Biology subjects

Khan, S.

Publications and source records attributed to Khan, S..

At least 73 records · Page 4Linked to original sources

bioRxiv2025

Proximate Composition and Mineral Analysis of Housefly Maggots and Mealworms Compared to Fish and Soybean Meals

The nutritional profiles of dried yellow mealworms and housefly maggots were analyzed and compared with conventional protein sources in poultry diets such as fish meal (FM) and soybean meal (SBM). Nutrient composition was determined through proximate analysis, while amino acid and mineral contents were analyzed using HPLC-based amino acid analyzer and atomic absorption spectrophotometer, respectively. Metabolizable energy (ME) was calculated to estimate energy content per kilogram of feed. The crude protein content of housefly maggots (57.8%) was comparable to that of fish meal (58.5%), which was the highest among the evaluated feeds, while mealworms had a slightly lower protein content (51.02%). The highest ether extract values were recorded for mealworms (27.3%) and maggots (26.9%), surpassing those in FM and SBM. The highest ME was calculated for housefly maggots (4,074 kcal/kg), followed by mealworms (3,988 kcal/kg) and FM (3,824 kcal/kg). Mineral profiling showed the highest calcium content in mealworms (5.23 g/kg), followed by maggots (5.13 g/kg). Phosphorus and zinc were recorded highest in housefly maggots, at 16.8 g/kg and 98.5 mg/kg, respectively. The limiting amino acids lysine, leucine, and isoleucine were highest in housefly maggots, followed by FM and mealworms, showing comparable values between the insect meals and FM. Methionine content was recorded highest in mealworms (2.3 g/100g), closely followed by housefly maggots (2.27 g/100g). The study demonstrated that housefly maggots and mealworms have a nutritive profile superior to soybean meal and comparable to fish meal.

zoology↗

bioRxiv2025

Bacteriophage-Loaded Microneedle Patches for Targeted andMinimally Disruptive Foodborne Pathogen Decontamination

Antibacterial additive use has surged due to rising incidences of food contamination, despite concerns over antibiotic resistance. Bacteriophage (bacterial viruses) represent a unique and promising opportunity as antibacterial agents, offering targeted bacterial lysis while being food safe. However, their commercial success has been limited by the significant diffusion barriers they face within food, preventing effective delivery at contamination sites. Here, we introduce bacteriophage-loaded microneedle patches that enable targeted phage delivery directly within food, eliminating internal pathogens in a minimally disruptive manner. The application of microneedles within food is first explored. The platform is then substantiated by comparing performance in raw beef and cooked chicken, where we achieved up to 3-logs reduction in Escherichia coli, thus providing complete decontamination according to regulatory limits. In contrast, conventional surface application of the same phage failed to provide significant decontamination. To ensure broad applicability, phage cocktails were also loaded into microneedles to demonstrate polymicrobial decontamination against other common food contaminants including Salmonella. This platform can also be adapted to extend food shelf-life by targeting spoilage-inducing bacteria.

bioengineering↗

bioRxiv2025

NF2 loss malignantly transforms human pancreatic acinar cells and enhances cell fitness under environmental stress

Pancreatic ductal adenocarcinoma (PDAC) occurs as a complex, multifaceted event driven by the interplay of tumor permissive genetic mutations, nature of cellular origin and microenvironmental stress. In this study, using primary human pancreatic acinar 3D organoids, we performed CRISPR knockout screen targeting 199 previously underappreciated potential tumor suppressors curated from clinical PDAC samples. Our data revealed significant enrichment of a list of candidates, with NF2 emerging as the top target. Functional validation confirmed that loss of NF2 promotes the transition of PDAC to an invasive state, potentially through extracellular matrix modulation. NF2 inactivation was found to enhance PDAC cell fitness under nutrient starvation. This adaptation not only reinforces the oncogenic state but also confers therapeutical resistance. Additionally, we found that NF2 loss is associated with the fibroblast heterogeneity and cancer-stroma communications in tumor evolution. These findings establish NF2 as a critical tumor suppressor in PDAC and uncover its role in mediating nutrient adaptation and drug resistance. Importantly, this study provides new insights into drug resistance mechanisms and potential therapeutic targets in PDAC.

