Biology subjects

Hall, K.

Publications and source records attributed to Hall, K..

14 recordsLinked to original sources

bioRxiv2026

In situ identification of pre-hematopoietic stem cells and their niche

Definitive hematopoietic stem cells (HSCs) emerge predominantly along the ventral surface of the dorsal aorta in the embryonic aorta-gonad-mesonephros (AGM) region, yet the spatial organization of the niche underlying this developmental asymmetry remains poorly understood. Defining the native niche of pre-HSCs has also been hindered by their rarity, transient nature and lack of a single definitive marker for their identification in situ. Here, we integrated single-cell and spatial transcriptomics to construct a spatiotemporal atlas of the niche in the AGM. Neural cells and chondrogenic mesenchyme predominated dorsally, whereas N-cadherin mesenchymal stromal cells (N-cad+ MSCs) formed a ventral layer between the aortic endothelium and mesonephric cells. BMP and SHH signaling showed overall dorsal enrichment, whereas WNT, NOTCH and KIT signaling were enriched ventrally, with these cellular and signaling patterns dynamically remodeled across HSC ontogeny. Imaging-based spatial transcriptomics validated the findings and further enabled the identification of individual pre-HSCs in situ and revealed a multicellular niche comprising endothelial cells, N-cad+ MSCs, intra-aortic hematopoietic cluster cells and macrophages. TGF{beta} and NOTCH signals were primarily supplied locally, whereas major sources of BMP and WNT were more distant. Functional perturbation identified niche-derived CD200 as an immune-regulatory signal promoting HSC development, validating a spatially predicted niche interaction. Together, our findings link tissue-scale spatial organization with the local multicellular niche supporting the preferential development of HSCs along the ventral aorta.

developmental biology↗

bioRxiv2026

The small RNA Teg16 represses rsbV and modulates SigB-dependent gene expression in Staphylococcus aureus

Staphylococcus aureus relies on coordinated regulatory networks to adapt to environmental stress and host-associated conditions. The alternative sigma factor SigB plays a central role in this process and is controlled by the anti-anti-sigma factor RsbV, which functions as a key regulatory node in the pathway. While numerous small regulatory RNAs (sRNAs) have been identified in S. aureus, relatively few have been directly linked to the SigB stress response network. Here, we investigated the role of the small RNA Teg16 in post-transcriptional regulation of the SigB stress response pathway. Computational prediction identified a region of complementarity between Teg16 and the translational initiation region of rsbV. To test a potential regulatory effect based on this prediction, teg16 was overexpressed, and rsbV transcript levels were measured by quantitative RT-PCR. Teg16 overexpression resulted in reduced rsbV transcript levels and decreased expression of SigB-dependent genes, including asp23 and the carotenoid (crt) biosynthesis operon responsible for staphyloxanthin pigment production. In addition, strains carrying the teg16 expression construct exhibited altered hemolytic activity under the conditions tested, suggesting effects on virulence-associated phenotypes. We further examined whether Teg16 influences the global regulator CodY and observed reduced codY transcript levels at early time points following teg16 overexpression. Together, these results extend a previously identified regulatory relationship between Teg16 and CodY and raise the possibility of a feedback relationship linking post-transcriptional regulation to metabolic control. These findings identify Teg16 as a previously uncharacterized regulator that connects small RNA-mediated control to the SigB stress response network in S. aureus. ImportanceThe alternative sigma factor SigB is a central regulator of stress adaptation in Staphylococcus aureus and influences both metabolism and virulence-associated phenotypes. While numerous small regulatory RNAs (sRNAs) have been identified in this organism, few have been functionally linked to control of the SigB pathway. Here, we identify the small RNA Teg16 as a regulator of rsbV, a key modulator of SigB activity. Teg16-dependent repression of rsbV is associated with reduced expression of SigB-dependent genes and measurable changes in phenotype, including decreased pigment production and altered hemolytic activity. In addition, our findings extend a previously identified relationship between Teg16 and the global regulator CodY, suggesting integration of post-transcriptional regulation with metabolic control. These results establish Teg16 as a previously uncharacterized component of the SigB regulatory network and provide new insight into how small RNAs contribute to stress adaptation in S. aureus.

microbiology↗

bioRxiv2025

Single-cell phylogenomics identifies major groups of marine eugregarine parasites (Apicomplexa)

