Biology subjects

He, Z.

Publications and source records attributed to He, Z..

At least 271 records · Page 15Linked to original sources

bioRxiv2020

Resolving brain organoid heterogeneity by mapping single cell genomic data to a spatial reference

Self-organizing tissues resembling brain regions grown in vitro from human stem cells (so-called organoids or spheroids) offer exciting possibilities to study human brain development, disease, and evolution. Brain organoids or spheroids are complex and can contain cells at various stages of differentiation from different brain structures. Single-cell genomic methods provide powerful approaches to explore cell composition, differentiation trajectories, gene regulation, and genetic perturbations in brain organoid systems. However, it remains a major challenge to understand the cellular heterogeneity observed within and between individual organoids. Here, we have developed a computational approach (VoxHunt) to assess brain organoid patterning, developmental state, and cell composition through systematic comparisons to three-dimensional in situ hybridization data from the Allen Brain Atlas. Cellular transcriptomes as well as accessible chromatin landscapes can be compared to spatial transcript patterns in the developing mammalian brain, which enables characterization and visualization of organoid cell compositions. VoxHunt will be useful to assess novel organoid engineering protocols and to annotate cell fates that emerge in organoids during genetic and environmental perturbation experiments.

bioinformatics↗

bioRxiv2020

Cryo-EM structures of the ATP release channel pannexin 1

The plasma membrane ATP release channel pannexin 1 has been implicated in numerous physiological and pathophysiological processes associated with purinergic signaling, including cancer progression, apoptotic cell clearance, inflammation, blood pressure regulation, oocyte development, epilepsy and neuropathic pain. Here, we present near-atomic resolution structures of Xenopus tropicalis and Homo sapiens PANX1 determined by cryo-electron microscopy that reveal a heptameric channel architecture. Compatible with ATP permeation, the transmembrane pore and cytoplasmic vestibule are exceptionally wide. An extracellular tryptophan ring located at the outer pore creates a constriction site, potentially functioning as a molecular sieve that restricts the size of permeable substrates. In combination with functional characterization, this work elucidates the previously unknown architecture of pannexin channels and establishes a foundation for understanding their unique channel properties as well as for developing rational therapies.

biophysics↗

bioRxiv2020

Single cell atlas of trisomy 21 cerebral cortex

Down syndrome (DS) is one of the most common human birth defects caused by trisomy 21 (T21), leading to a variety of cognitive impairments. The cellular composition of human brain has been explored using single cell RNA sequencing in both physiological and pathological conditions. However, the cellular heterogeneity of human brain with chromosome aneuploidy is largely unknown. Here, we profiled the transcriptome of 36046 cells in cerebral cortex of T21 human fetus, covering frontal lobe, parietal lobe, occipital lobe and temporal lobe. Intriguingly, we detected several genes positively associated with neurons maturation was dysregulated in T21 frontal cortex (HIC2, POU2F2, ZGLP1 and FOXK1). To share, explore and utilized the data resources of T21 cerebral cortex, we developed a comprehensive platform named T21atlas, composing of two functional modules (T21cluster and T21talk). Overall, our study provides, as far as we know, the first single cell atlas for T21 cerebral cortex, which could promote our understanding of the molecular mechanism of DS at an unprecedented resolution and could potentially facilitate the development of novel clinical therapeutics against T21.

neuroscience↗

bioRxiv2019

Single cell transcriptome of CD8+ T cells in multiple cancers reveals comprehensive exhaustion associated mechanisms

T cell exhaustion is one of the main reasons of tumor immune escape. Using single cell transcriptome data of CD8+ T cells in multiple cancers, we identified different cell types, in which Pre_exhaust and exhausted T cells participated in negative regulation of immune system process. By analyzing the co-expression network patterns and differentially expressed genes of Pre_exhaust, exhausted and effector T cells, we identified 35 genes related to T cell exhaustion, which high GSVA scores were associated with significantly poor prognosis in various cancers. In the differentially expressed genes, RGS1 showed the greatest fold change in Pre_exhaust and exhausted cells of three cancers compared with effector T cells, and high expression of RGS1 was also associated with poor prognosis in various cancers. Additionally, RGS1 protein was upregulated significantly in tumor tissues in the immunohistochemistry verification. Furthermore, RGS1 displayed positive correlation with the 35 genes, especially highly correlated with PDCD1, CTLA4, HAVCR2 and TNFRSF9 in CD8+ T cells and cancer tissues, indicating important roles of RGS1 in CD8+ T cell exhaustion. Considering the GTP-hydrolysis activity of RGS1 and significantly high mRNA and protein expression in cancer tissues, we speculated that RGS1 potentially mediate the T cell retention to lead to the persistent antigen stimulation, resulting in T cell exhaustion. In conclusion, our findings suggest that RGS1 is a new marker and promoting factor for CD8+ T cell exhaustion, and provide theoretical basis for research and immunotherapy of exhausted cells.

