Biology subjects

Liu, Z.

Publications and source records attributed to Liu, Z..

At least 397 records · Page 22Linked to original sources

bioRxiv2024

Arabidopsis SUFB and CLP protease regulate SUFBC2D to manipulate iron-sulfur cluster biosynthesis in chloroplast

Iron-sulfur (Fe-S) clusters are essential cofactors for Fe-S proteins. SUFBC2D complex is the scaffold responsible for Fe-S cluster assembly in chloroplasts. However, the regulatory mechanism on SUFBC2D remains elusive. In this study, we report that the transcription of SUFB responds rapidly to leaf senescence, whereas the transcription of SUFC and SUFD does not. Intriguingly, their protein contents remain stable during leaf senescence. We further found that leaf death was occurred only when SUFB RNAi was induced, and SUFB and SUFC contents decreased much faster in the SUFB-RNAi lines than in the SUFC-RNAi lines, indicating that SUFB had a faster turnover rate than SUFC. Moreover, overexpressing SUFB increased the contents of SUFC and SUFD, and SUFBC2D, whereas overexpressing SUFC did not increase SUFB and SUFD. Our findings reveal that SUFB stabilizes SUFC and SUFD via forming SUFBC2D, whereas SUFC lacks this function. Furthermore, SUFB expression was sharply downregulated when the plants were subjected to iron deficiency, whereas SUFC and SUFD expression was not. Interestingly, the contents of all three SUF members decreased, indicating that plants degrade SUFBC2D in response to iron deficiency by downregulating SUFB transcription. We subsequently studied the degradation mechanism of SUFBC2D. Our results indicated that all SUFs are substrates of the caseinolytic protease (CLP) because they all accumulated in the CLP impaired mutant, and they physically interact with CLPS1, the substrate recognition adaptor of CLP. Collectively, our findings provide novel insights into how plants regulate SUFBC2D complex via SUFB to adapt to leaf senescence and iron deficiency.

plant biology↗

bioRxiv2024

Age Prediction based on Blood DNA Methylation

ObjectiveIn the judicial field, traditional DNA methylation age prediction models have low accuracy and poor stability. Additionally, the use of linear regression models for detection is inefficient and costly. This study aims to utilize the prediction principles of the Support Vector Regression (SVR) model, based on preliminary laboratory data from blood DNA methylation detection using the Illumina 850K chip. By selecting low-dimensional and highly linear loci, we aim to establish a highly stable and accurate blood DNA methylation age prediction model. MethodsThis research is based on Illumina 850K chip technology. We conducted a literature review to select CpG sites and related primers, then employed SVR for model construction and age prediction. The model was built on the Matlab2022a platform. Standard parameters were selected, and optimal values for C and g were determined using grid search and cross-validation methods. During data processing, numerical values were normalized before calculation and de-normalized to obtain the predicted values. ResultsThe constructed model achieved an R2 of 0.91563 and a Mean Absolute Error (MAE) of 2.77 years. This indicates that the prediction accuracy for blood samples reached 91.56%, with an error of 2.77 years. Moreover, the accuracy of the models predictions decreases with increasing age.

genetics↗

bioRxiv2024

Mechanistic insights into structure-based design of a Lyme disease subunit vaccine

The quality of protective immunity plays a critical role in modulating vaccine efficacy, with native antigens often not able to trigger sufficiently strong immune responses for pathogen killing. This warrants creation of structure-based vaccine design, leveraging high-resolution antigen structures for mutagenesis to improve protein stability and efficient immunization strategies. Here, we investigated the mechanisms underlying structure-based vaccine design using CspZ-YA, a vaccine antigen from Borrelia burgdorferi, the bacteria causing Lyme disease (LD), the most common vector-borne disease in the Northern Hemisphere. Compared to wild-type CspZ-YA, we found CspZ-YAI183Y and CspZ-YAC187S required lower immunization frequency to protect mice from LD-associated manifestations and bacterial colonization. We observed indistinguishable human and mouse antigenicity between wild-type and mutant CspZ-YA proteins after native infection or active immunization. This supports our newly generated, high-resolution structures of CspZ-YAI183Y and CspZ-YAC187S, showing no altered surface epitopes after mutagenesis. However, CspZ-YAI183Y and CspZ-YAC187S favored the interactions between helices H and I, consistent with their elevated thermostability. Such findings are further strengthened by increasing ability of protective CspZ-YA monoclonal antibodies in binding to CspZ-YA at a physiological temperature (37{degrees}C). Overall, this study demonstrated enhanced intramolecular interactions improved long-term stability of antigens while maintaining protective epitopes, providing a mechanism for structure-based vaccine design. These findings can ultimately be extended to other vaccine antigens against newly emerging pathogens for the improvement of protective immunity.

