Accumulation Of Defects Research Articles

Styxl2 regulates de novo sarcomere assembly by binding to non-muscle myosin IIs and promoting their degradation.

Styxl2, a poorly characterized pseudophosphatase, was identified as a transcriptional target of the Jak1-Stat1 pathway during myoblast differentiation in culture. Styxl2 is specifically expressed in vertebrate striated muscles. By gene knockdown in zebrafish or genetic knockout in mice, we found that Styxl2 plays an essential role in maintaining sarcomere integrity in developing muscles. To further reveal the functions of Styxl2 in adult muscles, we generated two inducible knockout mouse models: one with Styxl2 being deleted in mature myofibers to assess its role in sarcomere maintenance, and the other in adult muscle satellite cells (MuSCs) to assess its role in de novo sarcomere assembly. We find that Styxl2 is not required for sarcomere maintenance but functions in de novo sarcomere assembly during injury-induced muscle regeneration. Mechanistically, Styxl2 interacts with non-muscle myosin IIs, enhances their ubiquitination, and targets them for autophagy-dependent degradation. Without Styxl2, the degradation of non-muscle myosin IIs is delayed, which leads to defective sarcomere assembly and force generation. Thus, Styxl2 promotes de novo sarcomere assembly by interacting with non-muscle myosin IIs and facilitating their autophagic degradation.

Styxl2 regulates de novo sarcomere assembly by binding to non-muscle myosin IIs and promoting their degradation

Styxl2, a poorly characterized pseudophosphatase, was identified as a transcriptional target of the Jak1-Stat1 pathway during myoblast differentiation in culture. Styxl2 is specifically expressed in vertebrate striated muscles. By gene knockdown in zebrafish or genetic knockout in mice, we found that Styxl2 plays an essential role in maintaining sarcomere integrity in developing muscles. To further reveal the functions of Styxl2 in adult muscles, we generated two inducible knockout mouse models: one with Styxl2 being deleted in mature myofibers to assess its role in sarcomere maintenance, and the other in adult muscle satellite cells (MuSCs) to assess its role in de novo sarcomere assembly. We find that Styxl2 is not required for sarcomere maintenance but functions in de novo sarcomere assembly during injury-induced muscle regeneration. Mechanistically, Styxl2 interacts with non-muscle myosin IIs, enhances their ubiquitination, and targets them for autophagy-dependent degradation. Without Styxl2, the degradation of non-muscle myosin IIs is delayed, which leads to defective sarcomere assembly and force generation. Thus, Styxl2 promotes de novo sarcomere assembly by interacting with non-muscle myosin IIs and facilitating their autophagic degradation.

METHODS OF INFLUENCE ON THE SYSTEM TO CHANGE THE ENERGY STATE OF SUBSTANCE: EXPERIENCE, STATE OF THE ISSUE

Methods of influencing the system, the ultimate goal of which is to destruct the natural structure of the material, can be divided as mechanical, physical, chemical, biological and complex. The changing the energy state of a substance is called activation. The current scientific field of ultradispersed materials and physical and chemical processes caused by dispersion is created by the researches of many scientists. Detailed consideration for the increasing reactivity of a solid substance compared to the change in its specific surface area during its mechanical activation showed that the share attributable to the growth of the specific surface area is only a few percent of the mechanical activation effect. The other part is due to the accumulation of defects in the crystals during the grinding process. According to the law of conservation of energy, when a crystal splits, the potential energy of interaction between lattice nodes is transferred to uncompensated surface energy. In addition, the value of the specific surface energy depends on the type of flat lattice used to split the crystal. Therefore, the activation processes and the application of the substance in the active state are relevant in the development of modern binders and concretes. The purpose of the article is to analyse the advantages and disadvantages of the existing methods of influencing the system with the ultimate goal of destruction of the natural structure of the material to changing the energy state of the substance, i.e. its activation. Conclusions. During the destruction of solids, the formation of new cleavage surfaces is accompanied by the breaking of bonds between the substance structural elements and the transition of the potential bond energy into surface energy. Ceteris paribus, the higher the ionic charges and the smaller the distance between them (between adjacent flat grids in the lattice), the greater the value of σ. In addition, the value of the specific surface energy depends on the type of flat grids used to split the crystal. It is worth mentioning that not all methods of activation for binder and concrete (soluble) mixtures are currently implemented on an i industry level. This is due to various reasons. The main method of activation used on an industry level is mechanochemical activation in various types of mills.

