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Biology subjects

Zhao, H.

Publications and source records attributed to Zhao, H..

At least 307 records · Page 17Linked to original sources
bioRxiv2023

Automated, self-resistance gene-guided, and high-throughput genome mining of bioactive natural products from Streptomyces

Natural products (NPs) produced by bacteria, fungi and plants are a major source of drug leads. Streptomyces species are particularly important in this regard as they produce numerous natural products with prominent bioactivities. Here we report a fully automated, scalable and high-throughput platform for discovery of bioactive natural products in Streptomyces (FAST-NPS). This platform comprises computational prediction and prioritization of target biosynthetic gene clusters (BGCs) guided by self-resistance genes, highly efficient and automated direct cloning and heterologous expression of BGCs, followed by high-throughput fermentation and product extraction from Streptomyces strains. As a proof of concept, we applied this platform to clone 105 BGCs ranging from 10 to 100 kb that contain potential self-resistance genes from 11 Streptomyces strains with a success rate of 95%. Heterologous expression of all successfully cloned BGCs in Streptomyces lividans TK24 led to the discovery of 23 natural products from 12 BGCs. We selected 5 of these 12 BGCs for further characterization and found each of them could produce at least one natural product with antibacterial and/or anti-tumor activity, which resulted in a total of 8 bioactive natural products. Overall, this work would greatly accelerate the discovery of bioactive natural products for biomedical and biotechnological applications. Graphic Abstracts O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=184 SRC="FIGDIR/small/564101v1_ufig1.gif" ALT="Figure 1"> View larger version (41K): org.highwire.dtl.DTLVardef@11068c9org.highwire.dtl.DTLVardef@4f68c5org.highwire.dtl.DTLVardef@16767edorg.highwire.dtl.DTLVardef@1d82eab_HPS_FORMAT_FIGEXP M_FIG C_FIG

synthetic biology↗
bioRxiv2023

ASCT2 is the primary serine transporter in cancer cells

The non-essential amino acid serine is a critical nutrient for cancer cells due to its diverse biosynthetic functions. While some tumors can synthesize serine de novo, others are auxotrophic for serine and therefore reliant on the uptake of exogenous serine. Importantly, however, the transporter(s) that mediate serine uptake in cancer cells are not known. Here, we characterize the amino acid transporter ASCT2 (coded for by the gene SLC1A5) as the primary serine transporter in cancer cells. ASCT2 is well-known as a glutamine transporter in cancer, and our work demonstrates that serine and glutamine compete for uptake through ASCT2. We further show that ASCT2-mediated serine uptake is essential for purine nucleotide biosynthesis and that ER promotes serine uptake by directly activating SLC1A5 transcription. Together, our work defines an additional important role for ASCT2 as a serine transporter in cancer and evaluates ASCT2 as a potential therapeutic target in serine metabolism.

cancer biology↗
bioRxiv2023

The role of YY2-mediated spindle assembly checkpoint activation on chromosomal instability and its consequences on colorectal cancer cell fate and tumor progression

Spindle assembly checkpoint (SAC) is a crucial safeguard mechanism of mitosis fidelity, which is fundamental for equal division of duplicated chromosomes to the two progeny cells. Impaired SAC can lead to chromosomal instability (CIN), a well-recognized hallmark of cancer that facilitates tumor progression; paradoxically, high CIN levels are associated with better drug sensitivity and prognosis. However, the mechanism by which CIN determines tumor cell fates and drug sensitivity remain poorly understood. In this study, using a cross-omics approach, we identified YY2 as a mitotic regulator that peaks at M phase and promotes SAC activity by positively regulating the transcriptional activity of budding uninhibited by benzimidazole 3 (BUB3), a component of SAC. While inducing CIN, YY2/SAC activity defect enhanced mitosis and tumor growth, whereas YY2/SAC hyperactivation, as a result of YY2 overexpression, triggered mitotic delay and growth suppression. Furthermore, we revealed that excessive CIN, caused by either YY2 overexpression or further inhibiting SAC activity in YY2-knocked out cells, leads to higher cell death rates. However, residual tumor cells that survived DNA damage-based therapy had moderate CIN and increased drug resistance; meanwhile YY2 overexpression in these cells sensitizes them to DNA-damage agents. Hence, this study provides insights into the regulatory mechanism of SAC activity as well as the role of YY2/BUB3 axis, SAC activity, and CIN levels in determining tumor cell fate. Furthermore, this study also links up tumor cells drug resistance with moderate CIN, and suggest a novel anti-tumor therapeutic strategy that combines SAC activity modulators and DNA-damage agents. SignificanceThis study identifies the novel role of YY2/BUB3 axis as a SAC modulator, as well as emphasizing the role of YY2-mediated SAC activity and CIN levels in determining tumor cell fates.