immunology↗

bioRxiv2024

SPP1+ tumor-associated macrophages induce radioresistance of nasopharyngeal carcinoma through crosstalk with the tumor microenvironment

The function and phenotype of tumor-associated macrophages (TAMs) influence the efficacy of radiotherapy. However, the effect of different subsets of TAMs on the radioresistance in nasopharyngeal carcinoma (NPC) still needs to be further explored. This study utilized single-cell RNA sequencing (scRNA-seq) to analyze 120,579 cells obtained from 15 NPC samples. Cell annotation, cell-cell communication analysis, and functional annotation were used to investigate the impact of TAMs on the effectiveness of radiotherapy in NPC patients. Additionally, we employed RNA-seq data and clinical information from many patients, including 24 NPC samples from Zhujiang Hospital, 3,934 samples from patients with a history of radiotherapy, for further validation. We identified a hub TAM subpopulation, SPP1+ TAMs, that induced radioresistance in NPC based on single-cell RNA sequencing (scRNA-seq) data. We combined many public datasets to confirm their prognostic value in radiotherapy patients. We found that SPP1+ TAMs had stronger protumorigenic and immunosuppressive effects in the postradiotherapy recurrent tumor (PRRT) group. SPI1 transcription factor efficiently regulates the expression level of SPP1 in macrophages. In addition, we validated the underlying mechanisms by molecular docking, multiplex immunofluorescence and cellular experiments. In conclusions, by forming an immunosuppressive microenvironment and promoting tumor cell proliferation, SPP1+ TAMs leading to radioresistance and poor clinical prognosis in NPC patients. Targeting SPP1+ TAMs could provide new insights into improving the efficacy of radiotherapy in NPC patients.

cancer biology↗

bioRxiv2024

Quantitative Resolving Cell Fate in the Early Embryogenesis of Caenorhabditis elegans

The nematode Caenorhabditis elegans exhibits an invariant cell lineage during its development where the gene-molecular network that regulates the development is crucial for the biological process. While there are many molecular cell atlases describing the phenomena and key molecules involved in cell transformation, the underlying mechanisms from a systems biology perspective have received less attention. Based on an endogenous molecular-cellular theory that relates the molecular mechanisms to biological phenotypes, we constructed a model of core endogenous network to describe the early stages of embryonic development of the nematode. Different cell types and intermediate cell states during development from zygotes to founder cells correspond to the steady states of the network as a nonlinear stochastic dynamical system. Connections between steady states form a topological landscape that encompasses known developmental lineage trajectories. By regulating the expression of agents in the network, we quantitatively simulated the effects of the Wnt and Notch signaling pathway on cell fate transitions and predicted the possible trajectories of transdifferentiation of the AB cell across the lineage. The success of the current study may help advance our understanding of the fundamental principles of developmental biology and cell fate determination, offering an effective tool for quantitative analysis of cellular processes.

developmental biology↗

bioRxiv2024

Substrate tunnel regulates substrate specificity switching in hyaluronan synthase

Hyaluronic acid (HA), a ubiquitous linear polysaccharide in the extracellular matrix of vertebrates and the capsule of certain pathogenic bacteria, is characterized by its unique structure of alternating {beta}-1,3-N-acetylglucosamine and {beta}-1,4-glucuronic acid units. HA is synthesized by Class I hyaluronan synthase (HAS) in the majority of organisms, but the molecular mechanisms determining the alternating sequence of HA remain unclear. Here, we demonstrated that HA synthesized in vitro using Streptococcus equisimilis HAS maintained its alternating sequence, regardless of substrate ratios and concentrations. While the active pocket lacks intrinsic selectivity, a distal allosteric regulation from the transmembrane tunnel is revealed. The lingering HA terminals in the active pocket ensure lower binding energies for alternating substrates through Coulombic repulsion and competitive binding. Moreover, the dynamic C-terminal loop at the substrate tunnel entrance reduces transport distance for alternating substrates. Our findings indicate that HA-substrate interactions and enzyme dynamics in the substrate tunnel collectively govern the alternating substrate specificity of HAS. This study provides the first molecular insight into precise substrate specificity control within a single active pocket during template-independent polymer synthesis.

