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Chan, Y.

Publications and source records attributed to Chan, Y..

15 recordsLinked to original sources

A Cell Viability and Utility Index (CVUI) for wildlife fibroblast biobanking: framework development and preliminary empirical validation

Wildlife biobanking depends on consistent, reproducible cell culture outcomes, yet no standardised framework exists for assessing culture quality across taxa or for integrating quality metrics into institutional collections management systems. Here, we present the Cell Viability and Utility Index (CVUI), a scored pipeline framework validated in a pilot study of 154 culture rounds from 46 species held in the Ian Potter Australian Wildlife Biobank at Museums Victoria Research Institute. The CVUI was adapted from the Wildlife Sperm Index (Jacobs et al., 2026) and assigns weighted scores encompassing four sequential culture stages -- establishment, first passage, expansion, and cryobanking -- with a continuous viability modifier applied at the cryobanking stage. Survival analysis identified individual animal identity as the primary source of variance in culture establishment, whereas taxon was the primary predictor of first-passage success. Beyond first passage, failure rates were too low to reliably assess either effect, with critical attrition concentrated at the earliest pipeline stages. These findings informed the differential weighting of CVUI components and have direct implications for workflow prioritisation and banking strategy. Monitoring can now be targeted at establishment and first passage, the stages where intervention has the greatest impact, with taxon-specific attention warranted at first passage and individual-level attention at establishment, while the robustness of the late-stage protocol means that banking yield is largely determined before a culture reaches P1. Integration of CVUI scores into collections management platforms such as Axiell EMu (Electronic Museum) would transform passive record-keeping into active decision support, enabling real-time quality tracking, early flagging of at-risk cultures, and longitudinal benchmarking of biobank performance across species, collectors, and tissue types. This framework provides a foundation for optimising wildlife fibroblast biobanking protocols, developing taxon-specific culture standards, and expanding standardised quality assessment across wildlife biobanks nationally and internationally.

zoology↗

MipSScs: Artificial neural network-based data integration of 2D/3D single-cell spatial RNA sequence data from virus-infected human cerebral organoids

There is interest in the use of recent single-cell spatial transcriptomic technologies to gain biological insights into disease mechanisms. Previously, we characterized the use of herpes simplex virus 1 (HSV-1) induced neuroinflammation in 2D dissociated cells from human cerebral organoids (dcOrgs) to model molecular and transcriptomic readouts associated with Alzheimers disease (AD). In this work, we generated two datasets by using single-cell non-spatial RNA sequencing and single-cell spatial RNA sequencing technologies on HSV-1-infected 2D dcOrgs and HSV-1-infected 3D cerebral organoids (cOrgs). We conducted cell type assignment for the cells in the 2D dcOrgs and 3D cOrgs, by using single-cell non-spatial RNA sequence data from human fetal brains and adult post-mortem brains, to infer the transcriptomic effects of AD-associated in-vitro perturbations through viral infections linked to AD. We evaluated computational and machine learning methods, including the use of multi-layer perceptrons (MLPs), and we used cross-2D/3D platform comparisons as a benchmark to evaluate the artificial neural network models. In the process, we found that the use of MLPs can lead to high validation rates for assigning cell type identities from 2D and 3D human cerebral organoids to cell types found in human adult post-mortem brain samples. Furthermore, the use of these technologies and systems enabled the identification of pseudotime trajectories and cell clusters associated with the viral transcriptional life cycle. We identified several cell types, including endothelial cells and astrocytes, with significantly more clustered cell-cell nearest neighbor distances in infected 3D cOrgs compared to mock 3D cOrgs. Permutation tests revealed that these differences in nearest neighbor distances are unlikely to be driven by overall structural differences between individual infected 3D cOrgs and mock 3D cOrgs, such as differences in the density of cells. Given that there are more large-scale single-cell non-spatial (2D) RNA sequence datasets that had been generated from human post-mortem brain samples, compared to single-cell spatial (3D) RNA sequence datasets from human post-mortem brain samples, the development of data integration approaches by using artificial neural networks such as MLPs, across 2D and 3D single-cell transcriptomics datasets generated from human post-mortem brain samples and human in-vitro systems such as brain organoids is likely to be critical to gain novel insights into neurodegenerative diseases such as AD.