cancer biology↗

bioRxiv2019

Maximum likelihood estimation of natural selection and allele age from time series data of allele frequencies

Temporally spaced genetic data allow for more accurate inference of population genetic parameters and hypothesis testing on the recent action of natural selection. In this work, we develop a novel likelihood-based method for jointly estimating selection coefficient and allele age from time series data of allele frequencies. Our approach is based on a hidden Markov model where the underlying process is a Wright-Fisher diffusion conditioned to survive until the time of the most recent sample. This formulation circumvents the assumption required in existing methods that the allele is created by mutation at a certain low frequency. We calculate the likelihood by numerically solving the resulting Kolmogorov backward equation backwards in time while re-weighting the solution with the emission probabilities of the observation at each sampling time point. This procedure reduces the two-dimensional numerical search for the maximum of the likelihood surface for both the selection coefficient and the allele age to a one-dimensional search over the selection coefficient only. We illustrate through extensive simulations that our method can produce accurate estimates of the selection coefficient and the allele age under both constant and non-constant demographic histories. We apply our approach to re-analyse ancient DNA data associated with horse base coat colours. We find that ignoring demographic histories or grouping raw samples can significantly bias the inference results.

genetics↗

bioRxiv2019

Upon microbial challenge human neutrophils undergo rapid changes in nuclear architecture to orchestrate an immediate inflammatory gene program

Differentiating neutrophils undergo large-scale changes in nuclear morphology. How such alterations in structure are established and modulated upon exposure to microbial agents is largely unknown. Here, we found that prior to encounter with bacteria, an armamentarium of inflammatory genes was positioned in a transcriptionally passive environment suppressing premature transcriptional activation. Upon microbial exposure, however, human neutrophils rapidly (<3 hours) repositioned the ensemble of pro-inflammatory genes towards the transcriptionally permissive compartment. We show that the repositioning of genes was closely associated with the swift recruitment of cohesin across the inflammatory enhancer landscape permitting an immediate transcriptional response upon bacterial exposure. These data reveal at the mechanistic level how upon microbial challenge human neutrophils undergo rapid changes in nuclear architecture to orchestrate an immediate inflammatory gene program.

genomics↗

bioRxiv2019

Low dose Cold Atmospheric Plasma induces membrane oxidation, stimulates endocytosis and enhances uptake of nanomaterials in Glioblastoma multiforme cells

Cold atmospheric plasma (CAP) has demonstrated synergistic cytotoxic effects with nanoparticles, especially promoting the uptake and accumulation of nanoparticles inside cells. However, the mechanisms driving the effects need to be explored. In this study, we investigate the enhanced uptake of theranostic nanomaterials by CAP. Numerical modelling of the uptake of gold nanoparticle into U373MG Glioblastoma multiforme (GBM) cells predicts that CAP may introduce a new uptake route. We demonstrate that cell membrane repair pathways play the main role in this stimulated new uptake route, following non-toxic doses of dielectric barrier discharge CAP (30 s, 75 kV). CAP treatment induces cellular membrane damage, mainly via lipid peroxidation as a result of reactive oxygen species (ROS) generation. Membranes rich in peroxidated lipids are then trafficked into cells via membrane repairing endocytosis. We confirm that the enhanced uptake of nanomaterials is clathrin-dependent using chemical inhibitors and silencing of gene expression. Therefore, CAP-stimulated membrane repair increases endocytosis and accelerates the uptake of gold nanoparticles into U373MG cells after CAP treatment. Our data demonstrate the utility of CAP to model membrane oxidative damage in cells and characterise a previously unreported mechanism of membrane repair to trigger nanomaterial uptake which will be useful for developing more efficient deliveries of nanoparticles and pharmaceuticals into cancer cells for tumour therapy and diagnosis. This mechanism of RONS-induced endocytosis will also be of relevance to other cancer therapies that induce an increase in extracellular RONS.\n\n\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=104 SRC=\"FIGDIR/small/805192v1_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (43K):\norg.highwire.dtl.DTLVardef@1487fd4org.highwire.dtl.DTLVardef@c05eeforg.highwire.dtl.DTLVardef@198c75aorg.highwire.dtl.DTLVardef@1481096_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2019

