Organelles Research Articles

Involvement of autophagy in germ cells in an experimental model of varicocele in rats before and after varicocelectomy.

Autophagy, a catabolic process enabling cellular organelles and proteins' reuse for energy, has been observed in varicocele models, but the effect of surgical treatment on this process remains unknown. This study aims to assess autophagy in varicocele models undergoing surgical correction. Twenty-one adolescent male rats were induced with varicocele and divided into three groups: sham, varicocele, and varicocele with varicocelectomy. After 21days, testicles were examined histologically for spermatogenesis (Jonhsen's score) and immunohistochemically for autophagy markers (LC3A, Beclin-1, Ambra-1, ULK-1, p62). Positive germ cells were quantitatively evaluated, and data were statistically analyzed (p < 0.05). Histological examination revealed significantly reduced Jonhsen's scores in varicocele compared to sham and varicocelectomy groups (p < 0.05). Expression of autophagy markers (LC3A, Beclin-1, Ambra-1, ULK-1, p62) was significantly higher in varicocele than sham and varicocelectomy groups (p < 0.05), and in varicocelectomy than sham (p < 0.05). Varicocele activates autophagy markers, with p62 potentially modulating autophagy despite being considered an inhibitor. While varicocelectomy improves histology, it doesn't fully inhibit autophagy, suggesting ongoing germ cell dysfunction despite treatment. This underscores varicocele's detrimental effects on germ cell functionality.

Mitochondrial and ER contact sites related to physiology and diseases

Mitochondria and the endoplasmic reticulum (ER) are indispensable organelles in eukaryotic cells, playing pivotal roles in energy production, calcium homeostasis, and lipid synthesis. The specialized contact sites between these two organelles, known as mitochondria-associated ER membranes (MERCs), facilitate fundamental cellular functions such as lipid metabolism, and apoptosis. Disruption of MERCs is implicated in various diseases, including neurodegenerative disorders, cardiovascular diseases, diabetes. This review delves into the dynamics of mitochondria, the importance of MERCs, and their implications in disease pathogenesis. We have explored the processes of mitochondrial fusion and fission, regulated by proteins such as mitofusins and dynamin-related protein 1, and their impact on mitochondrial quality control and cellular stress responses. Furthermore, we investigate the role of the ER in mitochondrial dynamics, with a focus on how ER-mitochondria interactions influence cellular homeostasis. By unraveling the complex mechanisms governing MERCs, we can identify potential therapeutic targets for diseases associated with MERC dysfunction, thereby offering new avenues for treatment.

Molecular Imaging of Nitric Oxide Surrogates with Organelle-Specific Fluorescent Probes.

Nitric oxide is an important signalling molecule responsible for maintaining body's homeostasis. Any dysregulation in NO can lead to many pathological conditions like atherosclerosis, cancers, neurodegenerative disorders, hypertension, and inflammation. Several, sensing technologies are used for sensing NO. Among these, fluorescent imaging is considered to be one of the most efficient. Till date, approximately 123 fluorescent probes are reported related to nitric oxide (NO) sensing fluorescent probes for the sensitive, selective, and real-time detection of NO at both the cellular and subcellular levels. In the past five years, around 41 fluorescent probes and four review articles have been published, specifically focusing on the detection of nitric oxide. Despite considerable advancements in this area, no systematic review has summarized various organelle-targeting NO-sensing fluorescent probes. Herein, we summarized last five years from 2019 to 2024 along with the key pioneering research in this field covering divergent roles of NO across various cellular organelles. We have included 41 probes by classifying into different organelle targeting sections. We strongly believe this review will provide an advanced summary of NO specific fluorescent probes and their applications for monitoring the progression of diseases in in vitro to in vivo models such as drosophila, zebrafish, mouse models.