cancer biology↗
bioRxiv2023

Amur grape genome sequence

To date, there is no high-quality sequence for genomes of the East Asian grape species, hindering biological and breeding research efforts to improve grape cultivars. This study presents a [~]522 Mb of the Vitis amurensis (Va) genome sequence containing 27,635 coding genes. Phylogenetic analysis indicated that V. riparia (Vr) may firstly split from the other two species, Va, V. Vinifera (Vv; Pinot Noir: PN40024 and Cabernet Sauvignon). Much divergent gene reservation among three grape duplicated gene sets suggests that the core eudicot common hexaploidy (ECH), 130 million years ago (Mya), has still played a non-negligible role in grape species divergence and biological innovation. Prominent accumulation of sequence variants might have improved cold resistance in Va, resulting in a more robust cold resistance gene regulatory network than those in Vv and Vr. In contrast, Va preserved much fewer NBS disease resistance genes than the other grapes. Notably, multi-omics analysis identified one trans-cinnamate 4-monooxygenase gene positively correlated to the resveratrol accumulated during Va berry development. A selective sweep analysis revealed a hypothetical Va sex-determination region (SDR). Besides, a PPR-containing protein-coding gene in the hypothetical SDR may be related with sex determination in Va. The content and arrangement order of genes in the putative SDR of female Va were similar to the SDR of female Vv. However, the putative SDR of female Va lost one Flavin-containing monooxygenases (FMO) and contained one extra uncharacterized protein-coding gene. These findings will improve the understanding of Vitis biology and contribute to the improvement of grape breeding.

genomics↗
bioRxiv2023

Decoding transcriptomic signatures of Cysteine String Protein alpha-mediated synapse maintenance

Synapse maintenance is essential for generating functional circuitry and decrement in this process is a hallmark of neurodegenerative disease. While we are beginning to understand the basis of synapse formation, much less is known about synapse maintenance in vivo. Cysteine string protein (CSP), encoded by the Dnajc5 gene, is a synaptic vesicle chaperone that is necessary for synapse maintenance and linked to neurodegeneration. To investigate the transcriptional changes associated with synapse maintenance, we performed single nucleus transcriptomics on the cortex of young CSP knockout (KO) mice and littermate controls. Through differential expression and gene ontology analysis, we observed that both neurons and glial cells exhibit unique signatures in CSP KO brain. Significantly all neurons in CSP KO brains show strong signatures of repression in synaptic pathways, while upregulating autophagy related genes. Through visualization of synapses and autophagosomes by electron microscopy, we confirmed these alterations especially in inhibitory synapses. By imputing cell-cell interactions, we found that neuron-glia interactions were specifically increased in CSP KO mice. This was mediated by synaptogenic adhesion molecules, including the classical Neurexin1-Neuroligin 1 pair, suggesting that communication of glial cells with neurons is strengthened in CSP KO mice in an attempt to achieve synapse maintenance. Together, this study reveals unique cellular and molecular transcriptional changes in CSP KO cortex and provides new insights into synapse maintenance and neurodegeneration. Significance statementSynapse maintenance is important for maintaining neuronal circuitry throughout life. However, little is known about molecules that affect synapse maintenance in vivo. CSP, encoded by the Dnajc5 gene, is a synaptic vesicle chaperone that is linked to synapse maintenance and neurodegeneration. Here, we show by performing single nucleus transcriptomics of CSP KO cortex that synapse instability is related to repression in synaptic pathways and elevation of autophagy in neurons. However, we find a heterogeneity of glial responses. Additionally, interactions between neurons and glia are increased in CSP KO, mediated by synaptogenic adhesion molecules. This study provides a novel perspective on into synapse maintenance and reveals unique cellular and molecular transcriptional changes in CSP KO brains.