Simulation Study on Defect Damage Behavior of Fe under Irradiation Environment

Abstract As a commonly used structural material in nuclear power plants, Reactor pressure vessel (RPV) steel is subjected to high-energy neutron irradiation from the reactor core for a long time, and the service environment is harsh. The accumulation of point defects (interstitial atoms and vacancies) generated by irradiation over a long period can seriously affect the microstructure of the material. The macroscopic properties of the material changed until the material failed, which threatened the safety and operation stability of nuclear power plants. This paper used the method of molecular dynamics to simulate the cascade collision process of Fe in the irradiation environment. The relationship between different factors and radiation damage defects was studied. Firstly, the quantity of the Frenkel pairs increases rapidly in the irradiation environment, and then recombination occurs after reaching the peak, which makes the quantity of the Frenkel pairs decrease rapidly. Finally, the quantity of Frenkel pairs is in a stable trend. When PKA energy and temperature increase, the higher the quantity of Frenkel pairs at the peak is, the higher the recombination rate of defects is. Meanwhile, the larger the cluster size of interstitial atoms and vacancies is, the greater the corresponding quantity of clusters is. As PKA energy increases, the quantity of residual Frenkel pairs at stability increases, while the number of residual Frenkel pairs at stability decreases with temperature. This is attributed to the intense thermal motion of molecules at high temperatures, resulting in the quantity of Frenkel pairs decreasing at the stable stage. Therefore, by simulating the irradiation damage process of Fe, the prediction of material irradiation damage under a neutron irradiation environment is provided, and the service life of materials can be provided with theoretical guidance.

A New Approach for Synthesis of 3D Tolerances with Consideration of Flatness Defects in Mechanical Assembly Using Jacobian Torsor Model

A New Approach for Synthesis of 3D Tolerances with Consideration of Flatness Defects in Mechanical Assembly Using Jacobian Torsor Model

Azoles activate type I and type II programmed cell death pathways in crop pathogenic fungi

Triazoles are widely used to control pathogenic fungi. They inhibit the ergosterol biosynthetic pathway, but the precise mechanisms leading to fungicidal activities in many fungal pathogens are poorly understood. Here, we elucidate the mode of action of epoxiconazole and metconazole in the wheat pathogen Zymoseptoria tritici and the rice blast fungus Magnaporthe oryzae. We show that both azoles have fungicidal activity and reduce fluidity, but not integrity, of the plasma membrane. This impairs localisation of Cdc15-like F-BAR proteins, resulting in defective actin ring assembly and incomplete septation. However, mutant studies and pharmacological experiments in vitro and in planta show that azole lethality is due to a combination of reactive oxygen species-induced apoptosis and macroautophagy. Simultaneous inhibition of both programmed cell death pathways abolishes azole-induced cell death. Other classes of ergosterol biosynthesis inhibitors also induce apoptosis and macroautophagy, suggesting that activation of these two cell death pathways is a hallmark of ergosterol synthesis-targeting fungicides. This knowledge will inform future crop protection strategies.

Loss of dihydroceramide desaturase drives neurodegeneration by disrupting endoplasmic reticulum and lipid droplet homeostasis in glial cells.

Dihydroceramide desaturases convert dihydroceramides to ceramides, the precursors of all complex sphingolipids. Reduction of DEGS1 dihydroceramide desaturase function causes pediatric neurodegenerative disorder hypomyelinating leukodystrophy-18 (HLD-18). We discovered that infertile crescent (ifc), the Drosophila DEGS1 homolog, is expressed primarily in glial cells to promote CNS development by guarding against neurodegeneration. Loss of ifc causes massive dihydroceramide accumulation and severe morphological defects in cortex glia, including endoplasmic reticulum (ER) expansion, failure of neuronal ensheathment, and lipid droplet depletion. RNAi knockdown of the upstream ceramide synthase schlank in glia of ifc mutants rescues ER expansion, suggesting dihydroceramide accumulation in the ER drives this phenotype. RNAi knockdown of ifc in glia but not neurons drives neuronal cell death, suggesting that ifc function in glia promotes neuronal survival. Our work identifies glia as the primary site of disease progression in HLD-18 and may inform on juvenile forms of ALS, which also feature elevated dihydroceramide levels.