genomics↗

Selective GSK3α Inhibition Promotes Self-Renewal Across Different Stem Cell States

Pan-GSK3/{beta} inhibition promotes stem cell self-renewal through activation of WNT/{beta}-catenin signaling, but its broad effects complicate the precise control of stem cell states. Here, we show that selective inhibition of GSK3 with BRD0705 supports the long-term self-renewal of mouse embryonic stem cells (ESCs), epiblast stem cells (EpiSCs), and neural stem cells (NSCs), independent of {beta}-catenin signaling. When combined with the tankyrase inhibitor IWR1, BRD0705 broadly supports the maintenance of diverse pluripotent stem cell states, including ESCs, EpiSCs, and formative pluripotent stem cells. This BRD0705/IWR1 cocktail enables stable co-culture of naive ESCs and primed EpiSCs while preserving their distinct molecular and functional identities. Single-cell transcriptomics, epigenomic profiling, and functional assays confirm sustained lineage-specific features across stem cell types. These findings demonstrate that selective GSK3 inhibition enhances stemness by buffering against differentiation cues and promoting intrinsic self-renewal capacity. This work identifies GSK3 as a key regulator of self-renewal across distinct stem cell states and establishes a versatile culture system with broad applications. In BriefWang et al. demonstrate that selective GSK3 inhibition with BRD0705 supports self-renewal of pluripotent and neural stem cells. Combined with IWR1, it enables long-term co-culture of naive and primed stem cells while preserving their distinct molecular and functional identities. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=181 HEIGHT=200 SRC="FIGDIR/small/653860v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@4e371eorg.highwire.dtl.DTLVardef@104b287org.highwire.dtl.DTLVardef@164bd96org.highwire.dtl.DTLVardef@daf1ba_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIGSK3 inhibition by BRD0705 promotes self-renewal of ESCs, EpiSCs, and NSCs C_LIO_LIBRD0705/IWR1 enables long-term co-culture of ESCs and EpiSCs C_LIO_LICo-cultured ESCs and EpiSCs retain distinct naive or primed identities C_LIO_LIBRD0705 preserves stem cell states independently of {beta}-catenin signaling C_LI

cell biology↗

The antigenic landscape of N1 neuraminidase in human influenza A virus strains isolated between 2009 and 2020

The clinical burden caused by influenza can be mitigated by the prophylactic use of seasonal influenza vaccines. Their immunogen composition is revised biannually to optimally match the antigenic drift of the hemagglutinin of circulating influenza virus strains. Antibodies directed against the influenza neuraminidase also correlate with protection against influenza, yet the antigenic evolution of influenza neuraminidase remains underexplored. To evaluate the antigenic diversity of N1 neuraminidase, we generated a panel of immune sera directed against 17 N1 neuraminidases derived from human H1N1 strains that were isolated between 2009 and 2020 and determined its neuraminidase inhibition titers against a panel of 15 HxN1 viruses. The resulting neuraminidase inhibition pattern revealed two antigenic groups that circulated in this period. A machine learning method identified K432E and I321V as key determinants of N1 neuraminidase antigenicity.

immunology↗

Unbiased multiplex antigen screening of Cerebrospinal Fluid detects microbial and autoantigenic epitopes associated with Multiple Sclerosis

To comprehensively investigate the intrathecal antibody profile of multiple sclerosis (MS), we examined the cerebrospinal fluid of 195 patients (92 MS and 103 non-MS) for antibodies using a multiplex unbiased bacteria peptide library. We first tested against Epstein-Barr nuclear antigen 1 (EBNA1) for epitope sites enriched in MS and found a significant enrichment at position 407-419. We then used the data to perform a high-throughput screen against a library of 129 viruses known to infect humans. We discovered several additional epitopes from viruses such as Hantaan virus, Human Herpesvirus 6A and Human respiratory syncytial virus B associated with MS. Besides viral epitopes, we also screened for potential autoantigens of the central nervous system (CNS). We discovered several autoantigenic epitopes in proteins such as ADRB3, HTR3A and MPO that were significantly enriched for MS. Because of previous associations of Toxoplasma gondii infection with MS, we also performed a Toxoplasma gondii specific analysis and discovered additional epitopes enriched for MS. We further assessed epitope-epitope correlations within the patient samples and found distinct patterns of association between these microbial and autoantigenic epitopes. Finally, we performed machine-learning to determine if these epitopes are predictive for MS and found that the model incorporating all the epitopes could most effectively discriminate between MS and non-MS (ROC-AUC score = 0.91). Our results demonstrate the effectiveness of multiplex unbiased screens to detect the identity of potentially cross-reactive antibodies targeting MS CNS epitopes and they can also be used as effective biomarkers for MS. One Sentence SummaryWe performed an unbiased multiplex bacteria peptide antibody library screen on cerebrospinal fluid samples of patients with multiple sclerosis (MS) as well as non-MS controls and detected multiple viral and autoantigenic epitopes that are significantly enriched in MS patient samples.