cancer biology↗

bioRxiv2025

SNX-2112 inhibits the ERBB3high tumor population in Plexiform Neurofibromas

Plexiform neurofibroma (PN) is a monogenic disorder affecting the Schwann cell lineage in approximately half of Neurofibromatosis type 1 patients. It often manifests in early childhood and carries a risk of malignant transformation at puberty. While MEK inhibitors have recently been approved for pediatric and adult patients, their long-term clinical benefits remain uncertain due to adverse effects, particularly in pediatrics. The ERBB3high stem-like tumor cell subpopulation reflects the intrinsic PN heterogeneity and can serve as alternative druggable targets. Characterization using molecular signatures also reveals the heterogeneity within the PN cell lines, and the PN drug screen analysis proposes that SNX-2112, an HSP90 inhibitor, can inhibit PN cell viability by targeting ERBB3-associated signaling. Our in vitro results demonstrated a significant viability reduction in ERBB3high PN cells compared to the controls. Treatment with SNX-2112 led to a decrease in total ERBB3, p-ERBB3 (Tyr1289), and the downstream total AKT and p-AKT (Ser473) levels. Furthermore, the significant in vivo inhibitory efficacy of SNX-2112 was revealed using a transplantation model from mouse PN with DhhCreNF1f/f;Luc configuration. These findings support the efficacy of SNX-2112 as a potential alternative therapeutic strategy, highlighting its possible application in PN patients.

cancer biology↗

bioRxiv2025

Understanding the selectivity of lysine negatively charged acyl modifications by OsCobB and its link with different plant stress condition

Recent proteomic studies have found several different lysine modifications in plants related to various important metabolic pathways. Lysine deacylation is a key feature of sirtuins for the regulation of several cellular processes in mammals. This may be involved in the tolerance against different stress conditions in case of plants. In this study, we deliver a comprehensive structural and kinetic analysis describing the selection of lysine acidic acyl groups by OsCobB. The catalytic efficiency (kcat/Km) of OsCobB to erase glutaryl, succinyl, and malonyl groups from the designated lysine site is favored due to the presence of Tyr55 and Arg58 at the active site. The selectivity of the substrate is further based on the OsCobB active site residues as well as residues next to the modified lysine. These modifications can be further linked to the plants mechanism to cope with stress due to dehydration, cold temperature and different metal toxicities.

plant biology↗

bioRxiv2025

Mechanistic insights and clinical implications of cross-reactive anti-prophage antibodies and bacterial heteroresistance on phage therapeutic failure

Phage therapy is an exciting strategy against antimicrobial-resistant bacterial infections, but critical knowledge gaps regarding its clinical application persist. Studying a patient with a life-threatening, chronic bacterial infection who failed phage therapy, we uncovered important biological concepts with direct translational impact. Using longitudinal clinical samples, we found that patients can harbour pre-existing antibodies against active prophages induced from the genome of the causative pathogen. Notably, these antibodies can contribute to clinical failure by cross-reacting with and effectively neutralising therapeutic phage. We also uncovered bacterial heteroresistance, characterised by bacterial subpopulations from the initial infection with reduced phage susceptibility, as a further contributor to treatment failure. These findings highlight the intricate interplay between host immunology, bacterial genetic diversity and phage biology, bearing broad significance for clinical phage therapy. Future phage therapy patients, especially those with chronic infections, should be screened for antiphage immunity and bacterial heteroresistance prior to phage treatment.

microbiology↗

bioRxiv2025

BioToken and BioFM - Biologically-Informed Tokenization Enables Accurate and Efficient Genomic Foundation Models

Genomic variation underlies human phenotypic diversity, disease susceptibility, and evolutionary adaptation. Although large-scale genomic sequencing has transformed our ability to map genetic variation, accurately modeling and interpreting this data remains a central challenge; while genomic foundation models (GFMs) are a promising approach, they suffer from fundamental limitations. Current GFMs typically treat DNA simplistically as nucleotide-only sequences, overlooking critical biological context, such as genomic annotations, regulatory elements, and functional contexts central to genomic interpretation. Here, we introduce BioToken, a modular and extendable tokenization framework designed to encode genomic variants and biologically relevant region annotations directly into genomic representations. By utilizing intrinsic inductive biases, BioToken facilitates meaningful representation learning and generalization across diverse molecular phenotypes, such as gene expression, alternative splicing, and variant pathogenicity prediction. Built on BioToken, our genomic foundation model, BioFM, achieves competitive or superior results relative to specialized models (e.g., Enformer, SpliceTransformer) and GFMs up to 7B parameters across a comprehensive suite of genomic benchmarks, including noncoding pathogenicity, expression modulation, sQTL prediction, and long-range genomic interactions. Notably, BioFM achieves state-of-the-art performance with significantly fewer parameters (265M), substantially reducing training costs and computational requirements. Our findings highlight the substantial advantages of integrating biologically-informed inductive biases into genomic foundation modeling, providing a robust and accessible path forward in genomics. We provide our code and model checkpoints to support further research in this direction.