Bone tissue condition in early dates of restoration after thermic exposure

BACKGROUND: Thermoablation is a promising method for treating bone tumors. It is important to select the optimal mode (dose/time) of high-temperature exposure to fully realize the potential of this method.AIM: to study in vivo the reaction of rabbits’ bone tissue (BT) in the dynamics of early (3-7 days) recovery after local intraoperative hyperthermic ablation in the temperature range in the bone marrow canal of 55-60℃.METHODS: The study involved 6 mongrel rabbits aged 15 weeks, weighing 3-4 kg. The animals were derived from the experiment on the 3rd and 7th days after local thermoablation of the femoral diaphysis. Histological assay of BT included overall examination (HE staining), assessment of the area of immature BT (Mallory staining), optical density and area of osteoblasts and osteocytes (Einarson staining). Statistical data processing was performed in the R programming language.RESULTS: HE staining showed no signs of pathological changes after high-temperature exposure of BT. Mallory staining revealed no negative effects of local thermoablation on the intercellular bone matrix. Morphometric analysis showed an overshoot in the area of osteoblasts by the 7th day against the background of reduced synthetic activity starting from the 3rd day of the experiment. By the 3rd day, there is also a decrease in the area and optical density of osteocytes in the diaphyses of bones subjected to thermoablation. However, by the 7th day, the area of mature bone cells doesn`t differ from the corresponding value in the contralateral limb.CONCLUSION: Local intraoperative thermoablation of rabbit femoral diaphyses at an intramedullary temperature of 55-60℃ significantly reduces the optical density of osteoblasts and osteocytes in the dynamics of early (3-7 days) recovery after extreme exposure, which suggests a violation of metabolic processes and intracellular organelles (nucleus, ribosomes) of bone cells. At the same time, signs of remodeling of the damaged area were noted, presumably through the mechanism of osteoconduction of endosteal and periosteal cells from metaphyses that were not subjected to direct hyperthermia. The results obtained may be useful in thermoablation of BT tumors with the condition of higher sensitivity of malignant cells to heating.

Drug-device-field integration for mitochondria-targeting dysfunction and tumor therapy by home-tailored pyroelectric nanocomposites

In spite of the hypoxia tumor microenvironment, an efficacious treatment with minimal invasiveness is highly desirable. Among common cellular organelles, mitochondria is a common target for inductive cellular apoptosis and tumor proliferation inhibition. Nevertheless, tumor hypoxic circumstances always give rise to poor therapeutic efficiency and instead lead to lesion recurrence and unsatisfactory prognosis. Herein, a home-tailored pyroelectric nanocomposites of BTO@PDA-FA-DOX-EGCG have been developed via a layer-by-layer synthesis to serve a cutting-edge tumor treatment with specific mitochondria-targeting, hypoxia-relieving, chemo-photodynamic performance and high anti-tumor efficacy. In particular, this therapeutic modality is featured as drug-device-field integration (DDFI) by combining chemo-drugs of DOX and EGCG, a commercially available medical laser and physical pyroelectric fields, which synergistically contributed to continuing ROS production and consequently cell apoptosis and tumor growth inhibition. Meanwhile, an anti-tumor mechanism of immune actuation and mitochondria dysfunction was elucidated by analyzing specific biomarkers of mitochondria complexes and MMPs, and therefore this research opened up a potential pathway for advanced tumor treatment by incorporating nanocomposites, medical devices and physical fields in a DDFI manner.