immunology↗

Development of a high-throughput, quantitative platform using human cerebral organoids to study virus-induced neuroinflammation in Alzheimer's disease

Neuroinflammation is a central process in the pathogenesis of several neurodegenerative diseases such as Alzheimers disease (AD), and there are active efforts to target pathways involved in neuroinflammation for molecular biomarker discovery and therapeutic development in neurodegenerative diseases. It was also proposed that there may be an infectious etiology in AD that is associated with viruses such as herpes simplex virus (HSV-1) and influenza A virus (IAV), leading to neuroinflammation-induced AD pathogenesis or disease progression. We sought to develop high-throughput, quantitative molecular biomarker assays using dissociated cells from human cerebral organoids (dcOrgs), that can used for screening compounds to reverse AD-associated neuroinflammation. We found that HSV-1 infection, but not IAV infection, in dcOrgs led to increased intracellular A{beta}42 and phosphorylated Tau-Thr212 (pTau-212) expression, lower ratios of secreted A{beta}42/40, as well as neuronal loss, and increased proportions of astrocytes and microglia, which are hallmarks of AD. Among the glia cell-type markers, Iba1 (microglia) and GFAP (astrocyte) expression were most strongly correlated with HSV-1 expression, which further supported that these biomarkers are perturbed by glia-mediated neuroinflammation. By performing large-scale RNA sequencing, we observed that differentially expressed transcripts in HSV-1 infected dcOrgs were specifically enriched for AD-associated GWAS genes, but not for genes associated with other common neurodegenerative, neuropsychiatric or autoimmune diseases. Immediate treatment of HSV-1 infected dcOrgs with anti-herpetic drug acyclovir (ACV) rescued most of the cellular and transcriptomic biomarkers in a dosage-dependent manner, indicating that it is possible to use our high-throughput platform to identify compounds or target genes that can reverse these neuroinflammation-induced biomarkers associated with AD.

genomics↗

Modeling of mitochondrial genetic polymorphisms reveals induction of heteroplasmy by pleiotropic disease locus MT:10398A>G

Mitochondrial (MT) dysfunction has been associated with several neurodegenerative diseases including Alzheimers disease (AD). While MT-copy number differences have been implicated in AD, the effect of MT heteroplasmy on AD has not been well characterized. Here, we analyzed over 1,800 whole genome sequencing data from four AD cohorts in seven different tissue types to determine the extent of MT heteroplasmy present. While MT-heteroplasmy was present throughout the entire MT genome for blood samples, we detected MT-heteroplasmy only within the MT control region for brain samples. We observed that an MT variant 10398A>G (rs2853826) was significantly associated with overall MT-heteroplasmy in brain tissue while also being linked with the largest number of distinct disease phenotypes of all annotated MT variants in MitoMap. Using gene-expression data from our brain samples, our modeling discovered several gene networks involved in mitochondrial respiratory chain and Complex I function associated with 10398A>G. The variant was also found to be an expression quantitative trait loci (eQTL) for the gene MT-ND3. We further characterized the effect of 10398A>G by phenotyping a population of lymphoblastoid cell-lines (LCLs) with and without the variant allele. Examination of RNA sequence data from these LCLs reveal that 10398A>G was an eQTL for MT-ND4. We also observed in LCLs that 10398A>G was significantly associated with overall MT-heteroplasmy within the MT control region, confirming the initial findings observed in post-mortem brain tissue. These results provide novel evidence linking MT SNPs with MT heteroplasmy and open novel avenues for the investigation of pathomechanisms that are driven by this pleiotropic disease associated loci.

