Biology subjects

Acharjee, S.

Publications and source records attributed to Acharjee, S..

8 recordsLinked to original sources

bioRxiv2026

Herbivory-induced alterations in cytosolic proteins of pigeon pea (Cajanus cajan) leaves

Insect herbivory triggers cytosolic proteome reprogramming by activating defense pathways and modulating key metabolic processes. We found that simulated herbivory in pigeon pea (Cajanus cajan) induced reactive oxygen species (ROS) production and molecular alterations within 12 hours (h) of post treatment. We compared the leaf proteome profiles of two cultivated genotypes, ICPL 332 (moderately resistant) and ICPL 87 (susceptible), using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) coupled with mass spectrometry (MS). More than 220 protein spots were detected in ICPL 332 and over 200 in ICPL 87. Comparative analysis revealed 75 differentially accumulated proteins (DAPs), of which 40 were consistently reproducible across biological replicates. These included 11 unique to ICPL 87, 9 unique to ICPL 332, and 10 common to both genotypes. Among the shared DAPs, ICPL 332 showed five upregulated and five downregulated, whereas ICPL 87 exhibited only two upregulated and eight downregulated. Functional categorization grouped DAPs into primary metabolism, stress response, and growth and development. Proteins related to primary metabolism were largely downregulated in both genotypes, while stress-associated proteins exhibited substantial downregulation in ICPL 87 compared to ICPL 332. Overall, the results demonstrate proteomic adjustments underlying defense responses in pigeon pea genotypes.

plant biology↗

bioRxiv2025

Modeling collective cell migration in a heterogeneous environment: Drosophila border cell migration as a model paradigm

Collective cell migration underpins development and disease progression, yet the influence of heterogeneous microenvironments on intercellular forces and migration dynamics remains elusive. Focusing on the chemotactic migration of border cell clusters in Drosophila egg chambers, we present a computational framework that integrates intercellular force dynamics and cell shape changes during large-scale migration, validated with live imaging data. Our model replicates in vivo observations, such as rotations of the cell cluster and its tendency to follow a central path in the egg chamber. Using the model, we discover instantaneous acceleration/deceleration phases as the cell cluster migrates through junctions of other cell types. We also predict how environmental tissue topology and perturbations in chemoattractant gradients and adhesion impact cluster speed and rotation. By addressing the limitations of prior models of border cell migration, our approach offers broad applicability to other migration contexts involving interactions among different cell types in complex environments.

biophysics↗

bioRxiv2025

Metabolic regulation of copper homeostasis governs the Sec61-dependent protein translocation process in Saccharomyces cerevisiae

Concentration of cellular labile pool of copper must be strictly regulated because disruption in copper homeostasis results in diseases. In Saccharomyces cerevisiae, elevated levels of labile copper impair cell viability by inhibiting Sec61-mediated protein translocation into the endoplasmic reticulum. We investigated how metabolic pathways, specifically mitochondrial respiration and autophagy, contribute to copper homeostasis and the translocation of secretory proteins. We show that copper selectively inhibits protein translocation in yeast cells grown in minimal medium but not in rich medium, highlighting a critical role of nutrients in modulating copper toxicity. Supplementation of specific amino acids suppresses the copper-induced defects in protein translocation and cell death, identifying amino acids suppressors of the copper toxicity. Using a panel of gene deletion mutants affecting mitochondrial functions, autophagy, peroxisomes, and lipid droplets, we demonstrate that metabolic pathways regulate sub-cellular distribution of copper and translocation of secretory proteins. Further, disruption of redox and pH homeostasis, and pharmacological inhibition of respiration, reveals that correct subcellular trafficking of copper is essential to prevent inhibitory effects on protein translocation process. Together, our findings provide mechanistic insights into how metabolic status influences cellular copper homeostasis and the secretory pathway of proteins, with broader implications for understanding diseases of copper metabolism.

