (I) have been analyzed using the line shape analysis, taking into account the temperature variation of paramagnetic chemical shifts, within the frame of the dynamic NMR method. Two kinds of molecular dynamics in I are reported for the CDCl3 solution. The first one conformational dynamics is conditioned by the pinched cone A ↔ pinched cone B interconversion with activation free energy ΔG≠(298 K) = 40 ± 3 kJ/mol (observed at low temperature). The second one dynamics is connected with rearrangements in coordination environment (with ΔG≠(298 K) = 58 ± 3 kJ/mol). Due to substantial temperature dependence of paramagnetic shifts, the complex I can be considered as NMR thermosensor reagent for local temperature monitoring. Owing to the large magnetic moments typical for many Ln-ions and especially high value of magnetic anisotropy for Er cation (III) adopting capped trigonal prismatic geometry of coordination sphere one may expect that 1-Er can potentially exhibit SMM behavior.

IntER-ACTINg: The structure and dynamics of ER and actin are interlinked.

The actin cytoskeleton is the driver of gross ER remodelling and the movement and positioning of other membrane-bound organelles such as Golgi bodies. Rapid ER membrane remodelling is a feature of most plant cells and is important for normal cellular processes, including targeted secretion, immunity and signalling. Modifications to the actin cytoskeleton through pharmacological agents such as Latrunculin B and phalloidin, or disruption of normal myosin function also affect ER structure and/or dynamics. Here, we investigate the impact of changes in the actin cytoskeleton on structure and dynamics on the ER as well as in return the impact of modified ER structure on the architecture of the actin cytoskeleton. By expressing actin markers that affect actin dynamics, or expressing of ER-shaping proteins that influence ER architecture, we found that the structure of ER-actin networks is closely inter-related; affecting one component is likely to have a direct effect on the other. Therefore, our results indicate that a complicated regulatory machinery and cross-talk between these two structures must exist in plants to co-ordinate the function of ER-actin network during multiple subcellular processes. In addition, when considering organelle structure and dynamics, the choice of actin marker is essential in preventing off-target organelle structure and dynamics modifications.

Er3+-doped LuYSGG crystal as a potential 2.79 μm radiation-resistant laser material

We demonstrate the influence of gamma-ray irradiation on the structure, spectroscopies, and laser performance of Er:LuYSGG crystal. After 100 Mrad 60Co gamma-ray irradiation, the crystal structure remains unchanged, the absorption near 968 nm and emission within 2.7 ∼ 3 μm are almost unaffected, the level lifetimes are reduced, and the maximum output power of 886 mW is achieved with a maximum slope efficiency of 20.8%. The maximum output power and slope efficiency decrease by only 2.5% and 3.7% after irradiation, respectively, and the M2 factor is little affected by irradiation. The results indicate that the Er:LuYSGG crystal is a potential mid-infrared radiation-resistant laser material applied in radiation environments.