Bacterial Hyperswarming as a Protective Response to Intestinal Stress

Bacterial swarming, a collective movement on a surface, has rarely been associated with human pathophysiology. Here, we report for the first time that bacterial swarmers are associated with protection against intestinal inflammation. We show that bacterial swarmers are highly predictive of intestinal stress in mice and humans. We isolated a novel Enterobacter swarming strain, SM3, from mouse feces. SM3 and other known commensal swarmers contrast to their respective swarming-deficient, but swimming-competent isogenic strains abrogated intestinal inflammation in mice. Treatment of colitic mice with SM3, but not its mutants, enriched beneficial fecal anaerobes belonging to the family, Bacteroidales S24-7. We observed SM3 swarming associated pathways in the in vivo fecal metatranscriptomes. In vitro growth of S24-7 was enriched in presence of SM3 or its mutants conjecturing that bacterial swarming in vivo might influence SM3s access to S24-7 in the intestines. Overall, our work identifies a new paradigm in which intestinal stress allows for the emergence of swarming bacteria, which can counterintuitively heal intestinal inflammation.

microbiology↗

bioRxiv2019

Culture under normoxic conditions and enhanced virulence of phase II Coxiella burnetii transformed with a RSF1010-based shuttle vector

Coxiella burnetii is a Gram-negative, facultative intracellular microorganism that can cause acute or chronic Q fever in human. It was recognized as an obligate intracellular organism until the revolutionary design of an axenic cystine culture medium (ACCM). Present axenic culture of C. burnetii strictly requires a hypoxic condition (<10% oxygen). Here we investigated the normoxic growth of C. burnetii strains in ACCM-2 with or without tryptophan supplementation. Three C. burnetii strains - Henzerling phase I, Nine Mile phase II and a Nine Mile phase II transformant, were included. The transformant contains a pMMGK plasmid that is composed of a RSF1010 ori, a repABC operon, an eGFP gene and a kanamycin resistance cassette. We found that, under normoxia if staring from an appropriate concentration of fresh age inocula, Nine Mile phase II can grow significantly in ACCM-2 with tryptophan, while the transformant can grow robustly in ACCM-2 with or without tryptophan. In contrast, long-term frozen stocks of phase II and its transformant, and Henzerling phase I of different ages had no growth capability under normoxia under any circumstances. Furthermore, frozen stocks of the transformant consistently caused large splenomegaly in SCID mice, while wild type Nine Mile phase II induced a lesser extent of splenomegaly. Taken together, our data show that normoxic cultivation of phase II C. burnetii can be achieved under certain conditions. Our data suggests that tryptophan and an unknown temperature sensitive signal are involved in the expression of genes for normoxic growth regulated by quorum sensing in C. burnetii.

microbiology↗

bioRxiv2019

Close homologue of L1 sensitizes lung cancer cells to cisplatin and paclitaxel via inhibition Akt pathway

Drug resistance is a serious promble during chemotherapy in lung cancer, which may lead to tumor relapse and further progression. CHL1 was a tumor suppressor in most malignancies, and it was found downregulated in NSCLC cisplatin-resistant cells H460. Thus, in this study, we investigated the role and mechanism of chemoresistance by CHL1 in lung cancer. Human lung adenocarcinoma cell lines A549 and its cisplatin resistant cells (A549/DDP) and paclitaxel resistant cells (A549/PTX) were applied in this research. CHL1 was found obvious downregulation in A549/DDP and A549/PTX cells versus A549 cells. Suppression of CHL1 in A549 cells, promoted cell survival rate and clone formation, decreased cell apoptosis when treated with or without DDP and PTX, respectively. While excessive CHL1 expression in A549/DDP and A549/PTX cells, the results were opposite. Moreover, CHL1 knockdown mediating chemoresistance was reversed by Akt inhibitor SC66 in A549 cells. In summary, overexpression of CHL1 reversed chemoresistance to cisplatin and PTX via suppressing Akt pathway in lung cancer, it was suggested that CHL1 maybe as a potential target for overcome chemoresistance in lung cancer.