biophysics↗

bioRxiv2024

The fourspine stickleback (Apeltes quadracus) has an XY sex chromosome system with polymorphic inversions on both X and Y chromosomes

Teleost fish are well-known for possessing a diversity of sex chromosomes and for undergoing frequent turnovers of these sex chromosomes. However, previous studies have mainly focused on variation between species, while comparatively little attention has been given to sex chromosome polymorphisms within species, which may capture early stages of sex chromosome changes. To better understand the evolution of sex chromosomes, we used the fourspine stickleback (Apeltes quadracus) as a model organism. Previously, it was believed that females of this species possessed a ZW heteromorphic sex chromosome system. However, genetic crosses and our whole-genome sequencing of wild populations revealed that A. quadracus has an XY sex chromosome on chromosome 23. This chromosome has not previously been identified as a sex chromosome in other stickleback species, indicating a recent sex chromosome turnover. We also identified two genes - rxfp2a and zar1l - as novel candidate sex determination genes. Notably, we observed inversions on both the X and Y chromosomes in different populations, resulting in distinctive patterns of differentiation between the X and Y chromosomes across populations. We propose that the inversion on the X chromosome may have been favored by sexually antagonistic selection. The new sex chromosome and intraspecies inversion polymorphisms observed in A. quadracus provide an excellent system for studying the evolution of sex chromosomes and their turnovers. Author SummaryAs compared to mammals and birds, teleost fish exhibit a very high level of diversity in their sex chromosomes, even among closely related species. Thus far, little attention has been paid to variation within species, although it offers a valuable opportunity to advance our understanding of the mechanisms underlying the formation and turnover of sex chromosomes. Through a quantitative trait locus (QTL) cross and sequencing diverse populations, we determined that instead of the previously reported ZW system, A. quadracus has an XY sex determination system on chromosome 23. Within the sex determining region, we identified rxfp2a and zar1l as putative sex determining genes. Notably, we also observed polymorphic inversions present on both the X and Y chromosomes that differ among populations. Based on our findings, we hypothesize that the X-linked inversions are favored by selection that differs between males and females. These observations represent a rare situation in which sex chromosomes are still polymorphic for sex-linked inversions, which offers important insights into the early stages of sex chromosome evolution.

evolutionary biology↗

bioRxiv2024

WRAD core perturbation impairs DNA replication fidelity promoting immunoediting in pancreatic cancer

It is unclear how cells counteract the potentially harmful effects of uncoordinated DNA replication in the context of oncogenic stress. Here, we identify the WRAD (WDR5/RBBP5/ASH2L/DPY30) core as a modulator of DNA replication in pancreatic ductal adenocarcinoma (PDAC) models. Molecular analyses demonstrated that the WRAD core interacts with the replisome complex, with disruption of DPY30 resulting in DNA re-replication, DNA damage, and chromosomal instability (CIN) without affecting cancer cell proliferation. Consequently, in immunocompetent models, DPY30 loss induced T cell infiltration and immune-mediated clearance of highly proliferating cancer cells with complex karyotypes, thus improving anti-tumor efficacy upon anti-PD-1 treatment. In PDAC patients, DPY30 expression was associated with high tumor grade, worse prognosis, and limited response to immune checkpoint blockade. Together, our findings indicate that the WRAD core sustains genome stability and suggest that low intratumor DPY30 levels may identify PDAC patients who will benefit from immune checkpoint inhibitors.

cancer biology↗

bioRxiv2024

S100a4+ alveolar macrophages accelerate the progression of precancerous atypical adenomatous hyperplasia by promoting fatty acid metabolism

Lung cancer is preceded by premalignant lesions, and what factors drive this transformation and the potential regulatory mode in the context of tumor initiation remain to be elucidated. In the course of precancerous lesions, we found a phasic shift in metabolic patterns. Macrophages are a heterogeneous cell population with high plasticity in the tumor microenvironment. Single-cell interaction and metabolic analyses highlighted a cellular state, S100a4+ alveolar macrophages, which exhibited distinct fatty acid metabolic activity, such as palmitic acid metabolism, at the atypical adenomatous hyperplasia stage, accompanied by an angiogenic-promoting function in a pre-neoplastic setting. These findings were reproducible in human single-cell transcriptomes and had been confirmed by histopathological staining and in vitro cell coculture assays. Taken together, the results from this study demonstrated that the S100a4+ alveolar macrophage subset contributes to tumorigenesis by altering its metabolic state, suggesting that metabolic interventions targeting this cell state in the early stage of disease may delay neoplastic transformation of the lung epithelium.