genomics↗

bioRxiv2025

Temporal coding enables hyperacuity in event based vision

The fact that the eyes are constantly in motion, even during fixation, entails that the spike times of retinal outputs carry information about the visual scene even when the scene is static. Moreover, this motion implies that fine details of the visual scene could not be decoded from pure spatial retinal representations due to smearing. Understanding the interplay of temporal and spatial information in visual processing is thus pivotal for both biological research and bio-inspired computer-vision applications. In this study, we consider data from a popular event-based camera that was designed to emulate the function of a biological retina in hardware. Similarly to biological eye, and in contrast to standard frame-based cameras, this camera outputs an asynchronous sequence of "spike" events. We used this camera to obtain dataset of event streams of tiny images, i.e., images whose recognition is impaired by photosensors pixelization and thus their recognition requires hyperacuity. Using these datasets we demonstrate here the superiority of event-based spatio-temporal coding over frame-based spatial coding in the recognition of tiny images by artificial neural networks (ANNs). We further demonstrate the benefits of event sequences for unsupervised learning. Interestingly, Vernier hyperacuity, which is a standard measure of shape hyperacuity, emerged in ANNs following training on tiny images, resembling the natural hyperacuity observed in humans. Our findings underscore the essential role of precise temporal information in visual processing, offering insights for advancing both biological understanding and bio-inspired engineering of visual perception.

neuroscience↗

bioRxiv2025

Vasopressin-Dependent β-Catenin Phosphorylation at Ser552 and Branching Structure of Mouse Collecting Duct System

BackgroundPhosphoproteomics studies in both cultured and native collecting duct (CD) cells showed that vasopressin strongly increases PKA-dependent phosphorylation of {beta}-catenin at Ser552. Relatively little is known about the role of Ser552 phosphorylation. MethodsTo address the role of {beta}-catenin Ser552 phosphorylation in the mature renal CD, we have inserted a Ser552Ala mutation in mice using CRISPR-Cas9. ResultsThe mutation did not affect the renal abundance of the vasopressin-regulated water channel aquaporin-2 (AQP2) or urinary osmolality. However, the structure of the CD system was altered. Specifically, the cortical branching ratio (the number of nephrons that merge to form one cortical CD) was reduced from 6.18 {+/-} 0.66 in control mice to 3.33 {+/-} 0.82 in Ser552Ala mutant mice. This was associated with a greater number of cortical and medullary CDs with smaller average diameter. The total number of nephrons (glomerular counts) was not different between control and Ser552Ala mutant mice (both [~]13,500 per kidney). RNA-seq in microdissected cortical CDs of the mice revealed a highly significant enrichment of genes involved in regulation of mitosis and the cell cycle, along with decreases in mRNAs coding for two CDK inhibitor proteins, Cdkn1b and Cdkn1c. At the same time, there were no changes in abundances of major transporter mRNAs, indicative of sustained CD differentiation. A subset of cortical CD cells showed an increase in DNA content, consistent with G2/M cell-cycle arrest. ConclusionsThe observed structural changes in the collecting duct system of adult mice point to a role of vasopressin-mediated post-translational modification of {beta}-catenin at Ser552 in collecting duct development, presumably PKA-mediated Ser552 phosphorylation. We speculate that vasopressin may act to slow or halt branching morphogenesis perinatally and may affect the collecting duct elongation process that normally produces the unbranched region of the CD system in the cortex and outer medulla. Key pointsO_LIVasopressin regulates collecting duct (CD) transport by triggering phosphorylation of multiple proteins including {beta}-catenin at Ser552. C_LIO_LIMutating Ser552 to a non-phosphorylable amino acid in mice resulted in altered CD branching without loss of differentiation in adult CDs. C_LIO_LIThe findings point to a role for {beta}-catenin Ser552 phosphorylation in CD branching and sub-segmental CD elongation. C_LI

physiology↗

bioRxiv2025

CREB-family transcription factors and vasopressin-mediated regulation of Aqp2 gene transcription