Mitochondrial phosphate carrier plays an important role in virulence of Candida albicans

ABSTRACT Candida albicans is a common fungal pathogen that can cause life-threatening infections. MIR1 is considered to be a mitochondrial phosphate carrier of C. albicans, while its role in virulence has not been fully elucidated. In this study, we found that mir1Δ/Δ mutant exhibited severe virulence defect in both nematode and murine models. Further mechanism studies revealed that the mir1Δ/Δ mutant grew more slowly than the wild-type strain and showed severe filamentation defects on the hypha-inducing agar media, including YPD + serum, Lee, Spider + glucose, SLAD, SLD, and YPS. Furthermore, the loss of MIR1 resulted in unfermentable carbon utilisation defect, ATP decrease, and reactive oxygen species (ROS) accumulation in C. albicans. Antioxidant proanthocyanidins, vitamin E, and N-acetyl cysteine (NAC) could reduce intracellular ROS levels and partially rescue the filamentation defects of the mir1Δ/Δ mutant. Accordingly, hypha-specific genes, as well as CEK1 and RIM101 were down-regulated in the mir1Δ/Δ mutant, and this down-regulation could be partially rescued by the addition of the antioxidant NAC. Collectively, MIR1 plays an important role in C. albicans mitochondrial function, filamentation and virulence, and would be a promising antifungal target.

Lysosomal Channels as New Molecular Targets in the Pharmacological Therapy of Neurodegenerative Diseases via Autophagy Regulation.

Besides controlling several organellar functions, lysosomal channels also guide the catabolic "self-eating" process named autophagy, which is mainly involved in protein and organelle quality control. Neuronal cells are particularly sensitive to the rate of autophagic flux either under physiological conditions or during the degenerative process. Accordingly, neurodegeneration occurring in Parkinson's (PD), Alzheimer's (AD), and Huntington's Diseases (HD), and Amyotrophic Lateral Sclerosis (ALS) as well as Lysosomal Storage Diseases (LSD) is partially due to defective autophagy and accumulation of toxic aggregates. In this regard, dysfunction of lysosomal ionic homeostasis has been identified as a putative cause of aberrant autophagy. From a therapeutic perspective, Transient Receptor Potential Channel Mucolipin 1 (TRPML1) and Two-Pore Channel isoform 2 (TPC2), regulating lysosomal homeostasis, are now considered promising druggable targets in neurodegenerative diseases. Compelling evidence suggests that pharmacological modulation of TRPML1 and TPC2 may rescue the pathological phenotype associated with autophagy dysfunction in AD, PD, HD, ALS, and LSD. Although pharmacological repurposing has identified several already used drugs with the ability to modulate TPC2, and several tools are already available for the modulation of TRPML1, many efforts are necessary to design and test new entities with much higher specificity in order to reduce dysfunctional autophagy during neurodegeneration.

Biofilm-associated metabolism via ERG251 in Candida albicans.

Biofilm formation by the fungal pathogen Candida albicans is the basis for its ability to infect medical devices. The metabolic gene ERG251 has been identified as a target of biofilm transcriptional regulator Efg1, and here we report that ERG251 is required for biofilm formation but not conventional free-living planktonic growth. An erg251Δ/Δ mutation impairs biofilm formation in vitro and in an in vivo catheter infection model. In both in vitro and in vivo biofilm contexts, cell number is reduced and hyphal length is limited. To determine whether the mutant defect is in growth or some other aspect of biofilm development, we examined planktonic cell features in a biofilm-like environment, which was approximated with sealed unshaken cultures. Under those conditions, the erg251Δ/Δ mutation causes defects in growth and hyphal extension. Overexpression in the erg251Δ/Δ mutant of the paralog ERG25, which is normally expressed more weakly than ERG251, partially improves biofilm formation and biofilm hyphal content, as well as growth and hyphal extension in a biofilm-like environment. GC-MS analysis shows that the erg251Δ/Δ mutation causes a defect in ergosterol accumulation when cells are cultivated under biofilm-like conditions, but not under conventional planktonic conditions. Overexpression of ERG25 in the erg251Δ/Δ mutant causes some increase in ergosterol levels. Finally, the hypersensitivity of efg1Δ/Δ mutants to the ergosterol inhibitor fluconazole is reversed by ERG251 overexpression, arguing that reduced ERG251 expression contributes to this efg1Δ/Δ phenotype. Our results indicate that ERG251 is required for biofilm formation because its high expression levels are necessary for ergosterol synthesis in a biofilm-like environment.