Gregarines are a large group of apicomplexan parasites that infect a wide range of invertebrate hosts, including diverse and speciose groups, such as annelids and arthropods. Marine eugregarines represent the majority of gregarine diversity, but remain poorly understood, especially their deepest phylogenetic relationships. To expand knowledge of marine eugregarine diversity and their evolutionary history, we surveyed marine invertebrates, with a particular focus on annelids, across multiple locations in British Columbia, Canada. From this effort, we obtained high-quality, single-cell transcriptomes from 20 different species of marine eugregarines, including nine previously described species and 11 novel ones, which more than doubles the amount of phylogenomic data for the group. These data, which comprehensively represent the known diversity of marine gregarines in annelid hosts, allowed us to construct an expanded phylogenetic tree based on small subunit ribosomal DNA sequences and a phylogenomic tree inferred from 142 proteins and 44,802 amino acid sequences. Our analyses identified five "superfamily-level" groups of marine eugregarines infecting annelid hosts: The Ancoroidea, Lecudinoidea, Loxomorphoidea n. superfam., Paralecudinoidea n. superfam., and Belladinoidea n. superfam., with the latter three newly established in this study. These findings contribute to ongoing efforts to build a robust molecular phylogenetic framework for gregarine diversity and refine gregarine classification, supporting the recognition of 11 eugregarine superfamilies. However, some of the deepest evolutionary relationships among these superfamilies remain unresolved, highlighting the need for expanded taxon sampling to better capture the true diversity of eugregarine parasites.

microbiology↗

bioRxiv2024

Barcoding-inferred biodiversity of shallow-water Indo-Pacific demosponges

AimThe Indo-Pacific is the worlds largest marine biogeographic region. It is characterised by different degrees of connectivity among its subregions, and harbours the majority of demosponge species currently known to science. Comparisons between several regional sponge faunas have been undertaken in the past, mostly based on identifying the sponge species morphologically. The Sponge Barcoding Project, in tandem with other regional DNA taxonomy campaigns, provides one of the largest DNA-based taxonomic data collections from sponges of the Indo-Pacific. Here, we utilise the sponge barcoding data in the largest molecular biodiversity study of sponges to date, which reveals patterns of shallow-water demosponge faunal connectivity, endemism, and distribution in the Indo-Pacific with a level of resolution unavailable in prior morphology-based studies. LocationDemosponge specimens in this study cover 13 marine provinces of the Indo-Pacific, from the Red Sea to South East Polynesia. MethodsWe classified demosponge barcodes using the ribosomal subunit (28S rDNA) of 1,910 sponge samples into molecular operational taxonomic units (MOTUs). MOTU composition of the 13 marine provinces was compared based on Jaccard and Sorenson dissimilarities, and other biodiversity indices. ResultsOur data corroborated high levels of endemism among demosponges. Faunal overlaps were revealed between the Red Sea and the Gulf, which displayed relatively small connectivity with other marine provinces of the Western Indian Ocean. In the Western Indian Ocean, we observed a strong faunistic boundary to the Central Indo-Pacific. The Polynesian sponge faunas were comparatively isolated marine provinces of the Central Indo-Pacific. Main conclusionsOur data corroborate case studies on sponges that generally reject the presence of cosmopolitan or otherwise widespread sponge species, instead revealing high levels of regional endemism. This is consistent with similar observations and hypotheses in other marine invertebrates. Connectivity among Indo-Pacific marine provinces differs for demosponges in many aspects from that of other marine taxa, such as corals and fishes, probably due to their shorter pelagic larval phase.

zoology↗

bioRxiv2024

Characterization of bacteria colonizing the mucosal layer of the gastrointestinal tract of Atlantic salmon farmed in a warm water region

Atlantic salmon (Salmo salar) farmed in seawater in Tasmania (lutruwita) can experience temperatures close to their thermotolerance limit during summer. Gut microbiome data from eight successive annual surveys and a specific survey of GI tract mucosa and digesta bacterial cross-sectional distributions indicated members of the genus Aliivibrio, Vibrio, and an unclassified Mycoplasmoidaceae are the main colonizers of the gut mucosal layer in Tasmanian farmed salmon. Peak abundance levels are reached after 7-8 months, corresponding to the late summer, following the transfer of hatchery smolt to seawater farms. Salmon Aliivibrio isolates comprise three novel non-bioluminescent species distinct from species found in the northern hemisphere growing regions. Along with other Aliivibrio species these species share many genes required for host colonization and biofilm formation and also include species and strain-level dependent features. Two of the novel Aliivibrio species surprisingly possessed genes for cytolethal distending toxin while the more predominant species lacked any known virulence genes. The overall observations suggest a small number of species actively colonize the mucosal layer of Atlantic salmon farmed in Tasmania and that this process is strongly influenced by the environmental temperature.