neuroscience↗
bioRxiv2023

KRAS inhibition activates an actionable CD24 do-not-eat-me signal in pancreas cancer

KRASG12C inhibitors (G12Ci) have produced encouraging, albeit modest and transient, clinical benefit in pancreatic ductal adenocarcinoma (PDAC). Identifying and targeting resistance mechanisms to G12Ci treatment is therefore crucial. To better understand the function of KRASG12C and possible G12Ci bypass mechanisms, we developed an autochthonous KRASG12C- driven PDAC model. Compared to the classical KRASG12D PDAC model, the G12C model exhibits slower tumor growth, yet similar histopathological and molecular features. Aligned with clinical experience, G12Ci treatment of KRASG12C tumors produced modest impact despite stimulating a hot tumor immune microenvironment. Immunoprofiling revealed that CD24, a dont eat me signal, is significantly upregulated on cancer cells upon G12Ci treatment. Blocking CD24 enhanced macrophage phagocytosis of cancer cells and significantly sensitized tumors to G12Ci treatment. Similar findings were observed in KRASG12D-driven PDAC. Together, this study reveals common and distinct oncogenic KRAS allele-specific biology and identifies a clinically actionable adaptive mechanism that may improve the efficacy of oncogenic KRAS inhibitor therapy in PDAC. SignificanceGeneration of an autochthonous KRASG12C-driven pancreatic cancer model enabled elucidation of specific effects of KRASG12C during tumor development, revealing CD24 as an actionable adaptive mechanism in cancer cells induced upon KRASG12C inhibition.

cancer biology↗
bioRxiv2023

CDK6-mediated endothelial cell cycle acceleration drives arteriovenous malformations in hereditary hemorrhagic telangiectasia

Increased endothelial cell (EC) proliferation is a hallmark of arteriovenous malformations (AVMs) in hereditary hemorrhagic telangiectasia (HHT). The underlying mechanism and disease relevance of this abnormal cell proliferative state of the ECs remain unknown. Here, we report the identification of a CDK6-driven mechanism of cell cycle progression deregulation directly involved in EC proliferation and HHT vascular pathology. Specifically, HHT mouse liver ECs exhibited defects in their cell cycle control characterized by a G1/S checkpoint bypass and acceleration of cell cycle speed. Phosphorylated retinoblastoma (p-RB1)--a marker of G1/S transition through the restriction point--significantly accumulated in ECs of HHT mouse retinal AVMs and HHT patient skin telangiectasias. Mechanistically, ALK1 loss of function increased the expression of key restriction point mediators, and treatment with palbociclib or ribociclib, two CDK4/6 inhibitors, blocked p-RB1 increase and retinal AVMs in HHT mice. Palbociclib also improved vascular pathology in the brain and slowed down endothelial cell cycle speed and EC proliferation. Specific deletion of Cdk6 in ECs was sufficient to protect HHT mice from AVM pathology. Thus, CDK6-mediated endothelial cell cycle acceleration controls EC proliferation in AVMs and is a central determinant of HHT pathogenesis. We propose that clinically approved CDK4/6 inhibitors have repurposing potential in HHT.

cell biology↗
bioRxiv2023

Evaluating the Utilities of Large Language Models in Single-cell Data Analysis

Foundation Models (FMs) have made significant strides in both industrial and scientific domains. In this paper, we evaluate the performance of FMs for single-cell sequencing data analysis through comprehensive experiments across eight downstream tasks pertinent to single-cell data. Overall, the top FMs include scGPT, Geneformer, and CellPLM by considering model performances and user accessibility among ten single-cell FMs. However, by comparing these FMs with task-specific methods, we found that single-cell FMs may not consistently excel than task-specific methods in all tasks, which challenges the necessity of developing foundation models for single-cell analysis. In addition, we evaluated the effects of hyper-parameters, initial settings, and stability for training single-cell FMs based on a proposed scEval framework, and provide guidelines for pre-training and fine-tuning, to enhance the performances of single-cell FMs. Our work summarizes the current state of single-cell FMs, points to their constraints and avenues for future development, and offers a freely available evaluation pipeline to benchmark new models and improve method development.

bioinformatics↗
bioRxiv2023

LUZP1 regulates the assembly of stress fibers by promoting maturation of contractile actomyosin bundles