Designing Surface Passivators Through Intramolecular Potential Manipulation for Efficient and Stable Perovskite Solar Cells.

The conjugation of terminal ammonium salt groups with perovskite surfaces is a frequently employed technique that aims to enhance the overall performance of perovskite materials, encompassing both bulk and surface properties. Particularly, it exhibits heightened efficacy when applied to surface modification, due to its ability to mitigate defect accumulation and facilitate facile binding with the receptive sites inherent to the perovskite structure. However, the interaction of the bulk ammonium group with PbI2 has the potential to form a low-dimensional phase of perovskite, which may obstruct carrier extraction at the interface. Therefore, the surface passivators (MeO-PFACl) are designed through intramolecular potential manipulation. The combinations of the electron-donating methoxy group and π-π conjugation of the phenyl ring reduce the local potential at the reactive site of formamidinium group, making it less likely to form a low-dimension phase with perovskite. This surface passivation strategy effectively suppresses the surface nonradiative recombination and promotes the interface carrier extraction. The devices treated with MeO-PFACl have demonstrated exceptional performance, achieving a peak power conversion efficiency (PCE) of 25.88%, with an average PCE of 25.37%. These works offer a novel principle for enhancing both the efficiency and stability of PSCs using ammonium-incorporated molecules without the induction of an additional phase layer.

Study on crystal to amorphous transition of nickel-based alloy processed by ultra-short pulsed laser shock peening

The main purpose was to investigate the process of crystal to amorphous transition in nickel-based alloy subjected to ultra-short pulsed laser shock peening. A molecular dynamics model of laser shock peened nanopolycrystalline nickel-based alloy was established using LAMMPS. The influence of shock velocity on the amorphous transformation in nickel-based alloy was analyzed. The results indicated that ultra-short pulsed laser shock peening with ultra-high strain rate plastic deformation promoted the increase and accumulation of defect for nickel-based alloy, contributing to the formation of amorphous structures.

PGE2 inhibits TIL expansion by disrupting IL-2 signalling and mitochondrial function

Expansion of antigen-experienced CD8+ T cells is critical for the success of tumour-infiltrating lymphocyte (TIL)-adoptive cell therapy (ACT) in patients with cancer1. Interleukin-2 (IL-2) acts as a key regulator of CD8+ cytotoxic T lymphocyte functions by promoting expansion and cytotoxic capability2,3. Therefore, it is essential to comprehend mechanistic barriers to IL-2 sensing in the tumour microenvironment to implement strategies to reinvigorate IL-2 responsiveness and T cell antitumour responses. Here we report that prostaglandin E2 (PGE2), a known negative regulator of immune response in the tumour microenvironment4,5, is present at high concentrations in tumour tissue from patients and leads to impaired IL-2 sensing in human CD8+ TILs via the PGE2 receptors EP2 and EP4. Mechanistically, PGE2 inhibits IL-2 sensing in TILs by downregulating the IL-2Rγc chain, resulting in defective assembly of IL-2Rβ–IL2Rγc membrane dimers. This results in impaired IL-2–mTOR adaptation and PGC1α transcriptional repression, causing oxidative stress and ferroptotic cell death in tumour-reactive TILs. Inhibition of PGE2 signalling to EP2 and EP4 during TIL expansion for ACT resulted in increased IL-2 sensing, leading to enhanced proliferation of tumour-reactive TILs and enhanced tumour control once the cells were transferred in vivo. Our study reveals fundamental features that underlie impairment of human TILs mediated by PGE2 in the tumour microenvironment. These findings have therapeutic implications for cancer immunotherapy and cell therapy, and enable the development of targeted strategies to enhance IL-2 sensing and amplify the IL-2 response in TILs, thereby promoting the expansion of effector T cells with enhanced therapeutic potential.

