Biology subjects

Bansal, H.

Publications and source records attributed to Bansal, H..

3 recordsLinked to original sources

bioRxiv2026

A pathogen-associated odorant induces fear-like response regulated by an olfactory receptor STR-211 in Caenorhabditis elegans

Exposure to chemical cues released by predator or pathogen can evoke anxiety or fear responses in prey/host animals such as fight, flight or freeze both at behavioral and molecular levels. Freezing is a fundamental anxiety response when fighting or fleeing arent feasible. Despite the potential relevance of freezing as a stress-coping mechanism, its behavioral and molecular underpinnings are not understood yet. At molecular level danger cues are perceived by chemosensory receptors expressed in sensory neurons which may further regulate the animals behavioral responses(Ye et al., 2024){Citation}. 2-nonanone (2-NA) is one of the principal volatile organic compounds secreted by many pathogenic bacteria infecting Caenorhabditis elegans as well as humans and may signal danger to worms. Here, we show that olfactory exposure to threat-associated cue 2-NA induces a reversible fear-like freezing response characterized by immobility and halted feeding in C. elegans. With the application of in silico and behavioral approaches we showed that 2-NA is one of the ligands for an olfactory G-protein Coupled Receptor (GPCR) STR-211 and RNAi knockdown of the receptor leads to a defect in 2-NA induced avoidance behavior in worms. We next discovered that STR-211 is required for immediate behavioral changes in C. elegans during freezing response against 2-NA. The study proposes an environment relevant animal model to mimic human anxiety and fear-like behavior, along with the identification of one of the olfactory GPCRs mediating this behavior. The model may help in understanding the neuromolecular basis of freezing response in human anxiety, contributing towards treatment of mental health disorders.

neuroscience↗

bioRxiv2026

Enriched-GF: A Reproducible High-Yield Autologous Blood-Derived Growth Factor Method for Regenerative Medicine

BackgroundPlatelet-derived Growth factors play key roles in tissue repair and regeneration, yet conventional platelet-rich plasma (PRP) formulations release these mediators inconsistently in vivo due to variability in platelet yield and activation dynamics. To overcome this limitation, direct administration of concentrated platelet-derived growth factor preparations has gained interest, though current manufacturing approaches for human platelet lysate (hPL), growth factor concentrates (GFC), and conditioned serum remain constrained by batch variability, incomplete platelet degranulation, and reliance on anticoagulants. Here, we examine alternative platelet activation workflows to establish a standardized, efficient, and reproducible method for high-yield growth factor recovery suitable for translational and clinical applications. MethodsNine GFC production protocols were compared, employing different combinations of freeze-thaw (FT) cycling, glass bead (GB) agitation, calcium (Ca2) activation, and a novel Enriched Growth Factor (Enriched-GF) method. The objective was to identify a protocol capable of maximizing growth factor yield within a three-hour workflow. Optimal Ca2 concentrations and GB conditions were determined from prior optimization studies and integrated into the Enriched-GF processing scheme. Platelet concentrates (n = 10 per protocol) were processed under each condition, and growth factor levels were quantified using ELISA. ResultsGrowth factor yields differed significantly across protocols. The greatest and most consistent increases in growth factor release were observed with the Enriched-GF method combining GB activation, FT cycling, and Ca2 stimulation. This approach resulted in markedly elevated concentrations of key regenerative mediators, including enhanced EGF release, a 4.5-fold increase in PDGF, maximal TGF-{beta} liberation, and a four-fold increase in FGF2 relative to conventional platelet lysate or conditioned serum preparations. These results were reproducible across independent donor pools, demonstrating robustness and batch-to-batch consistency. ConclusionWe describe a rapid and reproducible method for producing highly concentrated platelet-derived growth factors using a combined GB-FT-Ca2 activation strategy. The Enriched-GF protocol consistently outperformed existing platelet lysate, conditioned serum, and conventional GFC preparation methods, yielding a standardized product with enhanced growth factor content. This Enriched-GF approach offers a clinically practicable solution for applications in regenerative medicine requiring reliable and high-yield growth factor delivery. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/712883v2_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@ac60c3org.highwire.dtl.DTLVardef@104d8eborg.highwire.dtl.DTLVardef@13d5afcorg.highwire.dtl.DTLVardef@120645c_HPS_FORMAT_FIGEXP M_FIG C_FIG Schematic overview of platelet concentrate preparation from whole blood and the generation of different platelet lysates and growth factor-enriched serum using freeze-thaw, calcium gluconate, and glass bead activation methods.

biochemistry↗

bioRxiv2025

Motor protein disruption critically alters organelle trafficking, NMJ formation, and excitation contraction coupling.

Trafficking of intracellular cargoes along the neuronal axon microtubule tracks is a motor-protein-dependent process. It is well-established that the motor protein kinesin is responsible for anterograde trafficking of axonal cargo, while the dynein/dynactin complex regulates retrograde trafficking. However, there is still much to uncover regarding the various isoforms of these motor proteins as well as the adapter and cargo-associated proteins involved in the precise trafficking dynamics. Here we use a targeted genetic approach to knockdown candidate kinesin genes involved in trafficking organelles like synaptic vesicles, mitochondria, and dense core vesicles in motor neurons. Using fluorescently tagged cargo proteins; live-imaging experiments were conducted to quantify intracellular trafficking changes, and 2 genes, kinesins 1 and 3, were identified as critical regulators. Disruptions in either gene product, reduce rates of axonal trafficking in motor neurons, and lead to the formation of large intracellular aggregates in somas and axons. Downstream, disruptions in both kinesin 1 and 3 expression led to significant changes in neuropeptide (NP) abundance at boutons, and changes in synaptic morphology, including innervation length, bouton number, and active zone composition. Spinning disc confocal imaging revealed fewer NP trafficking through, or getting captured in kinesin knockdown experiments, and a dramatic reduction in NP release at motor neuron terminals. We go on to show profound reductions in neuromuscular transduction, and excitation-contraction coupling in kinesin 1 knockdowns, but not for kinesin 3. Changes in larval crawling as well as development were observed for kinesin 1 knockdowns. Taken together we have not only identified which kinesins are critically involved in organelle trafficking, but also revealed critical disruptions in cellular morphology, function, physiology, and behavior in genetically disrupted animals.

neuroscience↗