microbiology↗

bioRxiv2024

Characterization of Multicellular Niches Supporting Hematopoietic Stem Cells Within Distinct Zones

Previous studies of hematopoietic stem cells (HSCs) primarily focused on single cell-based niche models, yielding fruitful but conflicting findings1-5. Here we report our investigation on the fetal liver (FL) as the primary fetal hematopoietic site using spatial transcriptomics. Our study reveals two distinct niches: the portal-vessel (PV) niche and the sinusoidal niche. The PV niche, composing N-cadherin (N-cad)HiPdgfr+ mesenchymal stromal cells (MSCs), endothelial cells (ECs), and N-cadLoAlbumin+ hepatoblasts, maintains quiescent and multipotential FL-HSCs. Conversely, the sinusoidal niche, comprising ECs, hepatoblasts and hepatocytes, as well as potential macrophages and megakaryocytes, supports proliferative FL-HSCs biased towards myeloid lineages. Unlike prior reports on the role of Cxcl12, with its depletion from vessel-associated stromal cells leading to 80% of HSCs reduction in the adult bone marrow (BM)6,7, depletion of Cxcl12 via Cdh2CreERT (encoding N-cad) induces altered localization of HSCs from the PV to the sinusoidal niches, resulting in an increase of HSC number but with myeloid-bias. Similarly, we discovered that adult BM encompasses two niches within different zones, each composed of multi-cellular components: trabecular bone area (TBA, or metaphysis) supporting deep-quiescent HSCs, and central marrow (CM, or diaphysis) fostering heterogenous proliferative HSCs. This study transforms our understanding of niches by shifting from single cell-based to multicellular components within distinct zones, illuminating the intricate regulation of HSCs tailored to their different cycling states.

developmental biology↗

bioRxiv2022

Optimization of host cell-compatible, antimicrobial peptides effective against biofilms and clinical isolates of drug-resistant bacteria.

Here, we describe the continued synthetic molecular evolution of a lineage of host-compatible antimicrobial peptides (AMP) intended for the treatment of wounds infected with drug-resistant, biofilm-forming bacteria. The peptides tested are variants of an evolved AMP called D-CONGA, which has excellent antimicrobial activities in vitro and in vivo. In this newest generation of rational D-CONGA variants, we tested multiple sequence-structure-function hypotheses that had not been tested in previous generations. Many of the peptide variants have lower antibacterial activity against Gram-positive or Gram-negative pathogens, especially variants that have altered hydrophobicity, secondary structure potential, or spatial distribution of charged and hydrophobic residues. Thus, D-CONGA is generally well tuned for antimicrobial activity. However, we identified a variant, D-CONGA-Q7, with a polar glutamine inserted into the middle of the sequence, that has higher activity against both planktonic and biofilm-forming bacteria as well as lower cytotoxicity against human fibroblasts. Against clinical isolates of K. pneumoniae, innate resistance to D-CONGA was surprisingly common despite a lack of inducible resistance in P. aeruginosa reported previously. Yet, these same isolates were susceptible to D-CONGA-Q7. D-CONGA-Q7 is much less vulnerable to AMP resistance in Gram-negative bacteria than its predecessor. Consistent with the spirit of synthetic molecular evolution, D-CONGA-Q7 achieved a critical gain-of-function and has a significantly better activity profile.

biochemistry↗

bioRxiv2022

HNRNPH1 destabilizes the G-quadruplex structures formed by G-rich RNA sequences that regulate the alternative splicing of an oncogenic fusion transcript