genomics↗

Identification and characterization of a proliferative cell population in estrogen receptor-positive metastatic breast cancer through spatial and single-cell transcriptomics

BackgroundIntratumor heterogeneity is a hallmark of most solid tumors, including breast cancers. We applied spatial transcriptomics and single-cell RNA-sequencing technologies to profile spatially resolved cell populations within estrogen receptor-positive (ER+) metastatic breast cancers and elucidate their importance in estrogen-dependent tumor growth. MethodsSpatial transcriptomics and single-cell RNA-sequencing were performed on two patient-derived xenografts (PDXs) of "ER-high" metastatic breast cancers with opposite estrogen-mediated growth responses: estrogen-suppressed GS3 (80-100% ER) and estrogen-stimulated SC31 (30-75% ER) models. The analyses included samples treated with and without 17{beta}-estradiol. The findings were validated via scRNA-seq analyses on "ER-low" estrogen-accelerating PDX, GS1 (5% ER). The results from our spatial and single-cell analyses were further supported by the analysis of a publicly available single cell dataset and a protein-based dual immunohistochemical (IHC) evaluation using three important clinical markers [i.e., ER, progesterone receptor (PR), and Ki67]. The translational implication of these results was assessed by clinical outcome analyses on public breast cancer cohorts. ResultsOur novel space-gene-function study revealed a "proliferative" cell population in addition to three major spatially distinct compartments within ER+ metastatic breast cancers. These compartments showed functional diversity (i.e., estrogen-responsive, proliferative, hypoxia-induced, and inflammation-related). The "proliferative (MKI67+)" population, not "estrogen-responsive" compartment, was crucial for estrogen-dependent tumor growth, leading to the acquisition of luminal B features. The cells with induction of typical estrogen-responsive genes such as PGR were not directly linked to estrogen-dependent proliferation. Additionally, the dual IHC analyses demonstrated the distinct contribution of the Ki67+ proliferative cells toward estrogen-mediated growth and their response to palbociclib, a CDK4/6 inhibitor. The gene signatures developed from the proliferative, hypoxia-induced, and inflammation-related compartments were significantly correlated with worse clinical outcomes, while patients with the high estrogen-responsive scores showed better prognosis, confirming that the estrogen-responsive compartment would not be directly associated with estrogen-dependent tumor progression. ConclusionsFor the first time, our study elucidated a "proliferative" cell population distinctly distributed in ER+ metastatic breast cancers. They contribute differently toward progression of these cancers, and the gene signature in the "proliferative" compartment is an important determinant of luminal cancer subtypes.

cancer biology↗

Combined loss of obscurin and obscurin-like 1 in murine hearts results in impaired diastolic dysfunction, altered metabolism and deregulated mitophagy.

Muscle proteins of the obscurin protein family play important roles in sarcomere organization, sarcoplasmic reticulum (SR) and T-tubule architecture and function. However, their precise molecular functions and redundancies between protein family members as well as their involvement in cardiac diseases remain to be fully understood. To investigate the functional roles of obscurin and its close homologue obscurin-like 1 (Obsl1) in the heart, we generated and analyzed knockout mice for obscurin, Obsl1, as well as obscurin/Obsl1 double-knockouts (dKO). We show that dKO mice are viable but show postnatal deficits in cardiac muscle SR and mitochondrial architecture and function at the microscopic, biochemical and cellular level. Altered SR structure resulted in perturbed calcium cycling, while mitochondrial ultrastructure deficits were linked to decreased levels of Chchd3, a Micos complex protein. Hearts of dKO mice also show increased expression of Atg4d, a novel Obsl1 interacting protein, resulting in abnormal mitophagy and increased unfolded protein response. At the physiological level, loss of obscurin and Obsl1 resulted in a profound delay of cardiac relaxation, associated with metabolic signs of heart failure. Taken together, our data suggest that obscurin and Obsl1 play crucial roles in cardiac SR structure, calcium cycling, mitochondrial function, turnover and metabolism.

cell biology↗

Reliable multiplex generation of pooled induced pluripotent stem cells for genetic testing