A flexible, reusable and adjustable high-performance energy absorption system inspired by interlocking suture structures

Energy absorption systems play a very important role in impact protection under complex load conditions. However, traditional protective structures cannot adjust the mechanical properties on demand to accommodate variable load characteristics once manufactured. Therefore, inspired by the superior compression resistance of the diabolical ironclad beetle, a modular energy absorption system is developed by combining the efficient mechanical properties of thin-walled tubes and the robust connectivity of interlocking suture structures, which can be easily assembled from only bio-inspired tubes without external constraints. FEM simulations were performed to systematically investigate the static and dynamic mechanical properties of the developed system, and its crushing performance was demonstrated experimentally. Additionally, the influence of geometric parameters on the mechanical properties of the system has been investigated, and the insensitivity of secondary geometrical parameters and assembly defects has been verified, which shows that the system has a certain safety margin to avoid catastrophic accidents caused by fabrication defects. Moreover, the system exhibits excellent reusability under multi-impact load environments and its energy absorption capacity does not degrade after the primary impact. Furthermore, the system exhibits good designability thanks to the discrete modular structures, its mechanical properties can be tuned by stiffness design without affecting the energy absorption capacity, and its specific energy absorption can be effectively improved by lightweight design. This study provides a novel design strategy for the protection system applied in multiple complex environments.

Inactivation of the ribosome assembly factor RimP causes streptomycin resistance and impairs motility in Salmonella.

The ribosome is the central hub for protein synthesis and the target of many antibiotics. Although the majority of ribosome-targeting antibiotics inhibit protein synthesis and are bacteriostatic, aminoglycosides promote protein mistranslation and are bactericidal. Understanding the resistance mechanisms of bacteria against aminoglycosides is not only vital for improving the efficacy of this critically important group of antibiotics but also crucial for studying the molecular basis of translational fidelity. In this work, we analyzed Salmonella mutants evolved in the presence of the aminoglycoside streptomycin (Str) and identified a novel gene rimP to be involved in Str resistance. RimP is a ribosome assembly factor critical for the maturation of the 30S small subunit that binds Str. Deficiency in RimP increases resistance against Str and facilitates the development of even higher resistance. Deleting rimP decreases mistranslation and cellular uptake of Str and further impairs flagellar motility. Our work thus highlights a previously unknown mechanism of aminoglycoside resistance via defective ribosome assembly.

Extensive phase transformation in an equiatomic CrCoNi medium entropy alloy under extreme uniaxial tension

The dynamic tension behavior of an equiatomic CrCoNi medium entropy alloy (MEA) has been studied at both room temperature (RT, 298 K) and liquid nitrogen temperature (LNT, 77 K). Microstructural observations show that extensive phase transformations were activated in this alloy under dynamic tension at LNT instead of the activation of the deformation twins under high strain rate only or quasi-static loading at LNT. The appearance of massive nanoscale phase transformation bands along multiple slip directions even created a network structure of HCP lamellae in the FCC grains. This leads to defect accumulation at the intersection regions and results in the formation of new HCP variants, inverse phase transformations to FCC structure and even amorphous domains. Such transformation induced plasticity (TRIP) effects including the mutual interactions of crossover phase transformation bands on the plasticity and tension fracture of the MEA under extreme loading conditions were further discussed. These findings provide a deeper understanding of the deformation mechanisms in the equiatomic MEA under extreme loads.

Abstract 5269: Evaluation of mitotic spindle inhibitors as cell autonomous inflammatory stimulants in MYC overexpressing breast cancers

