Search bioRxiv⌕ Search

Biology subjects

Goyal, V.

Publications and source records attributed to Goyal, V..

10 recordsLinked to original sources

Early EEG responses indicate liking for artworks presented in rapid visual streams

When we appreciate visual art, we often take our time: We visit museums or galleries and deliberately engage with artworks and their meaning. Yet, our liking might at least partly be shaped by incidental encoding of the artworks' visual features, a process initially independent from sustained engagement. Here, we show that liking for visual art can be predicted from rapid and automatic responses in the visual brain. We recorded EEG responses while participants viewed 999 artworks from the Vienna Art Picture System (VAPS), which features complex artworks that span different categories and art styles. Artworks were shown with a 300ms stimulus-onset-asynchrony (150ms on, 150 off), and participants responded to occasional target images. Using representational similarity analysis, we predicted the geometry of neural representations from the artworks' similarity in liking (based on ratings from a different group of observers), while simultaneously controlling for similarities in other properties (category, art style, valence, arousal, and familiarity). Crucially, neural responses emerging within the first 150ms were robustly connected to liking, even though the task did not afford any liking judgments. Strikingly, this early neural correlate of liking was also observed in a second experiment, in which we presented the same 999 artworks with a 50ms stimulus-onset-asynchrony. Our results show that even under ultra-fast presentation conditions, automatic neural responses rapidly indicate liking. While fully appreciating an artwork may still need deliberate and prolonged engagement, the perceptual basis of whether we like or dislike an artwork seems to be laid in a split second.

neuroscience↗

Scientific computing in the age of agentic AI: an exploratory field report

Scientific computing has become a central component of modern scientific discovery. Yet many computational tools are developed by small, specialized teams under incentives that encourage the release of rapidly prototyped tooling without commensurate attention to engineering concerns, including performance and maintainability. These gaps are particularly visible in the life sciences, where the advent of high-throughput sequencing and molecular profiling has made the production and processing of datasets routine at scales that strain reliability and cost. Recently, LLM-based agents have become increasingly capable, with publicly available systems possessing both significant domain knowledge in many scientific fields and the ability to autonomously operate over complex and specialized codebases in pursuit of well-defined goals. Together, these developments create a practical opportunity for scientific computing. Many of the persistent weaknesses of the scientific computing ecosystem stem from technical debt and a shortage of sustained engineering labor and expertise. Here, we examine coding agents as a potential way to address these weaknesses: we present an exploratory field report of eight early case studies in the application of LLM agents to scientific computing across a range of project scopes, from lightweight maintenance tasks to full performance-oriented rewrites of scientific libraries, with a focus on the life sciences. Each of these case studies is accompanied by reflections from the individual or group responsible for the work, including lessons from the process. Overall, we find that the use of coding agents in scientific computing holds great promise for accelerating scientific research and increasing the reliability of critical systems, but that outstanding concerns remain, including responsibility and ownership for such projects, and we suggest collaboration and stewardship with existing maintainers when feasible.

bioinformatics↗

Genome-wide Analysis Reveals High Genomic Diversity and Panmixia in Bay Pipefish (Syngnathus leptorhynchus) from Coos Bay, Oregon

The over 300 species of fishes in the charismatic family Syngnathidae (seahorses, pipefish, pipehorses, and seadragons) exhibit remarkable morphological and reproductive adaptations. Most syngnathid species inhabit shallow coastal regions where they are vulnerable to human activities, including habitat degradation and collection for use in traditional medicine and the aquarium trade. A gap remains in our understanding of within-species genetic diversity and population structure for most of the species in this family--information that is crucial for establishing baselines to detect future human-driven changes. Here, we investigate fine-scale population structure and genomic diversity in the bay pipefish (Syngnathus leptorhynchus), one of the relatively few temperate lineages within the Syngnathidae. Bay pipefish are habitat specialists that are closely associated with eelgrass (Zostera marina) along the Pacific coast of North America. Due to the patchy and changing nature of eelgrass habitat, bay pipefish provide an instructive case for using population genomics to explore patterns of connectivity in a dynamic coastal environment. We sampled 116 individuals from two locations separated by approximately 17 km in the Coos Bay estuary (Oregon, USA) and used restriction site-associated DNA sequencing (RAD-seq) to discover high and consistent genetic diversity at both sampling locations, with no indication of inbreeding. Genome-wide patterns of genetic variation showed minimal differentiation between the sampling sites, with levels of divergence indistinguishable from those expected under random sampling. Linkage disequilibrium was low and declined rapidly, and estimates of effective population size indicate a large, well-connected population within Coos Bay. These results establish a crucial genomic baseline for understanding how bay pipefish populations may respond to ongoing changes in their eelgrass habitat and offer a genomic framework for conservation and comparative studies across the Syngnathidae.