Contractile actomyosin bundles play crucial roles in various physiological processes, including cell migration, morphogenesis, and muscle contraction. The intricate assembly of actomyosin bundles involves the precise alignment and fusion of myosin II filaments, yet the underlying mechanisms and factors involved in these processes remain elusive. Our study reveals that LUZP1, a leucine zipper protein, plays a central role in orchestrating the formation of thick actomyosin bundles. Loss of LUZP1 caused abnormal cell morphogenesis, migration, and the ability to exert forces on the environment. Importantly, knockout of LUZP1 results in significant defects in the concatenation and persistent association of myosin II filaments, severely impairing the assembly of myosin II stacks. The disruption of these processes in LUZP1 knockout cells provides mechanistic insights into the defective assembly of thick ventral stress fibers and the associated cellular contractility abnormalities. Overall, these results significantly contribute to our understanding of the molecular mechanism involved in actomyosin bundle formation and highlight the essential role of LUZP1 in this process.

cell biology↗
bioRxiv2023

CRISPR-COPIES: An in silico platform for discovery of neutral integration sites for CRISPR/Cas-facilitated gene integration

The CRISPR/Cas system has emerged as a powerful tool for genome editing in metabolic engineering and human gene therapy. However, locating the optimal site on the chromosome to integrate heterologous genes using the CRISPR/Cas system remains an open question. Selecting a suitable site for gene integration involves considering multiple complex criteria, including factors related to CRISPR/Cas-mediated integration, genetic stability, and gene expression. Consequently, identifying such sites on specific or different chromosomal locations typically requires extensive characterization efforts. To address these challenges, we have developed CRISPR-COPIES, a COmputational Pipeline for the Identification of CRISPR/Cas-facilitated intEgration Sites. This tool leverages ScaNN, a state-of-the-art model on the embedding-based nearest neighbor search for fast and accurate off-target search and can identify genome-wide intergenic sites for most bacterial and fungal genomes within minutes. As a proof of concept, we utilized CRISPR-COPIES to characterize neutral integration sites in three diverse species: Saccharomyces cerevisiae, Cupriavidus necator, and a human cell line. In addition, we developed a user-friendly web interface for CRISPR-COPIES (https://biofoundry.web.illinois.edu/copies/). We anticipate that CRISPR-COPIES will serve as a valuable tool for targeted DNA integration and aid in the characterization of synthetic biology toolkits, enable rapid strain construction to produce valuable biochemicals and support human gene and cell therapy applications. Graphical abstractOverview and application of CRISPR-COPIES in the field of biotechnology. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=93 SRC="FIGDIR/small/556564v1_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@c723a1org.highwire.dtl.DTLVardef@1f42594org.highwire.dtl.DTLVardef@1cf4bd6org.highwire.dtl.DTLVardef@7c1028_HPS_FORMAT_FIGEXP M_FIG C_FIG

synthetic biology↗
bioRxiv2023

Metagenomic analysis of individual mosquitos reveals the ecology of insect viruses

Mosquito transmitted viruses are responsible for an increasing burden of human disease. Despite this, little is known about the diversity and ecology of viruses within individual mosquito hosts. Using a meta-transcriptomic approach, we analysed the virome of 2,438 individual mosquitos (79 species), spanning [~]4000 km along latitudes and longitudes in China. From these data we identified 393 core viral species associated with mosquitos, including seven (putative) arbovirus species. We identified potential species and geographic hotspots of viral richness and arbovirus occurrence, and demonstrated that host phylogeny had a strong impact on the composition of individual mosquito viromes. Our data revealed a large number of viruses shared among mosquito species or genera, expanding our knowledge of host specificity of insect-associated viruses. We also detected multiple virus species that were widespread throughout the country, possibly facilitated by long-distance mosquito migrations. Together, our results greatly expand the known mosquito virome, linked the viral diversity at the scale of individual insects to that at a country-wide scale, and offered unique insights into the ecology of viruses of insect vectors.

ecology↗
bioRxiv2023

LncRNA SNHG16 modulates paclitaxel resistance in breast cancer by regulating Let-7a-5p/DUSP7

