Biology subjects

Nandi, C. K.

Publications and source records attributed to Nandi, C. K..

8 recordsLinked to original sources

bioRxiv2026

Euchromatin Peripheral Organization Follows Anterograde Signalling Under Anaesthetic Stress

Anterograde and retrograde signalling establish bidirectional communication between the nucleus and chloroplasts. Retrograde signals from chloroplasts regulate nuclear gene expression while anterograde signals from the nucleus coordinate chloroplast development and maintain cellular homeostasis. How this bidirectional signalling framework extends beyond locus-specific regulation to shape the global spatial organization of nuclear chromatin across tissues remains unclear. Although anaesthesia can alter chromatin organisation, the role of chloroplast dysfunction in these changes remains unclear. Here, we investigate how chloroplast dysfunction and anaesthesia influence euchromatin and heterochromatin organisation in Solanum lycopersicum seedlings across tissues with contrasting photosynthetic competence. Using confocal and super-resolution radial fluctuation (SRRF) imaging with quantitative multiparameter analysis, we identify distinct, tissue-specific chromatin responses to chloroplast disruption and anaesthesia. Notably, anaesthesia induces distinct spatial chromatin changes across tissues that are independent of chloroplast dysfunction, suggesting a direct nuclear response to anaesthesia rather than a chloroplast-mediated retrograde effect. These findings highlight chromatin topology as a potential quantitative biomarker of cellular disruption and provide a framework for investigating anterograde chloroplast-nucleus coordination and stress-responsive nuclear organisation in plants.

plant biology↗

bioRxiv2026

Efficient Mitigation of Copper Induced Cellular Dysfunction Using Chitosan Based Iron Oxide Nanoparticles

Copper is an essential redox-active micronutrient, but agricultural soils are increasingly contaminated by copper from mining, industrial discharge, and intensive agrochemical use, pushing concentrations beyond levels plants can tolerate. Excess copper triggers Fenton-like reactive oxygen species (ROS) generation, mitochondrial dysfunction, and impaired growth. Existing mitigation strategies, such as soil amendments, phytoremediation, antioxidants, and different chelators, have been explored to reduce copper toxicity, but their effectiveness can be limited by immobilization, poor specificity, and environmental persistence. The present work introduces a nanoparticle-based strategy for the direct sequestration of excess copper coupled with protection against the oxidative damage caused by copper stress. Here, we report MPA-iron oxide nanoparticles (MIONPs), sequentially functionalized with chitosan, glutathione, and 3-mercaptopropionic acid, designed to simultaneously scavenge ROS, restore redox homeostasis, and chelate copper via surface thiol groups. MIONPs showed a significant increase in copper binding capacity over bare iron oxide nanoparticles (BIONPs) and, in copper-stressed Solanum lycopersicum seedlings, significantly improved germination and root/shoot growth, reduced intracellular ROS, restored mitochondrial membrane potential, and preserved nuclear integrity. This integrated design establishes MIONPs as a promising, dual-function nanoplatform for sustainable copper stress management in agriculture.

plant biology↗

bioRxiv2025

Copper Stress Trigger Organelles Communication and Chromatin Condensation Leading to Cell Death in Solanum lycopersicum

Copper (Cu) is a vital micronutrient for plants but becomes highly toxic when present in excess, disrupting redox balance and damaging cellular structures. While the physiological and mitochondrial responses to Cu toxicity are well-documented, the nuclear-level consequences, particularly chromatin remodeling and gene regulatory changes, remain poorly understood. In this study, we used the root apex of Solanum lycopersicum as a model system to explore how increasing copper concentrations affect organelle integrity, stress signaling, and nuclear architecture. Using confocal and super-resolution imaging with organelle-specific markers and immunostaining, we observed that mitochondria was the earliest affected to Cu stress, exhibiting fragmentation, membrane depolarization, and cytochrome c release led to reactive oxygen species (ROS) accumulation, activation of AMPK, suppression of mTOR signaling, and nuclear translocation of NRF2. Critically, we found that copper exposure induced profound nuclear alterations, including shrinkage, lobulation, peripheral chromatin tethering, and global condensation events tightly correlated with stress signaling. H3K4me3 immunostaining revealed a shift from active euchromatin to condensed, transcriptionally silent states, leading to membrane rupture and cell death in root tip cells. Our findings show that the nucleus actively integrates organelle-derived stress signals, with chromatin remodeling as a key marker of copper toxicity. This highlights potential for chromatin-based diagnostics and stress-resilient crop breeding. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=86 SRC="FIGDIR/small/665307v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@15a3595org.highwire.dtl.DTLVardef@1740149org.highwire.dtl.DTLVardef@1007f24org.highwire.dtl.DTLVardef@19b1a20_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗

bioRxiv2025

Direct Visualization of Anesthesia-induced Subcellular Dysfunction in Non-Neuronal Tissues of C. elegans

Volatile anaesthetics such as isoflurane, halothane, and sevoflurane are extensively utilized for their reversible induction of unconsciousness, exhibiting well-defined impacts on neural networks. However, their influence on non-neuronal and developing tissues is inadequately comprehended, generating concerns for vulnerable categories, including children and individuals receiving extended anesthesia. To rectify this deficiency, we examined the subcellular impacts of anaesthetics utilizing HEK 293T and HepG2 cell lines, alongside with Caenorhabditis elegans as a comprehensive organismal model. In vitro treatment to lidocaine and isoflurane resulted in mitochondrial depolarization, lysosomal aggregation, and buildup of reactive oxygen species (ROS). In vivo, 8% isoflurane induced mitochondrial fragmentation, loss of branching, and disruption of tubular lysosomes, indicating compromised energy metabolism and autophagic stress. We detected selective transcriptional inhibition of neuron- and immune-related promoters, although RNA Pol I remained active, indicating energy-conservation strategies. Systemic oxidative stress was validated by TIR-1::GFP aggregation and lipofuscin accumulation. Our research is one of the initial investigations that defines anaesthesia-induced subcellular dysfunction beyond the nervous system, providing novel insights for safer anaesthetic protocols and informing long-term health evaluations, especially in individuals who are developing or chronically exposed. Significance statementWhile volatile anaesthetics are widely used for inducing unconsciousness, their effects beyond neurons remain poorly understood. This study reveals that clinically used anaesthetics such as isoflurane and lidocaine cause profound subcellular dysfunction in non-neuronal systems, including mitochondrial depolarization, lysosomal disruption, transcriptional repression, and systemic oxidative stress. Using both human cell lines and Caenorhabditis elegans, we uncover conserved patterns of organellar damage and stress responses. These findings have critical implications for pediatric, intensive care, and long-term anaesthesia cases, urging the need to reassess anaesthetic safety profiles and develop biomarkers for systemic toxicity. Our work opens new avenues for designing cell-type-specific protective strategies under anaesthetic exposure.

pharmacology and toxicology↗

bioRxiv2025

A Hierarchical Cascade of Organellar Silencing and their Regeneration under Anaesthetic Stress in Plants

Anaesthetics are pharmacological drugs that temporarily inhibit neural activity by acting on voltage-gated sodium channels and GABA receptors. Although their neurological mechanisms are well-defined, their wider cellular effects, especially in non-neuronal systems, are inadequately understood d. This study utilized Solanum lycopersicum plants root apex cells as a transparent model to examine anaesthetic-induced subcellular alterations via live-cell fluorescence imaging, immunostaining, and super-resolution microscopy. Our findings, first of its kind, demonstrate the initial comprehensive model of sequential causal structure and hierarchical cascade of organelle collapse of different but important organelles such as mitochondria, lysosome, vesicles trafficking and nuclear architectures under anaesthesia in plants. The nucleus is identified as the most important controller of recovery potential and cellular fate. In a time dependent experiment, we found that plant cells exposed to lidocaine for up to four hours could still recover mitochondrial potential, lysosomal function, and nuclear integrity when anaesthesia is removed. However, beyond four hours, the damage, especially to the nucleus, was irreversible, and cells proceeded to programmed cell death. Our data further demonstrate that organelle functions can recover after brief exposure to anaesthetic stress. However, prolonged exposure prevents recovery, resulting in the irreversible degradation of the nucleus leading to complete cell death. The results present novel targets for preventative therapies, such as mitochondrial antioxidants, lysosomal stabilizers, and nuclear structural protectants that could mitigate anaesthetic-induced damage.