Styryl dyes for viscosity measurement and detection of pathological processes in mitochondria of living cells using fluorescence lifetime imaging microscopy, a critical study

In the present work, two molecular rotors based on styryl dyes were synthesized and investigated. Both dyes showed significant sensitivity to the viscosity of the medium. Due to their significant positive charge, they efficiently accumulated in mitochondria of living cells. Binding to mitochondria resulted in increased fluorescence intensity and fluorescence lifetime of the dyes, allowing them to be visualized without washing off the unbound dye. We have also shown that the fluorescence lifetime of the studied molecular rotors is determined not only by the viscosity of the medium, but also by interactions with cell components such as proteins and nucleic acids. The present work clearly shows that these interactions do not allow a reliable estimation of viscosity in cell organelles using the synthesized dyes. This compromises the results of previous viscosity studies using molecular rotors at least of the styryl type. Nevertheless, induction of cell apoptosis by benzylviologen led to an increase in brightness and fluorescence lifetime of the dyes, which can be caused by both changes in viscosity and changes in the expression profile of proteins localized in mitochondria and interacting with the dyes. Thus, the obtained styryl dyes, like previously published homologous compounds, cannot be used for viscosity measurements, but can be used for identification of pathological states of the cell.

Concentration-dependent cellular responses of coontail (Ceratophyllum demersum) during the substitutions to perfluorooctanoic acid by its two alternatives

The substitutions of alternatives to legacy per- and polyfluoroalkyl substances (PFASs) may lead to unknown and variational joint toxicity on ecosystems. To comprehensively understand the effects of substitutions on aquatic ecosystems, the single and joint effects of perfluorooctanoic acid (PFOA) and its alternatives (perfluorobutanoic acid, PFBA; 2,3,3,3-tetrafluoro-2-(1,1,2,2,3,3,3,heptafluoropropoxy)propanoic acid, GenX) with various concentrations and compositions on a primary producer, coontail (Ceratophyllum demersum), were investigated at cellular level. Results showed that the substitutions of PFBA/GenX could alleviate the inhibition of PFOA on plant length, hydrogen peroxide accumulation, and chlorophyll b, due to the shifts of reactive oxygen species and their less toxicity to antioxidants. Significant up-regulations of superoxide dismutase, glutathione, and carotenoid implied their primary roles in defensing against PFASs (p<0.05). Catalase/peroxidase was significantly up-regulated in PFBA/GenX substitutions (p<0.05) to help alleviate stress. PFBA substitutions reduced 23.9% of PFOA in organelle and GenX reduced the subcellular concentrations of PFOA by 1.8%–17.4%. Redundancy analysis suggested that PFOA, PFBA, and GenX in cell wall and organelle, as well as GenX in soluble fractions, were responsible for the cellular responses. These findings were helpful to understand the integrated effects on aquatic ecosystems during the substitutions to legacy PFASs by alternatives.

Bioorthogonal Activation of Deep Red Photoredox Catalysis Inducing Pyroptosis.

The revolutionary impact of photoredox catalytic processes has ignited novel avenues for exploration, empowering us to delve into nature in unprecedented ways and to pioneer innovative biotechnologies for therapy and diagnosis. However, integrating artificial photoredox catalysis into living systems presents significant challenges, primarily due to concerns over low targetability, low compatibility with complex biological environments, and the safety risks associated with photocatalyst toxicity. To address these challenges, herein, we present a novel bioorthogonally activatable photoredox catalysis approach. In this approach, potent photocatalyst selection via atom replacement of the rhodamine core yielded the bioorthogonally activatable photocatalyst (PC-Tz). The introduction of 1,2,4,5-tetrazine quenched its photocatalytic properties, which were restored upon an intracellular inverse electron-demand Diels-Alder (iEDDA) reaction with trans-cyclooctene (TCO) localized in mitochondria. This reaction led to remarkable photocatalytic oxidation of nicotinamide adenine dinucleotide (NADH), effectively manipulating the mitochondrial electron transport chain (ETC) under hypoxic conditions in cancer cells. Additionally, photocatalytic pyroptotic cell death was observed through a caspase-3/gasdermin E (GSDME) pathway, achieving notable antitumor efficacy and adenosine triphosphate (ATP) reduction in tumor cells. To the best of our knowledge, this represents the first example of bioorthogonally activatable photoredox catalysis, opening new avenues for chemists to spatiotemporally control activity in specific cell organelles without disrupting other native biological processes.