evolutionary biology↗

NAC controls nascent chain fate through tunnel sensing and chaperone action

The nascent polypeptide-associated complex (NAC) is a conserved ribosome-bound factor with essential yet incompletely understood roles in protein biogenesis. Here, we show that NAC is a multifaceted regulator that coordinates translation elongation, cotranslational folding, and organelle targeting through distinct interactions with nascent polypeptides both inside and outside the ribosome exit tunnel. Using NAC-selective ribosome profiling in C. elegans, we identify thousands of sequence-specific NAC binding events across the nascent proteome, revealing broad cotranslational engagement with hydrophobic and helical motifs in cytosolic, nuclear, ER, and mitochondrial proteins. Unexpectedly, we discover an intra-tunnel sensing mode, where NAC engages ribosomes with extremely short nascent polypeptides inside the exit tunnel in a sequence-specific manner. These early NAC interactions induce an early elongation slowdown that tunes ribosome flux and prevent ribosome collisions, linking NACs chaperone activity to kinetic control of translation. We propose that NAC action protects aggregation-prone intermediates by shielding amphipathic helices thus promoting cytonuclear folding and supporting mitochondrial membrane protein biogenesis and ER targeting by early recognition of signal sequences and transmembrane domain. Our findings establish NAC as an early-acting, multifaceted orchestrator of cotranslational proteostasis, with distinct mechanisms of action on nascent chains depending on their sequence features and subcellular destinations.

biochemistry↗

SNHG10 promote tumorigenesis via miR-150/VEGFA/EGFR/AKT/ERK/mTOR axis and gemcitabine resistance in PDAC

SNHG10 emerged as a key regulator in progression and metastasis of cancers. However, potential of SNHG10 in PDAC tumorigenesis, gemcitabine resistance, and underlying mechanisms remains poorly understood. We observed significant upregulation of SNHG10 in 179 PDAC cases, revealing a positive correlation with clinical stages. Our results showed a significant SNHG10 overexpression in several PDAC cells. Downregulation of SNHG10 significantly decreased the proliferation, clonogenicity, EMT, tumor growth in the xenograft model, and the induction of cell cycle arrest and apoptosis of PDAC cells. Mechanistically, SNHG10 knockdown significantly inhibited the expression of vimentin, N-cadherin, survivin, CDK4, CDK6, cyclin B1, cyclin D1, aurora kinase A, and B, with an increased expression of E-cadherin and p21. RNA Immunoprecipitation data displayed physical interaction among SNHG10, miR-150-5p, and VEGFA in PDAC cells. SNHG10 silencing led to the significant induction of miR-150-5p, which repressed VEGFA expression in PDAC cells. SNHG10 downregulation enhanced gemcitabine sensitivity in PDAC cells. SNHG10 silencing suppressed the phosphorylation of EGFR, AKT, ERK1/2, mTOR, and c-MET pathways. Silencing SNHG10 and its regulated signalling offers a novel prospective therapeutic strategy.

cancer biology↗

Three-row stereocilia model predicts mammalian hair bundle behavior

Mammalian outer hair cells (OHCs) enhance sound amplification and frequency tuning through stereociliary hair bundles (HBs), which convert mechanical motion into electrical signals via mechano-electric transducer (MET) channels. Experiments show that the HB displacement creeps, and the MET current evinces dual timescales of adaptation in response to mechanical stimulus. Understanding these mechanisms is crucial for elucidating normal auditory function and disorders, yet their origins remain unclear. To address this, we developed a mathematical model of the OHC HB that incorporates three rows of stereocilia with distinct nonlinear adaptive gating mechanisms, nonlinear kinematics, and viscoelastic mechanics. Our model accurately replicates experimental responses to fluid-jet stimulation, predicting simultaneous mechanical creep and slow adaptation of the MET current. Using stiff probe stimulation, the same model reveals even faster adaptation, aligning with experimental observations and emphasizing the stimulus-dependence of the response. The model provides new insights into the functional importance of the three-row stereocilia configuration, offering a mechanistic explanation for its ubiquity in mammalian HBs and its role in facilitating the complex timescales of adaptation.

biophysics↗

Single Cell RNA Sequencing Provides Clues for the Developmental Genetic Basis of Syngnathidae's Evolutionary Adaptations

Seahorses, pipefishes, and seadragons are fishes from the family Syngnathidae that have evolved extraordinary traits including male pregnancy, elongated snouts, loss of teeth, and dermal bony armor. The developmental genetic and cellular changes that led to the evolution of these traits are largely unknown. Recent syngnathid genome assemblies revealed suggestive gene content differences and provide the opportunity for detailed genetic analyses. We created a single cell RNA sequencing atlas of Gulf pipefish embryos to understand the developmental basis of four traits: derived head shape, toothlessness, dermal armor, and male pregnancy. We completed marker gene analyses, built genetic networks, and examined spatial expression of select genes. We identified osteochondrogenic mesenchymal cells in the elongating face that express regulatory genes bmp4, sfrp1a, and prdm16. We found no evidence for tooth primordia cells, and we observed re-deployment of osteoblast genetic networks in developing dermal armor. Finally, we found that epidermal cells expressed nutrient processing and environmental sensing genes, potentially relevant for the brooding environment. The examined pipefish evolutionary innovations are composed of recognizable cell types, suggesting derived features originate from changes within existing gene networks. Future work addressing syngnathid gene networks across multiple stages and species is essential for understanding how their novelties evolved.