In the presence of physiological monovalent cations, thousands of RNA G-rich sequences can form parallel G-quadruplexes (G4s) unless RNA-binding proteins inhibit, destabilize, or resolve the formation of such secondary RNA structures. Here, we have used a disease-relevant model system to investigate the biophysical properties of the RNA-binding protein HNRNPH1s interaction with G-rich sequences. We demonstrate the importance of two EWSR1-exon 8 G-rich regions in mediating the exclusion of this exon from the oncogenic EWS-FLI1 transcripts expressed in a subset of Ewing sarcomas, using complementary analysis of tumor data, long-read sequencing, and minigene studies. We determined that HNRNPH1 binds the EWSR1-exon 8 G-rich sequences with low nM affinities irrespective of whether in a non-G4 or G4 state but exhibits different kinetics depending on RNA structure. Specifically, HNRNPH1 associates and dissociates from G4-folded RNA faster than the identical sequences in a non-G4 state. Importantly, we demonstrate using gel shift and spectroscopic assays that HNRNPH1, particularly the qRRM1-qRRM2 domains, destabilizes the G4s formed by the EWSR1-exon 8 G-rich sequences in a non-catalytic fashion. Our results indicate that HNRNPH1s binding of G-rich sequences favors the accumulation of RNA in a non-G4 state and that this contributes to its regulation of RNA processing.

molecular biology↗

bioRxiv2022

Molecular Control of Circuit Plasticity and the Permanence of Imprinted Odor Memory

Behavioral imprinting is a distinct form of learning that has a lifelong impact on social interactions and affectional behaviors1-4. Unlike other forms of memory, imprinting does not require conspicuous association of stimuli; exposure per se appears sufficient to induce memories that neither undergo extinction nor are altered by experience later in life. The site of storage of imprinted memory and the mechanisms that control its formation and permanence are unknown. Here we uncover a molecular mechanism that controls olfactory imprinting, which underlies behaviors including kin and nest recognition, maternal attachment, and homing5-10. We show that odor exposure during the perinatal period converts an innately aversive odor into a homing signal. The behavioral change is associated with odor-induced changes in the projection patterns of olfactory sensory neuron (OSN) expressing the cognate receptors for the exposed odor. We show that the Wnt signaling receptor Frizzled1 (Fzd1) acts as a master regulator of the critical period of OSN development and is responsible for closing the critical period to prevent further changes in the neural circuit. In Fzd1 knockout mice axon projection patterns are continually modified by sensory experience. As Fzd1 knockout abolishes the developmental critical period, it also abolishes odor imprinting. Specific knockout of Fzd1 in the OSNs have the same effect. Mechanistically, Fzd1 controls the critical period through an autoregulated shutdown and by controlling an activity-driven regulon in the OSNs. The transient expression and the subsequent downregulation of Fzd1 leads to the irreversible closure of the critical period to lock in circuits established during the critical period. The evidence suggests that imprinted odor memory is stored in the patterns of connectivity at the first synapse in the olfactory bulb. Early odor experience induces changes in the OSN projection to alter connectivity with innate circuits to establish a life-long memory.

neuroscience↗

bioRxiv2020

DNA ligase I fidelity mediates the mutagenic ligation of pol β oxidized nucleotide insertion products and base excision repair intermediates with mismatches

DNA ligase I (LIG1) completes base excision repair (BER) pathway at the last nick sealing step following DNA polymerase (pol) {beta} gap filling DNA synthesis. We previously reported that pol {beta} 8-oxo-2-deoxyribonucleoside 5-triphosphate (8-oxodGTP) insertion confounds LIG1 leading to the formation of ligation failure products with 5-adenylate (AMP) block. Here, we report the mutagenic ligation of pol {beta} 8-oxodGTP insertion products and an inefficient substrate-product channeling from pol {beta} Watson-Crick like dG:T mismatch insertion to DNA ligation by LIG1 mutant with perturbed fidelity (E346A/E592A) in vitro. Moreover, our results revealed that the substrate discrimination of LIG1 for the nicked repair intermediates with preinserted 3-8-oxodG or mismatches is governed by the mutations at both E346 and E592 residues. Finally, we found that Aprataxin (APTX) and Flap Endonuclease 1 (FEN1), as compensatory DNA-end processing enzymes, can remove 5-AMP block from the abortive ligation products with 3-8-oxodG or all possible 12 non-canonical base pairs. These findings contribute to understand the role of LIG1 as an important determinant of faithful BER, and how a multi-protein complex (LIG1, pol {beta}, APTX and FEN1) can coordinate to hinder the formation of mutagenic repair intermediates with damaged or mismatched ends at the downstream steps of the BER pathway.