Effect of Different Thawing Regimes on Cell Kinematics and Organelle Integrity of Nitrogen-Stored Wallachian Ram Spermatozoa

Artificial insemination is an advanced reproductive technology used to increase the number of lambs born from elite sires to accelerate genetic gain in a flock [...]

Ubiquitin and Ubiquitin-Like Modifications in Organelle Stress Signaling: Ub, Ub, Ub, Ub, Stayin' Alive, Stayin' Alive.

Due to various intracellular and external cues, cellular organelles are frequently stressed in both physiological and pathological conditions. Sensing these stresses initiates various signaling pathways which may lead to adaptation of the stressed cells or trigger its their death. At the unicellular level, this stress signaling involves a crosstalk between different organelles. At the multicellular level, such pathways can contribute to indicate the presence of a stressed cell to its neighboring cells. Here, we highlight the crucial and diverse roles played by Ubiquitin and Ubiquitin-like modification in organelle stress signaling.

Urolithin A Protects Hepatocytes from Palmitic Acid-Induced ER Stress by Regulating Calcium Homeostasis in the MAM

An ellagitannin-derived metabolite, Urolithin A (UA), has emerged as a potential therapeutic agent for metabolic disorders due to its antioxidant, anti-inflammatory, and mitochondrial function-improving properties, but its efficacy in protecting against ER stress remains underexplored. The endoplasmic reticulum (ER) is a cellular organelle involved in protein folding, lipid synthesis, and calcium regulation. Perturbations in these functions can lead to ER stress, which contributes to the development and progression of metabolic disorders such as metabolic-associated fatty liver disease (MAFLD). In this study, we identified a novel target protein of UA and elucidated its mechanism for alleviating palmitic acid (PA)-induced ER stress. Cellular thermal shift assay (CETSA)-LC-MS/MS analysis revealed that UA binds directly to the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA), an important regulator of calcium homeostasis in mitochondria-associated ER membranes (MAMs). As an agonist of SERCA, UA attenuates abnormal calcium fluctuations and ER stress in PA-treated liver cells, thereby contributing to cell survival. The lack of UA activity in SERCA knockdown cells suggests that UA regulates cellular homeostasis through its interaction with SERCA. Collectively, our results demonstrate that UA protects against PA-induced ER stress and enhances cell survival by regulating calcium homeostasis in MAMs through SERCA. This study highlights the potential of UA as a therapeutic agent for metabolic disorders associated with ER stress.

Visualizing the Internalization of Marburg Viruslike Particles into Living Cells.

Viral entry into cells is a pivotal stage of the infection process and, therefore, a prime target for the development of antiviral therapeutics. Here, we describe a system to monitor the internalization of lipophilic dye-labeled Marburg viruslike particles (VLPs) into living cells. Using cells stably expressing fluorescent protein-fused markers for specific cell organelles, the VLP entry process can be visualized. This procedure enables the characterization of the entry process by visualizing individual steps using specific bio-probes. Additionally, when combined with image analysis, this method allows for the quantification of the efficiencies of individual entry steps including particle adsorption, uptake by endocytosis, and membrane fusion. Finally, this method can be used for antiviral drug screening.

Overview of lysosome-mediated chemoresistance mechanisms in breast cancer: A mini review

It is widely acknowledged that chemoresistance is one of the major consequences that leads to chemotherapeutic treatment failure and cancer-related death. In recent studies, lots of attempts have been made to clarify the mechanisms that cancer cells utilize and/or modify to become resistant to chemotherapeutic drugs. Among these, lysosomes, also called ‘‘drug-safe house’’, have emerged as one of the crucial drivers of chemoresistance through trapping passively the chemotherapeutics, thereby preventing them from reaching their intracellular targets. Notably, lysosomes take part in regulating cellular metabolism, tumor growth and metastasis. Besides, lysosomes are a platform for inter- and intracellular communication among cellular organelles and/or cell surfaces and/or between tumor cells and extracellular microenvironment. In breast cancer (BCa), the mechanisms underlying chemotherapeutic resistance are perplexing and have not been fully understood. Therefore, in this review, we briefly highlight some aspects that describe lysosome-mediated regulation of chemoresistance in BCa.