BackgroundWater homeostasis is regulated by the peptide hormone arginine vasopressin (AVP), which promotes water reabsorption in the renal collecting duct. The regulation of Aqp2 gene transcription is a key mechanism through which AVP modulates water transport as disruption of this mechanism leads to water balance disorders. Therefore, an important goal is to understand the regulatory processes that control Aqp2 gene transcription. While CREB (CREB1) has been proposed as the primary transcription factor responsible for Aqp2 transcription, recent evidence challenges this view, suggesting that other CREB-like transcription factors, including ATF1 and CREM, may play a role. MethodsWe employed the CRISPR/Cas9 gene-editing system to delete Atf1, Creb1, and Crem in mpkCCD cells, an immortalized mouse collecting duct cell line. These cell lines were then exposed to the vasopressin analog, dDAVP, to assess the role of these transcription factors in regulating Aqp2 expression. AQP2 protein levels were measured by immunoblotting and RNA-seq was used to analyze changes in Aqp2 mRNA abundance, as well as other transcriptomic changes. ResultsDeletion of all three transcription factors (ATF1, CREB1, and CREM) led to a significant reduction in the vasopressin-induced upregulation of AQP2 protein, confirming their role in regulating Aqp2 expression. RNA-seq data showed that Aqp2 mRNA levels mirrored changes in protein abundance, supporting the idea that these transcription factors affect Aqp2 transcription. Rescue experiments in triple knockout cells showed that expressing any of the three transcription factors restored the response to vasopressin. ConclusionsOur findings demonstrate that ATF1, CREB1, and CREM have redundant roles in regulating Aqp2 transcription. Based on these results and prior data, we propose that these CREB-family transcription factors may regulate Aqp2 gene transcription indirectly by controlling the expression of additional unidentified transcription factors. Key PointsO_LICREB-family transcription factors (ATF1, CREB1, and CREM) were deleted in mpkCCD cells to assess their roles in Aqp2 gene transcription C_LIO_LICRISPR/Cas9 knockout of all three transcription factors strongly reduced the ability of vasopressin to increase AQP2 mRNA and protein C_LIO_LIRe-expression of any of the three restored the vasopressin response indicating redundant roles of the three transcription factors C_LI

physiology↗

bioRxiv2025

Electromotility can be disassociated from gating charge movement in outer hair cells of conditional alpha2 spectrin knockout mice.

Electromotility in mammalian outer hair cells (OHC) is the mechanism underlying cochlear amplification. It is brought about by the piezoelectric-like property of the membrane protein prestin (Slc26a5) that lies in the OHCs lateral plasma membrane. Prestin connects to an underlying cytoskeletal network of circumferential actin filaments that bridge longitudinal spectrin filaments. This network, in turn, lies between the plasma membrane and a closely apposed ER-like tubular array of subsurface cisternae (SSC). Two previous papers examining spectrin knockouts in embryonic hair cells were confined to analyzing the effects on the apical cuticular plate and overlying stereocilia. In this paper, we examine the effects of conditional knockouts of alpha2 spectrin in postnatal OHCs. We find a significant auditory phenotype likely due to the novel disassociation of prestins gating charge movement from OHC electromotility. In addition, OHCs show enlargement in their SSC and plasma membrane-SSC space with preserved cuticular plates and overlying stereocilia, which contrasts with the findings in embryonic knockouts.

physiology↗

bioRxiv2025

An Nlrp5-null mutation leads to attenuated de novo methylation in oocytes, accompanied by a significant reduction in DNMT3L