cancer biology↗

bioRxiv2019

Essential role of Bone morphogenetic protein 15 in porcine ovarian and follicular development and ovulation

Bone morphogenetic protein 15 (BMP15) is a multifunctional oocyte-specific secreted factor. It controls female fertility and follicular development in both species-specific and dosage-sensitive manners. Previous studies found that BMP15 played a critical role on follicular development and ovulation rate of mono-ovulatory mammalian species, but has minimal impact on poly-ovulatory mice. However, whether this is true in non-rodent poly-ovulatory species need to be validated. To investigate this question, we generated a BMP15 knockdown pig model. We found that BMP15 knockdown gilts showed markedly reduced fertility accompanied with phenotype of dysplastic ovaries containing significantly declined number of follicles, increased number of abnormal follicles, and abnormally enlarged antral follicles resulting in disordered ovulation. Molecular and transcriptome analysis revealed that knockdown of BMP15 significantly suppressed cell proliferation, differentiation, Fshr expression, leading to premature luteinization and reduced estradiol production in GCs, and simultaneously decreased the quality and meiotic maturation of oocyte. Our results provide in vivo evidences for the essential role of BMP15 in porcine ovarian and follicular development, and new insight into the complicated regulatory function of BMP15 in female fertility of poly-ovulatory species.

developmental biology↗

bioRxiv2019

Reversal of ageing- and injury-induced vision loss by Tet-dependent epigenetic reprogramming

Ageing is a degenerative process leading to tissue dysfunction and death. A proposed cause of ageing is the accumulation of epigenetic noise, which disrupts youthful gene expression patterns that are required for cells to function optimally and recover from damage1-3. Changes to DNA methylation patterns over time form the basis of an ageing clock4, 5, but whether old individuals retain information to reset the clock and, if so, whether this would improve tissue function is not known. Of all the tissues in the body, the central nervous system (CNS) is one of the first to lose regenerative capacity6, 7. Using the eye as a model tissue, we show that expression of Oct4, Sox2, and Klf4 genes (OSK) in mice resets youthful gene expression patterns and the DNA methylation age of retinal ganglion cells, promotes axon regeneration after optic nerve crush injury, and restores vision in a mouse model of glaucoma and in normal old mice. This process, which we call recovery of information via epigenetic reprogramming or REVIVER, requires the DNA demethylases Tet1 and Tet2, indicating that DNA methylation patterns dont just indicate age, they participate in ageing. Thus, old tissues retain a faithful record of youthful epigenetic information that can be accessed for functional age reversal.

molecular biology↗

bioRxiv2019

Single-cell profiles of retinal neurons differing in resilience to injury reveal neuroprotective genes

Neuronal types in the central nervous system differ dramatically in their resilience to injury or insults. Here we studied the selective resilience of mouse retinal ganglion cells (RGCs) following optic nerve crush (ONC), which severs their axons and leads to death of ~80% of RGCs within 2 weeks. To identify expression programs associated with differential resilience, we first used single-cell RNA-seq (scRNA-seq) to generate a comprehensive molecular atlas of 46 RGC types in adult retina. We then tracked their survival after ONC, characterized transcriptomic, physiological, and morphological changes that preceded degeneration, and identified genes selectively expressed by each type. Finally, using loss- and gain-of-function assays in vivo, we showed that manipulating some of these genes improved neuronal survival and axon regeneration following ONC. This study provides a systematic framework for parsing type-specific responses to injury, and demonstrates that differential gene expression can be used to reveal molecular targets for intervention.

neuroscience↗

bioRxiv2019

New genotype invasion of dengue virus serotype 1 drove massive outbreak in Guangzhou, China