cancer biology↗

bioRxiv2024

Stress-free Bioprinting of Human Primary and iPSC-derived Islets with Retained Functionality

Currently, Type 1 diabetes (T1D) can be treated through implantation of allogenic islets, which replenish the beta cell population, however this method requires an extensive post-implantation immunosuppressant regimen. Personalized cellular therapy can address this through implantation of an autologous cell population, induced pluripotent stem cells (iPSCs). Cellular therapy, however, requires an encapsulation device for implantation, and so to achieve this uniformly with cells in a clinical setting, bioprinting is a useful option. Bioprinting is dependent on having a bioink that is printable, retains structural fidelity after printing, and is supportive of cell type and function. While bioprinting of pancreatic islets has been demonstrated previously, success in maintaining islet function post-printing has been varied. The objective of this study is to investigate the feasibility of printing functional islets by determining the appropriate combination of bioink, printing parameters, and cell configuration. Here, we detail the successful bioprinting of both primary human islets and iPSC-derived islets embedded in an alginate/methylcellulose bioink, with functionality sustained within the construct for both cell lineages. Sc-RNAseq analysis also revealed that printing did not adversely affect the genetic expression and metabolic functionality of the iPSC-derived islets. Importantly, the iPSC-derived islets displayed comparable functionality to the primary islets, indicating the potential to act as a cell source alternative for T1D implantation.

bioengineering↗

bioRxiv2024

Splicing dysregulation in glioblastoma alters the function of cell migration-related genes

Glioblastoma (GBM) has a poor prognosis with a high recurrence and low survival rate. Previous RNA-seq analyses have revealed that alternative splicing (AS) plays a role in GBM progression. Here, we present a novel AS analysis method (Semi-Q) and describe its use to identify GBM-specific AS events. We analyzed RNA-seq data from normal brain (NB), normal human astrocytes (NHAs) and GBM samples, and found that comparison between NHA and GBM was especially informative. Importantly, this analysis revealed that genes encoding cell migration-related proteins, including filamins (FLNs) and actinins (ACTNs), were among those most affected by differential AS. Functional assays revealed that dysregulated AS of FLNA, B and C transcripts produced protein isoforms that not only altered transcription of cell proliferation-related genes but also led to enhanced cell migration, resistance to cell death and/or mitochondrial respiratory function, while a dysregulated AS isoform of ACTN4 enhanced cell migration. Together, our results indicate that cell migration and actin cytoskeleton-related genes are differentially regulated by AS in GBM, supporting a role for AS in facilitating tumor growth and invasiveness.

molecular biology↗

bioRxiv2024

Systems genetic dissection of Alzheimer's disease brain gene expression networks

In Alzheimers disease (AD), changes in the brain transcriptome are hypothesized to mediate the impact of neuropathology on cognition. Gene expression profiling from postmortem brain tissue is a promising approach to identify causal pathways; however, there are challenges to definitively resolve the upstream pathologic triggers along with the downstream consequences for AD clinical manifestations. We have functionally dissected 30 AD-associated gene coexpression modules using a cross-species strategy in fruit fly (Drosophila melanogaster) models. Integrating longitudinal RNA-sequencing and behavioral phenotyping, we interrogated the unique and shared transcriptional responses to amyloid beta (A{beta}) plaques, tau neurofibrillary tangles, and/or aging, along with potential links to progressive neuronal dysfunction. Our results highlight hundreds of conserved, differentially expressed genes mapping to human AD regulatory networks. To confirm causal modules and pinpoint AD network drivers, we performed systematic in vivo genetic manipulations of 357 conserved, prioritized targets, identifying 141 modifiers of A{beta}- and/or tau-induced neurodegeneration. We discover an up-regulated network that is significantly enriched for both AD risk variants and markers of immunity / inflammation, and which promotes A{beta} and tau-mediated neurodegeneration based on fly genetic manipulations in neurons. By contrast, a synaptic regulatory network is strongly downregulated in human brains with AD and is enriched for loss-of-function suppressors of A{beta}/tau in Drosophila. Additional experiments suggest that this human brain transcriptional module may respond to and modulate A{beta}-induced glutamatergic hyperactivation injury. In sum, our cross-species, systems genetic approach establishes a putative causal chain linking AD pathology, large-scale gene expression perturbations, and ultimately, neurodegeneration.