Abstract The oncogenic transcription factor MYC is overexpressed in most cancer types, including difficult to treat human malignancies such as receptor triple-negative breast cancers (TNBC). MYC overexpression induces aneuploidy and suppresses anticancer immunity. Elevated levels of MYC can induce mitotic spindle assembly defects and chromosomal instability (CIN) events, exemplified by an increase in cells with micronuclei. These defects are partially mitigated by concomitant upregulation of various mitotic spindle genes. Micronuclei result in cytosolic DNA which can activate cGAS-STING signaling, activating an interferon regulatory transcriptional program responsible for mounting an inflammatory immune response that potentially enhances immune cell recognition. We hypothesized that pharmacological inhibition of specific MYC deregulated mitotic spindle genes will further exacerbate mitotic defects in MYC high cells resulting in synthetic-lethal cell death and additional CIN to activate robust cGAS-STING activation. Interferon activation can increase surface expression of antigen presentation machinery, such as MHC-I, restoring the immunogenicity of MYC high cells. Here, we used mouse breast tumor cells in which MYC expression is conditionally expressed as well as human breast cancer cell lines with different levels of MYC expression. We assessed the anti-proliferative and cytotoxic effects of 9 mitotic small molecular inhibitors that affect spindle function. cGAS-STING activation in inhibitor treated and untreated samples was measured by immunoblotting for pathway proteins phosphorylated TBK1, total TBK1, and IFIT1. Differences in MHC-I cell surface expression was quantified using flow cytometry. Our findings revealed that inhibition of kinesin-like protein KIFC1 and transforming acidic coiled-coil-containing protein 3 (TACC3) induced greater levels of apoptosis in MYC high models. Moreover, inhibition of KIFC1 robustly triggered cGAS-STING activity in MYC high cells as evidenced by increased protein abundance of phospho-TBK1 and IFIT1 in a dose-dependent manner. In addition, sublethal KIFC1 inhibition resulted in increased levels of MHC-I surface expression in MYC high models. Our findings suggest that inhibition of MYC regulated mitotic spindle genes, specifically KIFC1, can serve to preferentially eliminate MYC overexpressing aggressive cancers. Furthermore, sublethal concentrations of a KIFC1 inhibitor can stimulate a tumor cell-intrinsic inflammatory-pathway. Future studies will determine if targeting KIFC1 can enhance the response of MYC high cancers to immunotherapy. Citation Format: Mauricio Jacobo, Andrei Goga. Evaluation of mitotic spindle inhibitors as cell autonomous inflammatory stimulants in MYC overexpressing breast cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5269.

The zinc finger motif in the mitochondrial large ribosomal subunit protein bL36m is essential for optimal yeast mitoribosome assembly and function

Ribosomes across species contain subsets of zinc finger proteins that play structural roles by binding to rRNA. While the majority of these zinc fingers belong to the C2-C2 type, the large subunit protein L36 in bacteria and mitochondria exhibits an atypical C2-CH motif. To comprehend the contribution of each coordinating residue in S. cerevisiae bL36m to mitoribosome assembly and function, we engineered and characterized strains carrying single and double mutations in the zinc coordinating residues. Our findings reveal that although all four residues markedly influence protein stability, C to A mutations in C66 and/or C69 have a more pronounced effect compared to those at C82 and H88. Importantly, protein stability directly correlates with the assembly and function of the mitoribosome and the growth rate of yeast in respiratory conditions. Mass spectrometry analysis of large subunit particles indicates that strains deleted for bL36m or expressing mutant variants have defective assembly of the L7/L12 stalk base, limiting their functional competence. Furthermore, we employed a synthetic bL36m protein collection, including both wild-type and mutant proteins, to elucidate their ability to bind zinc. Our data indicate that mutations in C82 and, particularly, H88 allow for some zinc binding albeit inefficient or unstable, explaining the residual accumulation and activity in mitochondria of bL36m variants carrying mutations in these residues. In conclusion, stable zinc binding by bL36m is essential for optimal mitoribosome assembly and function. MS data are available via ProteomeXchange with identifierPXD046465.

Detection of Rail Fastener Assembly Defects Using Axle-Box Acceleration

Detection of Rail Fastener Assembly Defects Using Axle-Box Acceleration

A physics-based tessellation algorithm for particle assemblies on arbitrary surfaces

Interacting particle assemblies embedded on a surface are often used to model biophysical systems and to study new colloidal materials. The configurations resulting from the particles interacting with each other and with their substrate affect the system's physical properties, which depend on local symmetries and defects. It is therefore important to identify the nature and location of defects in the particle assembly. This task is often achieved using either the Voronoi tessellation algorithm or order parameters. Although very useful, they present limitations, especially when the particle assemblies are embedded on irregular or highly deformed 3D surfaces. In this work, we present a novel algorithm to generate the tessellation of particle assemblies on 3D surfaces of arbitrary geometry. The algorithm is based on the particles' physical interactions and does not require a priori information on the surface geometry. The resulting cells in the tessellation represent each particle's interactions with its first ring of neighboring particles. The algorithm is tested using 2D and 3D surfaces, with or without periodic boundary conditions, with holes or fully covered by particles, of regular geometry or highly deformed shape, and in the presence of positive, zero, and negative Gaussian curvature. In all cases, the presented algorithm is capable of generating a tessellation representing the particle interactions and highlighting the location and nature of the assembly defects. Finally, the proposed algorithm is compared with both Voronoi and hexatic order parameters in several representative cases to highlight similarities with existing methods as well as the advantages of the newly proposed algorithm.