biochemistry↗

bioRxiv2020

Androgen regulation of bowel function in mice and humans

Many digestive disorders have prominent sex differences in incidence, symptomatology, and treatment response that are not well understood. Irritable bowel syndrome (IBS), for example, affects approximately 10% of the population worldwide and tends to have different manifestations in males and females. Androgens are steroid hormones present at much higher levels in post-pubertal males than females and could be involved in these sex differences, but their normal functions in the bowel are largely unknown. Here, we show that gonadal androgens are required for normal gastrointestinal motility in vivo. In the healthy mouse gut, we detected androgen receptors in smooth muscle cells and a subset of enteric neurons. Surgical or genetic disruption of androgen signaling in adult mice selectively and reversibly altered colonic motility by affecting neurons rather than smooth muscle. To determine if androgens also influence human bowel function, we measured androgen levels in 208 adults with IBS. Free testosterone levels were lower in patients with IBS compared to healthy controls and inversely correlated with symptom severity. Taken together, these observations establish a role for androgens in the regulation of colonic motility and link altered androgen signaling with a common digestive disorder. These findings advance the fundamental understanding of gut motility, with implications for normal aging and disorders involving the gut-brain axis.

neuroscience↗

bioRxiv2020

Germline gene de-silencing by a transposon insertion is triggered by an altered landscape of local piRNA biogenesis

Transposable elements (TE) are selfish genetic elements that can cause harmful mutations. In Drosophila, it has been estimated that half of all spontaneous visible marker phenotypes are mutations caused by TE insertions. Because of the harm posed by TEs, eukaryotes have evolved systems of small RNA-based genome defense to limit transposition. However, as in all immune systems, there is a cost of autoimmunity and small RNA-based systems that silence TEs can inadvertently silence genes flanking TE insertions. In a screen for essential meiotic genes in Drosophila melanogaster, a truncated Doc retrotransposon within a neighboring gene was found to trigger the germline silencing of ald, the Drosophila Mps1 homolog, a gene essential for meiosis. A subsequent screen for modifiers of this silencing identified a new insertion of a Hobo DNA transposon in the same neighboring gene. Here we describe how the original Doc insertion triggers flanking piRNA biogenesis and local gene silencing and how the additional Hobo insertion leads to de-silencing by reducing flanking piRNA biogenesis triggered by the original Doc insertion. These results support a model of TE-mediated silencing by piRNA biogenesis in cis that depends on local determinants of transcription. This may explain complex patterns of off-target gene silencing triggered by TEs within populations and in the laboratory. It also provides a mechanism of sign epistasis among TE insertions. Author SummaryTransposable elements (TEs) are selfish DNA elements that can move through genomes and cause mutation. In some species, the vast majority of DNA is composed of this form of selfish DNA. Because TEs can be harmful, systems of genome immunity based on small RNA have evolved to limit the movement of TEs. However, like all systems of immunity, it can be challenging for the host to distinguish self from non-self. Thus, TE insertions occasionally cause the small RNA silencing machinery to turn off the expression of critical genes. The rules by which this inadvertent form of autoimmunity causes gene silencing are not well understood. In this article, we describe a phenomenon whereby a TE insertion, rather than silencing a nearby gene, rescues the silencing of a gene caused by another TE insertion. This reveals a mode of TE interaction via small RNA silencing that may be important for understanding how TEs exert their effects on gene expression in populations and across species.

genetics↗

bioRxiv2018

p62-mediated Selective Autophagy Endows Virus-transformed Cells with Insusceptibility to DNA Damage under Oxidative Stress