systems biology↗

bioRxiv2024

Impact of Guanidine Hydrochloride on the shapes of Prothymosin-α and α-Synuclein is dramatically different

The effects of Guanidine Hydrochloride (GdmCl) on two Intrinsically Disordered Proteins (IDPs) are investigated using simulations of the Self-Organized Polymer-IDP (SOP-IDP) model. The impact of GdmCl is taken into account using the Molecular Transfer Model(MTM). We show that, due to dramatic reduction in the stiffness of the highly charged Prothymosin- (ProT) with increasing concentration of GdmCl ([GdmCl]), the radius of gyration (Rg) decreases sharply till about 1.0M. Above 1.0M, ProT expands, caused by the swelling effect of GdmCl. In contrast, Rg of -Synuclein (Syn) swells as continuously as [GdmCl] increases, with most of the expansion occurring at concentrations less than 0.2M. Strikingly, the amplitude of the Small Angle X-ray Scattering (SAXS) profiles for ProT increases till [GdmCl]{approx} 1.0M and decreases beyond 1.0M. The [GdmCl]-dependent SAXS profiles for Syn, which has a pronounced bump at small wave vector (q [~] 0.5nm-1) at low [GdmCl] ([≤] 0.2M), monotonically decrease at all values of [GdmCl]. The contrasting behavior predicted by the combination of MTM and SOP-IDP simulations may be qualitatively understood by modeling ProT as a strongly charged polyelectrolyte with nearly uniform density of charges along the chain contour and Syn as a nearly neutral polymer, except near the C-terminus where the uncompensated negatively charged residues are located. The precise predictions for the SAXS profiles as a function of [GdmCl] can be readily tested.

biophysics↗

bioRxiv2024

The C. elegans LON-1 protein requires its CAP domain for function in regulating body size and BMP signaling

The CAP (Cysteine-rich secretory proteins, Antigen-5, Pathogenesis-Related) proteins are widely expressed and have been implicated to play diverse roles ranging from mammalian reproduction to plant immune response. Increasing evidence supports a role of CAP proteins in lipid binding. The C. elegans CAP protein LON-1 is known to regulate body size and Bone Morphogenetic Protein (BMP) signaling. LON-1 is a secreted protein with a conserved CAP domain and a C-terminal unstructured domain with no homology to other proteins. In this study, we report that the C-Terminal Domain (CTD) of LON-1 is dispensable for its function. Instead, key conserved residues located in the CAP domain are critical for LON-1 function in vivo. We further showed that LON-1 is capable of binding sterol, but not fatty acid, in vitro, and that certain key residues implicated in LON-1 function in vivo are also important for LON-1 sterol binding in vitro. These findings suggest a role of LON-1 in regulating body size and BMP signaling via sterol binding. ARTICLE SUMMARYThe C. elegans LON-1 protein is known to regulate body size and Bone Morphogenetic Protein (BMP) signaling. However, its molecular mode of action remains elusive. This study shows that LON-1 can bind sterol, but not fatty acid, in vitro. Furthermore, key conserved residues in the CAP domain of LON-1 are required for LON-1 function in vivo. These findings suggest a role of LON-1 in regulating body size and BMP signaling via sterol binding.

genetics↗

bioRxiv2024

The dynamics of wild Vitis species in response to climate change facilitate the breeding of grapevine and its rootstocks with climate resilience