cell biology↗

bioRxiv2025

Combined genetic and environmental factors shape the landscape of anti-fungal tolerance in Nakaseomyces glabratus

The rising incidence of fungal infections caused by Candida species is compounded by increasing antifungal resistance, compromising treatment efficacy. In Candida albicans, antifungal drug tolerance (AFDT) has emerged as a distinct, clinically relevant phenotype. However, AFDT remains underexplored in other clinically significant Candida species, and its prevalence across the genus is unclear. Here, we characterize AFDT in Nakaseomyces glabratus (formerly Candida glabrata), the second most common cause of candidiasis. Using disk diffusion and supra-MIC growth assays, we quantified AFDT across six clinical isolates and a reference strain. Our results mirror findings in C. albicans, demonstrating reproducible AFDT across N. glabratus strains in response to multiple azoles. Importantly, tolerance did not correlate with resistance profiles, underscoring AFDT as a distinct phenotype. Isolates were categorized into high- medium- and low-tolerance groups based on variability. Highly tolerant strains showed reduced clearance in a Galleria mellonella infection model, aligning with previous AFDT studies. Tolerance was modulated by environmental factors such as media, temperature, and azole, yet relative strain tolerance remained stable--suggesting a heritable, strain-specific trait shaped by genetic and environmental factors. These findings underscore the clinical relevance of AFDT in N. glabratus and support further investigation into its molecular underpinnings and therapeutic impact.

microbiology↗

bioRxiv2024

Elucidating Molecular Mechanism and Chemical Space of Chalcones through Knowledge Graph and Machine Learning: A Combined Bio-Cheminformatic Pipeline

We developed a bio-cheminformatics method, exploring disease inhibition mechanisms using machine learning-enhanced quantitative structure-activity relationship (ML-QSAR) models and knowledge-driven neural networks. ML-QSAR models were developed using molecular fingerprint descriptors and the Random Forest algorithm to explore the chemical spaces of Chalcones inhibitors against diverse disease properties, including antifungal, anti-inflammatory, anticancer, antimicrobial, and antiviral effects. We generated and validated robust machine learning-based bioactivity prediction models ((https://ashspred.streamlit.app/) for the top genes. These models underwent ROC and applicability domain analysis, followed by molecular docking studies to elucidate the molecular mechanisms of the molecules. Through comprehensive neural network analysis, crucial genes such as AKT1, HSP90A1, SRC, and STAT3 were identified. The PubChem fingerprint-based model revealed key descriptors: PubchemFP521 for AKT1, PubchemFP180 for SRC, PubchemFP633 for HSP90, and PubchemFP145 and PubchemFP338 for STAT3, consistently contributing to bioactivity across targets. Notably, chalcone derivatives demonstrated significant bioactivity against target genes, with compound RA1 displaying a predictive pIC50 value of 5.76 against HSP90A and strong binding affinities across other targets. Compounds RA5 to RA7 also exhibited high binding affinity scores comparable to or exceeding existing drugs. These findings emphasize the importance of knowledge-based neural network-based research for developing effective drugs against diverse disease properties. These interactions warrant further in vitro and in vivo investigations to elucidate their potential in rational drug design. The presented models provide valuable insights for inhibitor design and hold promise for drug development. Future research will prioritize investigating these molecules for mycobacterium tuberculosis, enhancing the comprehension of effectiveness in addressing infectious diseases.

bioinformatics↗

bioRxiv2023

Cdc73 majorly regulates apoptosis-inducing factor (AIF1) in Saccharomyces cerevisiae via the H3K36 methylation