ObjectiveTo investigate the effect of long chain non coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG16) on paclitaxel (PTX) resistance in breast cancer and to understand its underlying mechanism, to lay a foundation for decreasing the PTX resistance in breast cancer treatment and improving the therapeutic quality for breast cancer patients. MethodsPTX was used to induce the establishment of PTX resistant breast cancer cell lines; the control group (normal cultured MCF-7/PTX cells), si-NC group, si-SNHG16 group, si-SNHG16+anti miR-NC group, and si-SNHG16 +anti-Let-7a-5p group were set to compared the effect of SNHG16 on the PTX resistance in MCF-7 cells; MTT assay, Flow cytometry, and Transwell invasion assay were used to determine the PTX resistance, apoptosis, and invasion ability of MCF-7 cells in different groups, respectively; for further assess the effect of SNHG16 on the PTX resistance, nude mouse tumor transplantation experiment was used; and the potential mechanism of SNHG16 regulated the PTX resistance in MCF-7 cells was explored by double luciferase reporter gene detection method and gene silencing technology. ResultsThe expression of SNHG16 gene and DUSP7 protein in MCF-7 cell line was the highest, and the expression of Let-7a-5p was the lowest compared with the various breast cancer cell lines (human breast epithelial cell line MCF-10A and human breast cancer cell lines MDA-MB-468 and MDA-MB-453) (P<0.05); PTX could increase the expression of SNHG16 gene and DUSP7 protein, and reduce the expression of Let-7a-5pin MCF-7 cell line (P<0.05); the results of cell experiment and nude mouse transplantation tumor experiment demonstrated that inhibiting the expression of SNHG16 gene could reduce the invasive ability and promote cell apoptosis of MCF-7/PTX cells (P<0.05), and inhibit tumor growth and reduce the PTX resistance in breast cancer transplantation models; simultaneous inhibition of Let-7a-5p and SNHG16 had a weakening effect in MCF-7/PTX cells (P<0.05). Double luciferase reporter gene detection and gene silencing technology demonstrated that inhibiting SNHG16 gene expression could increase the expression of Let-7a-5p and decrease the expression of DUSP7 (P<0.05); inhibiting the Let-7a-5p gene could increase the expression of DUSP7. ConclusionsInhibiting SNHG16 gene could upregulate Let-7a-5p expression and downregulate the expression of DUSP7 to inhibit MCF-7 cell invasion, promote MCF-7 cell apoptosis, and reduce the PTX resistance in MCF-7 cells and nude mouse tumor transplantation models, those data demonstrated that SNHG16-Let-7a-5p-DUSP7 axis maybe a potential therapeutic strategy for decreasing the PTX resistance in breast cancer in the future.

cancer biology↗
bioRxiv2023

Herpes zoster mRNA vaccine induces superior vaccine immunity over licensed vaccine in mice and rhesus macaques

Herpes zoster remains an important global health issue and mainly occurs in aged and immunocompromised individuals with an early exposure history to Varicella Zoster Virus (VZV). Although the licensed vaccine Shingrix has a remarkably high efficacy, undesired reactogenicity and increasing global demand causing vaccine shortage urged the development of improved or novel VZV vaccines. In this study, we developed a novel VZV mRNA vaccine candidate (named as ZOSAL) containing sequence-optimized mRNAs encoding full-length glycoprotein E encapsulated in an ionizable lipid nanoparticle. In mice and rhesus macaques, ZOSAL demonstrated superior immunogenicity and safety in multiple aspects over Shingrix, especially in the induction of strong T cell immunity. Transcriptomic analysis revealed that both ZOSAL and Shingrix could robustly activate innate immune compartments, especially Type-I IFN signaling and antigen processing/presentation. Multivariate correlation analysis further identified several early factors of innate compartments that can predict the magnitude of T cell responses, which further increased our understanding of the mode of action of two different VZV vaccine modalities. Collectively, our data demonstrated the superiority of VZV mRNA vaccine over licensed subunit vaccine. The mRNA platform therefore holds prospects for further investigations in next-generation VZV vaccine development.