Nlrp5 encodes a core component of the subcortical maternal complex (SCMC) a cytoplasmic protein structure unique to the mammalian oocyte and cleavage-stage embryo. NLRP5 mutations have been identified in patients presenting with early embryo arrest, recurrent molar pregnancies and imprinting disorders. Correct patterning of DNA methylation over imprinted domains during oogenesis is necessary for faithful imprinting of genes. It was previously shown that oocytes with mutation in the human SCMC gene KHDC3L had globally impaired methylation, indicating that integrity of the SCMC is essential for correct establishment of DNA methylation at imprinted regions. Here, we present a multi-omic analysis of an Nlrp5- null mouse model, which in GV oocytes displays a misregulation of a broad range of maternal proteins, including proteins involved in several key developmental processes. This misregulation likely underlies impaired oocyte developmental competence. Amongst impacted proteins are several epigenetic modifiers, including a substantial reduction in DNMT3L; we show that de novo DNA methylation is attenuated in Nlrp5-null oocytes. This provides evidence for mechanisms leading to downstream misregulation of imprinted genes, which in turn, may result in imprinting syndromes, multi-locus imprinting disturbances (MLID) and hydatidiform moles.

developmental biology↗

bioRxiv2025

Soil and water microbial communities: A source of novel antibiotics for sustainable plant disease control

Pathogenic microorganisms pose a significant threat to plant health and agricultural productivity worldwide. Herein, this study explores the potential of natural microbial communities as sources of biopesticides. We analyzed 20 soil and water samples from remote areas, isolating 121 colonies using nutrient agar. Antibacterial activity was assessed through agar diffusion, revealing that 12 colonies exhibited significant inhibitory effects against various pathogenic bacteria. Measurement of inhibition zones indicated that these colonies could produce antibiotics. Subsequently, molecular characterization with 16S rRNA and BLAST searches of 12 unidentified sequences highlighted substantial microbial diversity within the samples. This research underscores the promise of these natural microbial communities in developing biocontrol agents for managing plant diseases in greenhouse and field environments. Extraction and purification techniques could further refine these antibiotics, advancing sustainable agricultural practices.

microbiology↗

bioRxiv2025

Fatty Acid Transport Protein-2 (FATP2) Inhibition Enhances Glucose Tolerance through α-Cell-mediated GLP-1 Secretion

Type 2 diabetes affects more than 30 million people in the US, and a major complication is kidney disease. During the analysis of lipotoxicity in diabetic kidney disease, global fatty acid transport protein-2 (FATP2) gene deletion was noted to markedly reduce plasma glucose in db/db mice due to sustained insulin secretion. To identify the mechanism, we observed that islet FATP2 expression was restricted to -cells, and -cell FATP2 was functional. Direct evidence of FATP2KO-induced -cell-mediated GLP-1 secretion included increased GLP-1-positive -cell mass in FATP2KO db/db mice, small molecule FATP2 inhibitor enhancement of GLP-1 secretion in TC1-6 cells and human islets, and exendin[9-39]-inhibitable insulin secretion in FATP2 inhibitor-treated human islets. FATP2-dependent enteroendocrine GLP-1 secretion was excluded by demonstration of similar glucose tolerance and plasma GLP-1 concentrations in db/db FATP2KO mice following oral versus intraperitoneal glucose loading, non-overlapping FATP2 and preproglucagon mRNA expression, and lack of FATP2/GLP-1 co-immunolocalization in intestine. We conclude that FATP2 deletion or inhibition exerts glucose-lowering effects through -cell-mediated GLP-1 secretion and paracrine {beta}-cell insulin release. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=136 SRC="FIGDIR/small/635976v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@190c799org.highwire.dtl.DTLVardef@203076org.highwire.dtl.DTLVardef@14dbf26org.highwire.dtl.DTLVardef@140869e_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗

bioRxiv2025

Visualizing sub-organellar lipid distribution using correlative light and electron microscopy

Lipids and proteins compartmentalize biological membranes into nanoscale domains which are crucial for signaling, intracellular trafficking and many other cellular processes. Studying nanodomain function requires the ability to measure protein and lipid localization at the nanoscale. Current methods for visualizing lipid localization do not meet this requirement. Here, we introduce a correlative light and electron microscopy workflow to image lipids (Lipid-CLEM), combining near-native lipid probes and on-section labeling by click chemistry. This approach enables the quantification of relative lipid densities in membrane nanodomains. We find differential partitioning of sphingomyelin into intraluminal vesicles, recycling tubules, and the boundary membrane of the early endosome, representing a degree of nanoscale organization previously observed only for proteins. We anticipate that our Lipid-CLEM workflow will greatly facilitate the mechanistic analysis of lipid functions in cell biology, allowing for the simultaneous investigation of proteins and lipids during membrane nanodomain assembly and function.