Bioinformatic Analysis and Molecular Docking to Elucidate the Anticancer Effect of Silver Nanoparticles in Hepatocellular Carcinoma

Background: Hepatocellular carcinoma is the cancer with the highest mortality rate worldwide. Currently, existing treatments are not very effective for this disease. Different science areas have focused on developing new therapies, including nanomedicine. In-vitro studies have reported the anticancer activity of silver nanoparticles, particularly those coated with polyvinylpyrrolidone (AgNPs-PVP). Aims: Characterize the effect of AgNPs on the HepG2 by bioinformatics analysis. Methods: From a list of proteins, we performed in-silico analysis to predict protein-protein interaction, hub gene, gene ontology, KEGG pathways, hub gene expression, protein expression, survival, cell infiltration immune, and molecular docking of AgNPs-PVP to target proteins. Cytoscape and UCSF Chimera software, DAVID, UALCAN, TISIDB, and HDOCK databases were included in the predictive analysis. Results: Gene ontology and KEGG pathways showed that AgNP exposure causes cellular organelles dysregulation and deregulation of protein production mechanisms. Additionally, metabolic pathways were altered, including glycolysis, gluconeogenesis, and amino acid biosynthesis. Hub genes RPS15, RPLP0, EEF1B2, RPL12, and NACA showed differential expression for gene expression, protein, and survival analysis. Furthermore, RPS15 and RPL12 were positively correlated with CD8+ T cell infiltration, and RPLP0, EEF1B2, and NACA were negatively correlated with NK cell infiltration. Finally, molecular docking showed that AgNPs-PVP interacts highly with the target proteins. Conclusion: AgNPs cause alterations in cell viability. Furthermore, the deregulation of hub genes and the modulation of the immune system are associated with anticancer effects, and molecular docking demonstrated high interaction with the target proteins that should be studied experimentally.

Packaging "vegetable oils": Insights into plant lipid droplet proteins.

Plant neutral lipids, also known as "vegetable oils", are synthesized within the endoplasmic reticulum (ER) membrane and packaged into subcellular compartments called lipid droplets (LDs) for stable storage in the cytoplasm. The biogenesis, modulation, and degradation of cytoplasmic LDs in plant cells are orchestrated by a variety of proteins localized to the ER, LDs, and peroxisomes. Recent studies of these LD-related proteins have greatly advanced our understanding of LDs not only as steady oil depots in seeds but also as dynamic cell organelles involved in numerous physiological processes in different tissues and developmental stages of plants. In the past 2 decades, technology advances in proteomics, transcriptomics, genome sequencing, cellular imaging and protein structural modeling have markedly expanded the inventory of LD-related proteins, provided unprecedented structural and functional insights into the protein machinery modulating LDs in plant cells, and shed new light on the functions of LDs in nonseed plant tissues as well as in unicellular algae. Here, we review critical advances in revealing new LD proteins in various plant tissues, point out structural and mechanistic insights into key proteins in LD biogenesis and dynamic modulation, and discuss future perspectives on bridging our knowledge gaps in plant LD biology.