plant biology↗

bioRxiv2024

Super Resolved Structural Imaging of Mitochondrial Network using Orange Emissive Carbon Nanodot as Fluorescent Probe

Super-resolution microscopy (SRM), coupled with appropriate bright and photostable fluorescent probes, has revolutionized the ability to study organelle dynamics with unprecedented spatial and temporal resolution. An increasing trend of designing nanomaterial probes that has unprecedented advantages over the organic molecular probes has become the frontier in SRM based imaging of subcellular organelles. Herein, we report the development of orange-emissive fluorescent carbon nanodots (CNDs) via a one-pot synthesis that has excellent capabilities to target mitochondria. Spectroscopic analysis confirms the presence of guanidine on the surface of CNDs, thus facilitating its ability to selectively target mitochondria. The CNDs were highly capable for the super resolution radial fluctuation (SRRF) imaging of mitochondrial network and the morphology. The synthesized CNDs exhibited excellent photoluminescent properties along with high biocompatibility and non-toxicity, which could be used for their application in mitochondria-based imaging modalities.

biochemistry↗

bioRxiv2024

Carbon nanodots as a red emissive fluorescent probe for the super-resolution microscopy of DNA dynamics during paclitaxel treatment

Paclitaxel is a commonly used frontline chemotherapeutic drug for cancer treatment. It is known to be functional by arresting the microtubule disassembly during mitosis. Recently, a non-mitotic pathway has been evolving and thus contemplating the mitotic mechanism. Here, using super-resolution microscopy (SRM), we directly visualized the nuclear dynamics and unveiled the mechanism of paclitaxel treatment. A new class of non-toxic, biocompatible and highly fluorescent carbon nanodots (CNDs) were used as a fluorescent probe that were highly capable to directly stain the nuclear DNA, capture the SRM imaging of chromosome and the chromatin structures. Apart from SRM imaging of chromosomes during all stages of normal mitotic cell division, CNDs successfully visualized the formation of lagging, mis-segregated and bridging chromosomes which leads to the multi-micronucleus formation upon paclitaxel treatment. A detailed chromatin remodelling analysis suggested that heterochromatin played an important role in the formation of condensed multi-micronucleus, ultimately leading to cell death. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/620846v1_ufig1.gif" ALT="Figure 1"> View larger version (59K): org.highwire.dtl.DTLVardef@1d5bb12org.highwire.dtl.DTLVardef@ecd313org.highwire.dtl.DTLVardef@15bb3corg.highwire.dtl.DTLVardef@b79273_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2024

Synchronized Chromatin Organization Serves as Potent Biomarker in Anaesthesia-based Plant Consciousness

Anaesthesia has been used for centuries for medical purposes. With the application of anaesthesia, organisms lose their conscious awareness. It provides a temporary loss of sensation, which enables painless performance during surgery. However, the cellular mechanisms underlying the effects of anaesthesia are not clearly understood. It has been proposed that plant root function is analogous to the human brain. Here, using super-resolution imaging technique, we explored an organelle-level understanding of the effect of anaesthesia on plant roots and the stem connecting to the root. Our results showed that the nuclei organized themselves in an orchestrated manner upon treatment with both local and general anaesthesia without damaging their structure. Euchromatin within the nucleus was found to be reorganized in the nuclear periphery, and this process was found to be independent of ATP. In contrast, mitochondria, microtubules, endocytic vesicles, and chloroplasts, which are other important organelles in plant cells, were highly altered or damaged under the same experimental conditions. Eventually, the cellular homeostasis again maintained and process is reversible upon the removal of anaesthesia. Our results suggest that such orchestrated chromatin organization without disturbing the overall structure of the nucleus could be used as a potent biomarker for conscious awareness in plants. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=184 HEIGHT=200 SRC="FIGDIR/small/615456v1_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@18e5582org.highwire.dtl.DTLVardef@1900826org.highwire.dtl.DTLVardef@1073002org.highwire.dtl.DTLVardef@e100f7_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