AIF1 overexpression is intimately linked to the sensitivity of the yeast cells towards hydrogen peroxide or acetic acid. Therefore, studying the mechanism of its regulation in the cell would provide a significant understanding of the factors ultimately guiding yeast apoptosis. In this report, we establish the time-dependent induction of AIF1 in hydrogen peroxide stress. Additionally, the AIF1 expression in hydrogen peroxide is mediated by two transcription factors, Yap5 (DNA binding) and Cdc73 (non-DNA binding). Furthermore, substituting the H3K36 residue with another significantly abrogates the AIF1 expression. However, substituting H3K4 or H3K79 with A does not affect the AIF1 expression level under hydrogen peroxide stress. Altogether, the significant reduction of AIF1 expression in cdc73{Delta} cells plausibly reflects the reduced H3K36me3 modification and is independent of the H3K4me3 modification.

genetics↗

bioRxiv2022

Germline protein, Cup, non-cell autonomously limits migratory cell fate in Drosophila oogenesis.

Attaining migratory fate from a stationary cell population is complex and indispensable both for the multicellular organism development as well for the pathological condition like tumor metastasis. Though widely prevalent in the metazoans, the molecular understanding of this phenomenon remains elusive. Specification of migratory border cells from the follicular epithelium during Drosophila oogenesis has emerged as one of the excellent model systems to study how motile cell are specified. JAK-STAT activation in 6-10 anterior most follicle cells of the Drosophila egg chamber transforms them to a migratory cluster called the border cells. We show that a nurse cell protein, Cup, non-cell autonomously restricts the domain of JAK-STAT activation in the anterior follicle cells. Further examination suggests that Cup functions through Rab11GTPase to regulate Delta trafficking in the nurse cells potentiating Notch activation in the anterior follicle cells. Since Notch activity in the follicle cells modulates the JAK-STAT, any perturbation in Notch activation affects the border cell fate. Altogether, we propose that germline Cup affects the border cell fate through appropriate activation of Notch and JAK-STAT signaling in the follicle cells.

developmental biology↗

bioRxiv2018

Vitexin alters Staphylococcus aureus surface hydrophobicity to interfere with biofilm formation.

Bacterial surface hydrophobicity is one of the determinant biophysical parameters of bacterial aggregation for being networked to form biofilm. Phytoconstituents like vitexin have long been in use for their antibacterial effect. The present work is aimed to characterise the effect of vitexin on S. aureus surface hydrophobicity and corresponding aggregation to form biofilm. We have found that vitexin shows minimum inhibitory concentration at 252 g/ml against S. aureus. Vitexin reduces cell surface hydrophobicity and membrane permeability at sub-MIC dose of 126 g/ml. The in silico binding analysis showed higher binding affinity of vitexin with surface proteins of S. aureus. Down regulation of dltA, icaAB and reduction in membrane potential under sub-MIC dose of vitexin, explains reduced S. aureus surface hydrophobicity. Vitexin has substantially reduced the intracellular adhesion of planktonic cells to form biofilm through interference of EPS formation, motility and subsequent execution of virulence. This was supported by the observation that vitexin down regulates the expression of icaAB and agrAC genes of S. aureus. In addition, vitexin also found to potentiate antibiofilm activity of sub-MIC dose of gentamicin and azithromycin. Furthermore, CFU count, histological examination of mouse tissue and immunomodulatory study justifies the in vivo protective effect of vitexin from S. aureus biofilm associated infection. Finally it can be inferred that, vitexin has the ability to modulate S. aureus cell surface hydrophobicity which can further interfere biofilm formation of the bacteria.\n\nImportanceThere has been substantial information known about role of bacterial surface hydrophobicity during attachment of single planktonic bacterial cells to any surface and the subsequent development of mature biofilm. This study presents the effect of flavone phytoconstituent vitexin on modulation of cell surface hydrophobicity in reducing formation of biofilm. Our findings also highlight the ability of vitexin in reducing in vivo S. aureus biofilm which will eventually outcompete the corresponding in vitro antibiofilm effect. Synergistic effect of vitexin on azithromycin and gentamicin point to a regime where development of drug tolerance may be addressed. Our findings explore one probable way of overcoming drug tolerance through application of vitexin in addressing the issue of S. aureus biofilm through modulation of cell surface hydrophobicity.

microbiology↗