evolutionary biology↗

Age at cancer diagnosis by breed, weight, sex, and cancer type in a cohort of over 3,000 dogs: determining the optimal age to initiate cancer screening in canine patients

The goal of cancer screening is to detect disease at an early stage when treatment may be more effective. Until recently, cancer screening in dogs has relied upon annual physical examinations and routine laboratory tests, which are largely inadequate for detecting preclinical disease. With the introduction of non-invasive "liquid biopsy" cancer detection methods, the discussion is shifting from "How to screen dogs for cancer" to "When to screen dogs for cancer". To address this question, data from 3,452 cancer-diagnosed subjects were analyzed to determine the age at which dogs of certain breeds and weights are typically diagnosed with cancer. In the study population, the median age at cancer diagnosis was 8.8 years, with males diagnosed at younger ages than females, and spayed/neutered dogs diagnosed at significantly later ages than intact dogs. Overall, weight was inversely correlated with age at cancer diagnosis, and purebred dogs were diagnosed at significantly younger ages than mixed-breed dogs. For breeds with 10 or more subjects, a breed-based median age at diagnosis was calculated. A weight-based linear regression model was developed to predict the median age at diagnosis for breeds represented by fewer than 10 subjects and for mixed-breed dogs. The study findings support a general recommendation to start cancer screening for all dogs at the age of 7, and as early as 4 years of age for breeds with a lower median age at cancer diagnosis, in order to increase the chances of early detection and treatment.

cancer biology↗

Altered neuromechanical strategies of the paretic hip and knee joints during a step-up task

Stroke often leads to chronic motor impairments in the paretic lower limb that can constrain lower extremity movement and negatively impact the ability to navigate stairs or curbs. This exploratory study investigated the differences in hip and knee biomechanical strategies during a step-up task between 5 adults with hemiparetic stroke and 5 age-matched adults without stroke. Participants were instructed to step up onto a 4-inch platform, where joint biomechanics were quantified for the hip in the frontal plane and the hip and knee in the sagittal plane. Peak joint kinematics were identified during the leading limb swing phase and peak joint moments and power were identified during the leading limb pull-up phase of stance. Mixed effects regression models estimated fixed effects of limb (3 levels: control dominant, stroke non-paretic, and stroke paretic) on biomechanical outcomes, while a random effect of participant controlled for within-participant correlations. Repeated assessments within participants (approximately 60 trials per lower limb) increased the effective sample size from 10 to between 12.0 to 19.6. Altered biomechanical strategies of the paretic lower limb included reduced flexion angles and increased pelvic obliquity angles during swing, decreased power generation in the hip frontal plane during stance, and decreased moment and power generation in the knee sagittal plane during stance. A strategy of substantial interest was the elevated hip sagittal plane moment and power generation in both stroke limbs. Overall, our findings suggest that chronic motor impairments from stroke can lead to inefficient biomechanical strategies when stepping up.

bioengineering↗

Dopamine 2 receptor signaling controls the daily burst in phagocytic activity in the mouse retinal pigment epithelium

PurposeA burst in phagocytosis of spent photoreceptor outer fragments by retinal pigment epithelium (RPE) is a rhythmic process occurring 1-2 hours after the onset of light. This phenomenon is considered crucial for the health of the photoreceptors and RPE. We have recently reported that dopamine, via dopamine 2 receptor (D2R), shifts the circadian rhythm in the RPE.\n\nMethodsHere, we first investigated the impact of the removal of D2R on the daily peak of phagocytosis by RPE and then we analyzed the function and morphology of retina and RPE in the absence of D2R.\n\nResultsD2R KO mice do not show a daily burst of phagocytic activity after the onset of light. Also, in contrast to control, phosphorylation of FAK did not increase significantly in KO mice at ZT1. RNA sequencing revealed a total of 394 differentially expressed genes (DEGs) between ZT23 and ZT1 in the control mice, whereas in D2R KO mice, we detected 1054 DEGs. Pathway analysis of the gene expression data implicated integrin signaling to be one of the upregulated pathways in control but not in D2R KO mice. No difference in retinal thickness, visual function, or morphology of RPE cells was observed between WT and D2R KO mice at the age of 3 and 12 months.\n\nConclusionsOur data suggest that removal of D2R prevents the burst in phagocytosis and a related increase in the phosphorylation of FAK after light onset. The pathway analysis points towards a putative role of D2R in controlling integrin signaling, which is known to play an important role in the control of the daily burst of phagocytosis by the RPE. Our data also indicate that the absence in the burst of phagocytic activity in the early morning does not produce any apparent deleterious effect on the retina or RPE up to one year of age.

cell biology↗