Inducing somatic cells into pluripotent stem cells (iPSCs) provides an excellent model for studying systems in-vitro. Understanding the impact of individual donor genetic backgrounds on reprogramming ability would allow researchers to harness these genetic differences and increase the efficiency of the reprogramming process. To better understand the genetic basis of reprogramming cells into iPSCs, we present Induction of Pluripotency from Pooled Cells (iPPC) - an efficient, scalable, and reliable reprogramming procedure. Using our deconvolution algorithm that employs low-coverage pooled sequencing and single nucleotide polymorphisms (SNPs), we estimate individual donor proportions of cell lines within large cohorts. With iPPC, we concurrently reprogrammed over one hundred donor LCLs into iPSCs and found strong correlations of individual donors reprogramming ability across multiple experiments. We note that individual donors reprogramming ability remains consistent across both same-day replicates and multiple experimental runs, and that the expression of certain immunoglobulin precursor genes (IGLV10-54, IGLV3-9, IGLV1-17, IGLV1-6, and IGLV3-1) may impact reprogramming ability. Our process enables a multiplex framework to study the reprogramming ability of different donor cells into iPSCs and also provides a reliable method along with a pooled library of donor iPSCs for downstream research and investigation of other in-vitro phenotypes.

molecular biology↗

CRISPR-Mediated Generation and Characterization of a Gaa Homozygous c.1935C>A (p.D645E) Pompe Disease Knock-in Mouse Model Recapitulates Human Infantile Onset-Pompe Disease

Pompe disease (PD) is an autosomal recessive disorder caused by deficient lysosomal acid -glucosidase (GAA), leading to reduced degradation and subsequent accumulation of intra-lysosomal glycogen in tissues, especially skeletal and oftentimes cardiac muscle. The c.1935C>A (p.Asp645Glu) variant is the most frequent GAA pathogenic mutation in people of Taiwanese and Southern Chinese ethnicity, causing infantile-onset PD (IOPD), which presents neonatally with severe hypertrophic cardiomyopathy, profound muscle hypotonia, and respiratory failure leading to premature death if untreated. To further investigate the pathogenic mechanism and facilitate development of therapies pertaining to this variant, we applied CRISPR-Cas9 homology-directed repair (HDR) using a novel dual sgRNA approach flanking the target site to generate a GaaEm1935C>A knock-in mouse model as well as a myoblast cell line carrying the Gaa c.1935C>A mutation. Herein we describe the molecular, biochemical, physiological, histological, and behavioral characterization of 3-month-old homozygous GaaEm1935C>A mice. Homozygous GaaEm1935C>A knock-in mice exhibited normal Gaa mRNA expression levels relative to wild-type mice, but GAA enzymatic activity was almost completely abolished, leading to a substantial increase in tissue glycogen storage, and significant concomitant impairment of autophagy. Echocardiography of 3-month-old knock-in mice revealed significant cardiac hypertrophy. The mice also demonstrated skeletal muscle weakness but, paradoxically, not early mortality. Longitudinal studies of this model, including assessment of its immune response to exogenously supplied GAA enzyme, are currently underway. In summary, the GaaEm1935C>A knock-in mouse model recapitulates the molecular, biochemical, histopathologic, and phenotypic aspects of human IOPD caused by the GAA c.1935C>A pathogenic variant. It is an ideal model to assess innovative therapies to treat IOPD, including personalized therapeutic strategies that correct pathogenic variants, restore GAA activity and produce functional phenotypes.

genetics↗

Response of Endozoicomonas montiporae to heat stress and coral host lysates

Endozoicomonas, a core bacterial group in corals, may also be a coral symbiont. Endozoicomonas communities often decrease rapidly in corals under heat stress. However, how the bacteria respond to changes in temperature and coral host during heat stress is unknown. Here, we employed the cultivable, dominant species E. montiporae as a working organism to explore how Endozoicomonas responds to heat stress. We designed two experiments to clarify the extent to which E. montiporae is influenced by temperature and coral host. We detected differentially expressed protein (DEP) profiles in this bacterium at 31{degrees}C and 33{degrees}C compared to 25{degrees}C by tandem mass tags-based quantitative proteome analysis. Fifty DEPs, including many heat shock proteins, were detected when the temperature changed. The expression of antioxidant defense proteins and key pyruvate synthase proteins decreased, suggesting that E. montiporae were in a physiology of stress at 33{degrees}C. Furthermore, some proteins were differentially expressed because of the heat-stress-treated coral lysate specifically, suggesting that not only heat but also heat-induced host factors can affect the protein expression of the bacterium. This study provides an in-depth analysis of how the molecular mechanisms of Endozoicomonas are affected by heat stress and coral host.