Genomic survey and evolution analysis of calcium-dependent protein kinases in plants and their stress-responsive patterns in populus

BackgroundCalcium-dependent protein kinases (CDPKs) phosphorylate downstream target proteins in response to signals transmitted by free calcium ions (Ca2+, one of the second messengers) and thus play important regulatory roles in many biological processes, such as plant growth, development, and stress response.ResultsA bioinformatic analysis, as well as thorough evolutionary and expression investigations, were conducted to confirm previous reports of functional evidence for plant CDPKs. Using the Phytozome database’s BLAST search engine and the HMM search tool in TBtools software, we discovered that CDPKs are well conserved from green algae to flowering angiosperms in various gene family sizes. Additional investigations of the obtained CDPKs revealed high conservation of domain and motif numbers, gene architectures, and patterns. However, this conservation differed among plant species. Phylogenetic analysis demonstrated that the CDPK gene family diverged from a common ancient gene. Similarly, investigations into plant interspecies evolutionary relationships revealed common ancestral plant species, suggesting speciation of plants and evolution based on plant adaptation and diversification. A search for the driving force of CDPK gene family expansion revealed that dispersed duplication events, among other duplication events, contributed largely to CDPK gene family expansion. Gene localization analysis in P. trichocarpa demonstrated that most CDPK genes are localized within several cell organelles and bind other kinases and proteins to perform their biological functions efficiently. Using RNA-seq data and qPCR analyses, we postulated that PtCDPKs play functional roles in abiotic stress responses by regulating cold, heat, drought and salt stress to varying extents.ConclusionThe CDPK genes are well conserved in plants and are critical entities in abiotic stress regulation, and further exploration and manipulation of these genes in the future may provide solutions to some of the challenges in agriculture, forestry and food security.

Construction of molecular subtype and prognostic model for gastric cancer based on nucleus-encoded mitochondrial genes

Gastric cancer (GC) is a common digestive system cancer, characterized by a significant mortality rate. Mitochondria is an indispensable organelle in eukaryotic cells. It was previously revealed that a series of nucleus-encoded mitochondrial genes (NMG) mutations and dysfunctions potentially contribute to the initiation and progression of GC. However, the correlation between NMG mutations and survival outcomes for GC patients is still unclear. In this study, NMG expression profile and clinical information in GC samples were collected from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Through consistent clustering and functional enrichment analysis, we have identified three NMG clusters and three gene clusters that are associated with patterns of immune cell infiltration. Prognostic genes were identified through Univariate Cox regression analysis. The principal component analysis was conducted to set up a scoring system. Subsequently, the Single‑cell RNA sequencing (scRNA-seq) data of GC patients and cancer cell drug sensitivity data were retrieved from the GEO database. Patients with high NMG scores exhibited increased microsatellite instability status and a heightened tumor mutation rate compared to those with low NMG scores. Survival analysis revealed that GC samples with high NMG scores could achieve a better prognosis. Additionally, These patients were observed to be more responsive to immunotherapy. Moreover, we delved into prognostic genes at the level of single cells, revealing that MRPL4 and MRPL37 exhibit high expression in epithelial cells, while TPM1 demonstrates high expression in tissue stem cells. Utilizing cancer cell drug sensitivity data from the Drug Sensitivity in Cancer (GDSC) database, we noted a heightened sensitivity to chemotherapy in the high NMG group. Furthermore, we discovered a significant enrichment of cuproptosis-related genes in clusters with high NMG scores. Consequently, employing the scoring system could facilitate the prediction of GC patients’ sensitivity to cuproptosis-induced therapy. Our study confirmed the potency of this scoring system as a therapeutic response biomarker for gastric cancer, potentially informing clinical treatment strategies.

Mitochondrial Dysfunction: Effects and Therapeutic Implications in Cerebral Gliomas.