BackgroundDengue fever is a mosquito-borne infectious disease that has caused major health problems. Variations in dengue virus (DENV) genes are important features of epidemic outbreaks. However, the associations of DENV genes with epidemic scale have not been extensively examined. Here, we assessed new genotype invasion of DENV-1 isolated from Guangzhou in China to evaluate associations with epidemic outbreaks.\n\nMethodology/Principal FindingsWe used DENV-1 strains isolated from sera of dengue cases from 2002 to 2016 in Guangzhou for complete genome sequencing. A neighbor-joining phylogenetic tree was constructed to elucidate the genotype characteristics and determine if new genotype invasion correlated with major outbreaks. In our study, a new genotype invasion event was observed during each significant outbreak period in 2002-2003, 2006-2007 and 2013-2014. Genotype II was the main epidemic genotype in 2003 and before. Invasion of genotype I in 2006 caused an unusual outbreak with 765 cases (relative risk (RR)=16.24, 95% confidence interval (CI) =12.41-21.25). At the middle and late stages of the 2013 outbreak, genotype III was introduced to Guangzhou as a new genotype invasion responsible for 37340 cases with RR 541.73 (95%CI=417.78-702.45), after which genotypes I and III began co-circulating. Base mutations occurred after new genotype invasion, and the gene sequence of NS3 protein had the lowest average similarity ratio (99.82%), followed by the gene sequence of E protein (99.86%), as compared to the 2013 strain.\n\nConclusions/SignificanceGenotype replacement and co-circulation of multiple DENV-1 genotypes were observed. New genotype invasion was highly correlated with local unusual outbreaks. In addition to DENV-1 genotype I in the unprecedented outbreak in 2014, new genotype invasion by DENV-1 genotype III occurred in Guangzhou.\n\nAuthor SummaryNew genotype invasion of dengue virus highly correlates with the massive outbreaks. In this study, we examined the association of the genotype of dengue virus serorype 1 (DENV-1) from human cases through complete genome sequencing with outbreak scale during 2002 and 2016 in Guangzhou, China. It was observed that genotype replacement and co-circulation of multiple genotypes occurred. Most importantly, it indicated that new genotype invasion was highly related with local unusual outbreaks in major outbreak periods in 2002-2003, 2006-2007 and 2013-2014. DENV-1 genotype II was the main epidemic genotype in 2003 and before. Invasion of genotype I in 2006 caused an unusual outbreak with 765 cases reported. In addition to genotype I circulation, new genotype invasion by genotype III was the key determinant for the 2014 massive outbreak reaching the highest number of cases with 37340. Furthermore, base mutations appeared after genotype III invasion, and the gene sequence of NS3 protein had the lowest average similarity ratio, followed by the gene sequence of E protein, as compared to the 2013 strain.

epidemiology↗

bioRxiv2019

Functional analysis of KIT gene structural mutations causing porcine dominant white phenotype by using genome edited mouse models

Dominant white phenotype in pigs is considered to be caused by two structural mutations in KIT gene, including a 450-kb duplication encompassing the entire KIT gene, and a splice mutation (G > A) at the first base in intron 17, which leads to the deletion of exon 17 in mature KIT mRNA, and the production of KIT protein lacking a critical catalytic domain of kinase. However, this speculation has not yet been validated by functional studies. Here, by using CRISPR/Cas9 technology, we created two mouse models mimicing the structural mutations of KIT gene in dominant white pigs, including the splice mutation mouse model KIT D17/+ with exon 17 of one allele of KIT gene deleted, and duplication mutation mouse model KIT Dup/+ with one allele of KIT gene coding sequence (CDS) duplicated. We found that each mutation individually can not cause dominant white phenotype. Splice mutation homozygote is lethal and heterozygous mice present piebald coat. Inconsistent with previous speculation, we found KIT gene duplication mutation did not confer the patched phenotype, and had no obvious impact on coat color. Interestingly, combination of these two mutations lead to dominant white phenotype. Further molecular analysis revealed that combination of these two structural mutations could inhibit the kinase activity of the KIT protein, thus reduce the phosphorylation level of PI3K and MAPK pathway associated proteins, which may be related to the observed impaired migration of melanoblasts during embryonic development, and eventually lead to dominant white phenotype. Our study provides a further insight into the underlying genetic mechanisms of porcine dominant white coat colour.\n\nAuthor summaryKIT plays a critical role in control of coat colour in mammals. Two mutation coexistence in KIT are considered to be the cause of the Dominant white phenotype in pigs. One mutation is a 450-kb large duplication encompassing the entire KIT gene, another mutation is a splice mutation causing the skipping of KIT exon 17. The mechanism of these two mutations of KIT on coat color formation has not yet been validated. In this study, by using genome edited mouse models, we found each structural mutation individual does not lead dominant white phenotype, but combination of these two mutations could lead to a nearly complete white coat colour similar to pig dominant white phenotype, possibly due to the inhibition of the kinase activity of the KIT protein, thus its signalling function on PI3K and MAPK pathways, leading to impaired migration of melanoblasts during embryonic development, and eventually lead to dominant white phenotype. Our study provides a further insight into the underlying genetic mechanisms of porcine dominant white coat colour.