microbiology↗

Diversity of Treponema denticola and other oral treponeme lineages in subjects with periodontitis and gingivitis

More than 75 species/species-level phylotypes of taxa belonging to the genus Treponema inhabit the human oral cavity. Treponema denticola is commonly associated with periodontal disease, but the etiological roles and ecological distributions of other oral treponemes remain more obscure. Here, we compared the clinical distributions of phylogroup 1 and 2 oral treponemes in subgingival plaque sampled from Chinese subjects with periodontitis (n=10) and gingivitis (n=8), via the sequence analysis of the highly-conserved pyrH housekeeping gene. Two PCR primer sets that respectively targeted oral phylogroup 1 and 2 treponeme pyrH genes were used to construct plasmid clone-amplicon libraries for each subject, which were sequenced for bioinformatic analysis. 1,204 quality-filtered, full-length pyrH gene sequences were obtained from the cohort (median: 61.5; range: 59-83 of cloned pyrH sequences per subject), which were assigned to 34 pyrH genotypes (pyrH001-pyrH034; 97% sequence-identity cut-off). 18 pyrH genotypes (536 pyrH sequences) corresponded to phylogroup 1 treponeme taxa (including Treponema vincentii, Treponema medium). 16 pyrH genotypes (668 pyrH sequences) corresponded to T. denticola and other phylogroup 2 treponemes. Periodontitis subjects contained a greater diversity of phylogroup 2 pyrH genotypes, compared to gingivitis subjects (Mann-Whitney U-test). One T. denticola pyrH genotype (pyrH001) was highly prevalent: detected in 10/10 periodontitis and 6/8 gingivitis subjects. Several subjects harboured multiple T. denticola pyrH genotypes. Non-metric multidimensional scaling and PERMANOVA tests revealed no significant differences in overall pyrH genotype compositions between periodontitis and gingivitis subjects. In conclusion, our results clearly show that subjects with periodontitis and gingivitis commonly harbour highly-diverse oral treponeme communities.

microbiology↗

CRISPR-Cas9 generated Pompe knock-in murine model exhibits early-onset cardiomyopathy and impaired skeletal muscle function

Infantile-onset Pompe Disease (IOPD), caused by mutations in lysosomal acid alpha-glucosidase (Gaa), manifests rapidly progressive fatal cardiac and skeletal myopathy incompletely attenuated by synthetic GAA intravenous infusions. The currently available murine model does not fully simulate human IOPD, displaying skeletal myopathy with late-onset hypertrophic cardiomyopathy. Bearing a Cre-LoxP induced exonic disruption of the murine Gaa gene, this model is also not amenable to genome-editing based therapeutic approaches. We report the early onset of severe hypertrophic cardiomyopathy in a novel murine IOPD model generated utilizing CRISPR-Cas9 homology-directed recombination to harbor the orthologous Gaa mutation c.1826dupA (p.Y609*), which causes human IOPD. We demonstrate the dual sgRNA approach with a single-stranded oligonucleotide donor is highly specific for the Gaac.1826 locus without genomic off-target effects or rearrangements. Cardiac and skeletal muscle were deficient in Gaa mRNA and enzymatic activity and accumulated high levels of glycogen. The mice demonstrated skeletal muscle weakness but did not experience early mortality. Altogether, these results demonstrate that the CRISPR-Cas9 generated Gaac.1826dupA murine model recapitulates hypertrophic cardiomyopathy and skeletal muscle weakness of human IOPD, indicating its utility for evaluation of novel therapeutics.

molecular biology↗

High-throughput creation and functional profiling of eukaryotic DNA sequence variant libraries using CRISPR/Cas9

Construction of genetic variant libraries with phenotypic measurement is central to advancing todays functional genomics, and remains a grand challenge. Here, we introduce a Cas9-based approach for generating pools of mutants with defined genetic alterations (deletions, substitutions and insertions), along with methods for tracking their fitness en masse. We demonstrate the utility of our approach in performing focused analysis of hundreds of mutants of a single protein and in investigating the biological function of an entire family of poorly characterized genetic elements. Our platform allows fundamental biology questions to be investigated in a quick, easy and affordable manner.

bioengineering↗