Climate change poses significant challenges to agricultural suitability and food security due to the limited adaptability of domesticated crops, however, our understanding of their climate adaptability is still limited. In this study, we compare the potential distributional dynamics in response to future climate change between grapevine and its wild relatives (Vitis L.) based on ecological niche models (ENMs). We reveal that the annual mean temperature is the primary factor influencing the potential distribution of cultivated grapes (V. vinifera L.). By 2080, under RCP 8.5, suitable areas for wine and table grapes from V. vinifera are predicted to reduced by 15.04x105 km{superscript 2} and 13.26x105 km{superscript 2}, respectively. The results suggest that grape cultivation, particularly for table grapes, will face serious threats from future climate change. In contrast, seventy percent of wild grapes are well able to withstand future climate conditions. For example, under RCP 8.5, North American wild grapes like V. rotundifolia and V. labrusca, as well as East Asian wild grapes such as V. heyneana and V. davidii, are projected to demonstrate significant adaptability. These wild grapes have the potential to provide rootstocks that could enhance the adaptability of cultivated grapes and serve as invaluable resources for breeding programs aimed at developing new cultivars better suited to withstand the environmental pressures of climate change. Our results not only predict potential suitable distribution areas of wild grapes in the future, but also emphasize the essential impact of these wild genetic resources on grape breeding for promoting adaptation to future climate change.

plant biology↗

bioRxiv2024

An all-in-one AAV vector for cardiac-specific gene silencing by an adenine base editor

ABE editing outcomes are highly variable and unpredictable, depending on various factors. Therefore, the success rate of creating targeted A*T-to-G*C conversions using ABE is not high. But utilizing ABE to target RNA splicing sites for gene silencing has a higher success rate. Another challenge for base editing in the heart is that traditional ABE is too large in size, necessitating dual AAV delivery. Whether single AAV delivery can be achieved remains to be explored. In this study, we demonstrated how the diversity of Cas9 homologs and screening of sgRNAs can facilitate cardiac base editing. Single-AAV base editing outperformed dual-AAV systems in the heart, potentially benefiting from chromatin accessibility-guided sgRNA selection. These findings have important implications for the development of more effective and predictable base editing tools for cardiac gene therapy.

molecular biology↗

bioRxiv2024

Rapid prediction of thermodynamically destabilizing tyrosine phosphorylations in cancers

Tyrosine phosphorylations are a prominent characteristic of numerous cancers, necessitating the use of computational tools to comprehensively analyze phosphoproteomes and identify potentially (dys)functional phosphorylations. Here we propose a machine learning-based method to predict the thermodynamic stability change resulting from tyrosine phosphorylation. Our approach, based on prediction of phosphomimetic delta-delta-G from structural features, strongly correlates with experimental mutational scanning cDNA proteolysis data (R = 0.71). We predicted the destabilizing effects of all 384,857 tyrosine residues from the Alphafold2 database. We then applied our approach to a pan-cancer phosphoproteomics dataset, comprising over 600 unique tyrosine phosphorylations across 11 cancer subtypes. We predict destabilizing phosphorylations in both oncogenes and tumor suppressors, where the former likely reflects a generalized relief of auto-inhibition or activating conformational change. We find that the number of circuit topological parallel relations with respect to residues contacting the phosphorylated site is greater for autoinhibited oncogenes than for other proteins (Wilcoxon p = 0.03). Utilizing an extreme gradient-boosting machine learning approach, we obtain an AUC of 0.85 for the prediction of autoinhibited phosphorylation states from circuit topological features. The top destabilized proteins from the pan-cancer data are enriched for chemical and oxidative stress pathways. Among metabolic proteins, highly destabilizing phosphorylations tend to occur in more peripheral proteins with lower network centrality measures (Wilcoxon p = 0.005). We predict 58% of recurrent tyrosine cancer phosphorylations to be destabilizing at the 1 kcal/mol threshold. Our approach can enable rapid screening of destabilizing phosphorylations and phosphomimetic mutations.

systems biology↗

bioRxiv2024

Comparative Analysis of AAV Serotypes for Transduction of Olfactory Sensory Neurons

Olfactory sensory neurons within the nasal epithelium detect volatile odorants and relay odor information to the central nervous system. Unlike other sensory inputs, olfactory sensory neurons interface with the external environment and project their axons directly into the central nervous system. The use of adeno-associated viruses to target these neurons has garnered interest for applications in gene therapy, probing olfactory sensory neuron biology, and modeling disease. To date, there is no consensus on the optimal AAV serotype for efficient and selective transduction of olfactory sensory neurons in vivo. Here we utilized serial confocal imaging and single-nucleus RNA sequencing to evaluate the efficacy of 11 different AAV serotypes in transducing murine olfactory sensory neurons via non-invasive nasal inoculation. Our results reveal that AAV1, while highly effective, exhibited broad tropism, whereas AAV-DJ/8 showed the greatest specificity for olfactory sensory neurons.

neuroscience↗