cell biology↗

bioRxiv2025

Diet links gut chemistry with cancer risk in C57Bl/6 mice and human colorectal cancer patients

The gastrointestinal tract is a complex ecosystem in which host tissues, microbial communities, and dietary inputs interact to shape metabolic outputs and epithelial homeostasis. Western-style diets, characterized by high fat and protein and low micronutrient content, represent a sustained ecological perturbation linked to colorectal cancer (CRC), yet specific mechanisms that impact risk remain poorly defined. Here, using a purified Western-style diet (NWD1) that induces sporadic intestinal and colon tumors in wild-type C57BL/6 mice we demonstrate how chronic dietary disturbance restructures gut community composition and sulfur metabolism, and how these changes modulate intestinal stem cell responses. Mice fed NWD1 for 24 weeks exhibited consistent shifts in ecosystem function, including a threefold increase in fecal sulfide production (P < 0.00001) and expansion of Erysipelotrichaceae family taxa. This altered chemical landscape associates with increased expression of mitochondrial sulfide oxidation pathways in Lgr5hi intestinal stem cells. Meta-analysis of human CRC cohorts revealed concordant enrichment of Erysipelotrichaceae, alongside established CRC-associated taxa such as Solobacterium moorei, indicating conserved ecological signatures across systems. Together, these findings support a model in which the Western-style diet drives a persistent shift in gut ecosystem structure and function toward a sulfide producing state that challenges epithelial homeostasis, with conserved microbial and metabolic configurations emerging prior to overt disease in mouse models.

cancer biology↗

bioRxiv2025

Stress Granules Underlie Acute Myeloid Leukemia Stem Cell Survival and Stress Adaptation

The link between cancer maintenance and an ability to sustain continued growth through stresses conferred by the cancer state itself is growing. However, there are significant gaps in our understanding of how this stress is managed, particularly at the level of cancer initiating cells. Here, we identify proteins comprising the dynamic, stress-adaptive ribonucleoprotein complexes known as stress granules (SG) to be enriched among the factors essential for leukemic stem cell (LSC)-driven leukemic propagation. Focusing on core SG nucleator G3BP1, we dissect the role of SGs in human acute myeloid leukemia (AML), their targetability, and the mechanisms they govern to uncover a novel propensity for AML, and in particular LSC-enriched fractions, to prime the expression of SG components, form SGs with greater fidelity and to be reliant on their establishment and continued integrity for LSC maintenance. We further unveil the transcript and protein interactome of G3BP1 in the AML context and show that consolidated control of innate immune signaling, and apoptosis repression is executed through regional binding specificity of G3BP1 to highly structured 3UTRs and cooperation with the RNA helicase UPF1 to mediate transcript decay in SGs. Altogether our findings advance novel fundamental principles of stress adaptation exploited in AML and LSCs that may extend to other cancers and uncover SGs as a novel axis for therapy development.

cancer biology↗

bioRxiv2025

Decreased auditory cortical activations and altered long-range alpha-band connectivity characterize passive auditory spatial attention in ASD

Autism Spectrum Disorder (ASD) is a developmental condition characterized by difficulties in social interaction, communication and sensory processing. The ability to orient towards sounds is a key component of social interactions, yet auditory spatial attention remains relatively understudied in ASD, despite prior research indicating differences in this domain. Here, we investigate the neural signatures associated with passive auditory spatial attention in children with ASD (n = 21, ages 6-17) relative to age- and IQ-matched typically developing (TD) children (n = 31), using source-localized magnetoencephalography (MEG). Participants listened passively, while watching a silenced movie, to non-social auditory stimuli designed to either remain lateralized to one hemifield (stay trials), or to change in location from one side to the contralateral hemifield (jump trials). Linear mixed effects modeling showed lower cortical activation in the auditory cortex in the ASD group in response to jump trials, relative to the TD group. Additionally, functional connectivity analyses showed higher alpha-band functional connectivity in the ASD group between left auditory cortex seeds and right prefrontal and left parietal regions known to be recruited during auditory spatial attention. Right prefrontal alpha-band connectivity estimates were associated with behaviorally assessed auditory processing scores, whereas left parietal connectivity estimates were associated with ASD symptomatology. Our results align with the hypothesis that auditory spatial attention generally, and specifically orientation to sounds even when experienced passively, differs in ASD individuals.

neuroscience↗