molecular biology↗

bioRxiv2019

Single-cell genomic atlas of great ape cerebral organoids uncovers human-specific features of brain development

The human brain has changed dramatically since humans diverged from our closest living relatives, chimpanzees and the other great apes1-5. However, the genetic and developmental programs underlying this divergence are not fully understood6-8. Here, we have analyzed stem cell-derived cerebral organoids using single-cell transcriptomics (scRNA-seq) and accessible chromatin profiling (scATAC-seq) to explore gene regulatory changes that are specific to humans. We first analyze cell composition and reconstruct differentiation trajectories over the entire course of human cerebral organoid development from pluripotency, through neuroectoderm and neuroepithelial stages, followed by divergence into neuronal fates within the dorsal and ventral forebrain, midbrain and hindbrain regions. We find that brain region composition varies in organoids from different iPSC lines, yet regional gene expression patterns are largely reproducible across individuals. We then analyze chimpanzee and macaque cerebral organoids and find that human neuronal development proceeds at a delayed pace relative to the other two primates. Through pseudotemporal alignment of differentiation paths, we identify human-specific gene expression resolved to distinct cell states along progenitor to neuron lineages in the cortex. We find that chromatin accessibility is dynamic during cortex development, and identify instances of accessibility divergence between human and chimpanzee that correlate with human-specific gene expression and genetic change. Finally, we map human-specific expression in adult prefrontal cortex using single-nucleus RNA-seq and find developmental differences that persist into adulthood, as well as cell state-specific changes that occur exclusively in the adult brain. Our data provide a temporal cell atlas of great ape forebrain development, and illuminate dynamic gene regulatory features that are unique to humans.

developmental biology↗

bioRxiv2019

Genomic islets in a sea of introgressions between sympatric species

In the conventional view, species are separate gene pools delineated by reproductive isolation (RI). However, species may also be delineated by merely a small set of "speciation genes" without full RI. It is thus important to know whether "good species" (defined by the "secondary sympatry" test) do continue to exchange genes. Here, we carry out sequencing and de novo high-quality assembly of the genomes of two closely related mangrove species (Rhizophora mucronata and R. stylosa). Whole-genome re-sequencing of individuals across their range on the tropical coasts shows their genomes to be well delineated in allopatry. They became sympatric in northeastern Australia but remain distinct species in contact. Nevertheless, their genomes harbor [~] 4,000 to 10,000 introgression blocks, each averaging only about 3-4 Kb. These fine-grained introgressions indicate that gene flow has continued long after speciation. Non-introgressable "genomic islets," averaging only 1.4 Kb, may contribute to speciation as they often harbor diverging genes underlying flower development and gamete production. In conclusion, RI needs not be the main criterion of species delineation even though all species would eventually be fully reproductively isolated.

evolutionary biology↗

bioRxiv2019

Single cell RNA sequencing reveals cellular diversity of trisomy 21 retina

Retina is a crucial tissue for the capturing and processing of light stimulus. Characterization of the retina at single cell level is essential for the understanding of its biological functions. A variety of abnormalities in terms of morphology and function were reported in T21 retina. To evaluate the effects of chromosome aneuploidy on retina development, we characterized single cell transcriptional profiles of a T21 fetus and performed comprehensive bioinformatic analyses. Our data revealed the diversity and heterogeneity of cellular compositions in T21 retina. In total, we identified seven major cell types, and detected several subtypes within each cell type, followed by the detection of corresponding molecular markers including previously reported ones and a series of novel markers. Our analyses identified extensive communication networks between distinct cellular types, among which a few ligand-receptor interactions were associated with the development of retina and immunoregulatory interactions. Taken together, our data provided the first single cell transcriptome profile for human T21 retina which facilitates our understanding on the dosage effects of chromosome 21 on the development of retina.

cell biology↗