Gliomas are the most common primary brain tumors, representing approximately 28% of all central nervous system tumors. These tumors are characterized by rapid progression and show a median survival of approximately 18 months. The therapeutic options consist of surgical resection followed by radiotherapy and chemotherapy. Despite the multidisciplinary approach and the biomolecular role of targeted therapies, the median progression-free survival is approximately 6-8 months. The incomplete tumor compliance with treatment is due to several factors such as the presence of the blood-brain barrier, the numerous pathways involved in tumor transformation, and the presence of intra-tumoral mutations. Among these, the interaction between the mutations of genes involved in tumor bio-energetic metabolism and the functional response of the tumor has become the protagonist of numerous studies. In this scenario, the main role is played by mitochondria, cellular organelles delimited by a double membrane and containing their own DNA (mtDNA), which participates in numerous cellular processes such as the regulation of cellular metabolism, cellular proliferation, and apoptosis and is also the main source of cellular energy production. Therefore, it is understood that the mitochondrion, specifically its functional alteration, is a leading figure in tumor transformation, including brain tumors. The acquisition of mutations in the mitochondrial DNA of tumor cells and the subsequent identification of the so-called mitochondria-related genes (MRGs), both functional (mutation of Complex I) and structural (mutations of Complex III/IV), have been seen to play an important role in metabolic reprogramming with increased proliferation, resistance to apoptosis, and the progression of tumorigenesis. This demonstrates that these mitochondrial alterations could have a role not only in the intrinsic tumor biology but also in the extrinsic one associated with the therapeutic response. We aim to summarize the main mitochondrial dysfunction interactions present in gliomas and how they might impact prognosis.

Combining NeuroPainting with transcriptomics reveals cell-type-specific morphological and molecular signatures of the 22q11.2 deletion.

Neuropsychiatric conditions pose substantial challenges for therapeutic development due to their complex and poorly understood underlying mechanisms. High-throughput, unbiased phenotypic assays present a promising path for advancing therapeutic discovery, especially within disease-relevant neural tissues. Here, we introduce NeuroPainting, a novel adaptation of the Cell Painting assay, optimized for high-dimensional morphological phenotyping of neural cell types, including neurons, neuronal progenitor cells, and astrocytes derived from human stem cells. Using NeuroPainting, we quantified cell structure and organelle behavior across various brain cell types, creating a public dataset of over 4,000 cellular traits. This extensive dataset not only sets a new benchmark for phenotypic screening in neuropsychiatric research but also serves as a gold standard for the research community, enabling comparisons and validation of results. We then applied NeuroPainting to identify morphological signatures associated with the 22q11.2 deletion, a major genetic risk factor for schizophrenia. We observed profound cell-type-specific effects of the 22q11.2 deletion, with significant alterations in mitochondrial structure, endoplasmic reticulum organization, and cytoskeletal dynamics, particularly in astrocytes. Transcriptomic analysis revealed reduced expression of cell adhesion genes in 22q11.2 deletion astrocytes, consistent with recent post-mortem findings. Integrating the RNA sequencing data and morphological profiles uncovered a novel biological link between altered expression of specific cell adhesion molecules and observed changes in mitochondrial morphology in 22q11.2 deletion astrocytes. These findings underscore the power of combined phenomic and transcriptomic analyses to reveal mechanistic insights associated with human genetic variants of neuropsychiatric conditions.

Synthesis of coumarin based Tb3+ complex and its application in cell imaging

Mitochondria is an important site for ATP production from oxidative phosphorylation, and plays a crucial role in biochemical processes. It is a significant site for the production of ATP via oxidative phosphorylation, and plays crucial in regulation of apoptosis, redox homeostasis and calcium signalling. In the present work, Tb3+ complex was synthesized using coumarin based ligand L and 1, 10-phenanthroline as coligand. The coumarin is well known for its photophysical and medicinal importance in therapeutic research. Photophysical characterizations of the complex indicated that the ligand efficiently sensitizes the emissive level of Tb3+ ion. Thus, the long-excited state lifetime of 0.75 ms and high quantum yield of 57 % exhibited by the complex led to its employment in imaging of cellular organelles. Interestingly, the complex was found to be selectively localized to mitochondria, its positively charged chemical structure being permeable to the cell membrane and accumulating in mitochondria, which is well visualized under confocal microscopy. An attempt has been made to understand how the Tb3+ complex can be taken up by mitochondria and become a better target for drugs that exhibit therapeutic effect.