DNA damage response (DDR) and selective autophagy both can be activated by reactive oxygen/nitrogen species (ROS/RNS), and both are of paramount importance in cancer development. The selective autophagy receptor and ubiquitin (Ub) sensor p62 plays a key role in their crosstalk. ROS production has been well documented in latent infection of oncogenic viruses including Epstein-Barr Virus (EBV). However, p62-mediated selective autophagy and its interplay with DDR have not been investigated in these settings. In this study, we provide evidence that considerable levels of p62-mediated selective autophagy are constitutively induced, and correlates with ROS-Keap1-NRF2 pathway activity, in virus-transformed cells. Inhibition of autophagy results in p62 accumulation in the nucleus, and promotes ROS-induced DNA damage and cell death, as well as downregulates the DNA repair proteins CHK1 and RAD51. In contrast, MG132-mediated proteasome inhibition, which induces rigorous autophagy, promotes p62 degradation but accumulation of the DNA repair proteins CHK1 and RAD51. However, pretreatment with an autophagy inhibitor offsets the effects of MG132 on CHK1 and RAD51 levels. These findings imply that p62 accumulation in the nucleus in response to autophagy inhibition promotes proteasome-mediated CHK1 and RAD51 protein instability. This claim is further supported by the findings that transient expression of a p62 mutant, which is constitutively localized in the nucleus, in B cell lines with low endogenous p62 levels recaptures the effects of autophagy inhibition on CHK1 and RAD51 protein stability. These results indicate that proteasomal degradation of RAD51 and CHK1 is dependent on p62 accumulation in the nucleus. However, small hairpin RNA (shRNA)-mediated p62 depletion in EBV-transformed lymphoblastic cell lines (LCLs) had no apparent effects on the protein levels of CHK1 and RAD51, likely due to the constitutive localization of p62 in the cytoplasm and incomplete knockdown is insufficient to manifest the effects on its nuclear function. Furthermore, shRNA-mediated p62 depletion in EBV-transformed LCLs results in significant increases of endogenous RNF168-{gamma}H2AX damage foci and chromatin ubiquitination, indicative of activation of RNF168-mediated DNA repair mechanisms. Our results have unveiled a pivotal role for p62-mediated selective autophagy that governs DDR in the setting of oncogenic virus latent infection, and provide a novel insight into virus-mediated oncogenesis. Author SummaryReactive oxygen/nitrogen species (ROS/RNS) can induce both DNA damage response (DDR) and selective autophagy, which play crucial roles in cancer development. The selective autophagy receptor and ubiquitin (Ub) sensor p62 links their crosstalk. However, p62-mediated selective autophagy and its interplay with DDR have not been investigated in latent infection of oncogenic viruses including Epstein-Barr Virus (EBV). In this study, we provide evidence that p62-mediated selective autophagy is constitutively induced in virus-transformed cells, and that its inhibition exacerbates ROS-induced DNA damage, and promotes proteasomal degradation of CHK1 and RAD51 in a manner depending on p62 accumulation in the nucleus. However, rigorous autophagy induction results in accumulation of DNA repair proteins CHK1 and RAD51, and p62 degradation. Further, transient expression of a constitutive nucleus-localizing mutant of p62 recaptured the effects of autophagy inhibition on CHK1 and RAD51 protein stability. These findings support the claim that p62 accumulation in the nucleus in response to autophagy inhibition promotes proteasome-mediated CHK1 and RAD51 protein instability. However, small hairpin RNA (shRNA)-mediated p62 depletion did not affect CHK1 and RAD51 protein levels; rather, shRNA-mediated p62 depletion activates RNF168-dependent DNA repair mechanisms. Our results have unveiled a pivotal role for p62-mediated selective autophagy in regulation of DDR by overriding traditional DDR mechanisms in the setting of oncogenic virus latent infection, and provide a novel insight into the etiology of viral cancers.

cancer biology↗

bioRxiv2018

Single cell RNA-Seq reveals distinct stem cell populations that drive sensory hair cell regeneration in response to loss of Fgf and Notch signaling

Loss of sensory hair cells leads to deafness and balance deficiencies. In contrast to mammalian hair cells, zebrafish ear and lateral line hair cells regenerate from poorly characterized, proliferating support cells. Equally ill-defined is the gene regulatory network underlying the progression of support cells to cycling hair cell progenitors and differentiated hair cells. We used single cell RNA-Sequencing (scRNA-Seq) of lateral line sensory organs and uncovered five different support cell types, including quiescent and activated stem cells. In silico ordering of support cells along a developmental trajectory identified cells that self-renew and new groups of genes required for hair cell differentiation. scRNA-Seq analyses of fgf3 mutants, in which hair cell regeneration is increased, demonstrates that Fgf and Notch signaling inhibit proliferation of support cells in parallel by inhibiting Wnt signaling. Our scRNA-Seq analyses set the foundation for mechanistic studies of sensory organ regeneration and is crucial for identifying factors to trigger hair cell production in mammals. As a resource, we implemented a shiny application that allows the community to interrogate cell type specific expression of genes of interest.

developmental biology↗