immunology↗
bioRxiv2023

Diversity of Short Linear Interaction Motifs in SARS-CoV-2 Nucleocapsid Protein

Molecular mimicry of short linear interaction motifs has emerged as a key mechanism for viral proteins binding host domains and hijacking host cell processes. Here, we examine the role of RNA-virus sequence diversity in the dynamics of the virus-host interface, by analyzing the uniquely vast sequence record of viable SARS-CoV-2 species with focus on the multi-functional nucleocapsid protein. We observe the abundant presentation of motifs encoding several essential host protein interactions, alongside a majority of possibly non-functional and randomly occurring motif sequences absent in subsets of viable virus species. A large number of motifs emerge ex nihilo through transient mutations relative to the ancestral consensus sequence. The observed mutational landscape implies an accessible motif space that spans at least 25% of known eukaryotic motifs. This reveals motif mimicry as a highly dynamic process with the capacity to broadly explore host motifs, allowing the virus to rapidly evolve the virus-host interface.

biophysics↗
bioRxiv2023

Melatonin alleviates valproic acid-induced neural tube defects by modulating Src/PI3K/ERK signaling and oxidative stress

Neural tube defects (NTDs) represent a developmental disorder of the nervous system that can lead to significant disability in children and impose substantial social burdens. Valproic acid (VPA), a widely prescribed first-line antiepileptic drug for epilepsy and various neurological conditions, has been associated with a fourfold increase in the risk of NTDs when used during pregnancy. Consequently, urgent efforts are required to identify innovative prevention and treatment approaches for VPA-induced NTDs. Studies have demonstrated that the disruption in the delicate balance between cell proliferation and apoptosis is a crucial factor contributing to NTDs induced by VPA. Encouragingly, our current data reveal that melatonin (MT) exerts significant inhibition on apoptosis while promoting the restoration of neuroepithelial cells proliferation impaired by VPA. Moreover, further investigations demonstrate that MT substantially reduces the incidence of neural tube malformations resulting from VPA exposure, primarily achieved by suppressing apoptosis through the modulation of intracellular reactive oxygen species levels. In addition, the Src/PI3K/ERK signaling pathway appears to play a pivotal role in VPA-induced NTDs, with a significant inhibition observed in the affected samples. Notably, MT treatment successfully reinstates the Src/PI3K/ERK signals, thereby offering a potential underlying mechanism for MTs protective effects against VPA-induced NTDs. In summary, our current study substantiates the considerable protective potential of MT in mitigating VPA-triggered NTDs, thereby offering valuable strategies for the clinical management of VPA-related birth defects.

developmental biology↗
bioRxiv2023

Epigenomic Analyses Identify FOXM1 As a Key Regulator of Anti-Tumor Immune Response in Esophageal Adenocarcinoma

Unlike most cancer types, the incidence of esophageal adenocarcinoma (EAC) has rapidly escalated in the western world over recent decades. Using whole genome bisulfite sequencing (WGBS), we identify the transcription factor (TF) FOXM1 as an important epigenetic regulator of EAC. FOXM1 plays a critical role in cellular proliferation and tumor growth in EAC patient-derived organoids and cell line models. We identify ERBB2 as an upstream regulator of the expression and transcriptional activity of FOXM1. Unexpectedly, Gene Set Enrichment Analysis (GSEA) unbiased screen reveals a prominent anti-correlation between FOXM1 and immune response pathways. Indeed, syngeneic mouse models show that FOXM1 inhibits the infiltration of CD8+ T cells into the tumor microenvironment. Consistently, FOXM1 suppresses CD8+ T cell chemotaxis in vitro and antigen-dependent CD8+ T cell killing. This study characterizes FOXM1 as a significant EAC-promoting TF and elucidates its novel function in regulating anti-tumor immune response.

cancer biology↗
bioRxiv2023

Human receptive endometrial organoid for deciphering the implantation window

Human endometrial receptivity is a critical determinant of pregnancy success; however, in vivo studies of its features and regulation are particularly challenging due to ethical restriction. Recently, the development of human endometrial assembloids has provided a powerful model to investigate this intricate biological process. In this study, we established a specialized human window-of-implantation (WOI) endometrial assembloid system that mimics the in vivo receptive endometrium. It not only reproduces the structural attributes of pinopodes and cilia, but also molecular characteristics of mid-secretory endometrium. Furthermore, the WOI endometrial assembloid exhibits hormone responsiveness, an energy metabolism profile characterized by larger and functionally enhanced mitochondria, increased ciliary assembly and motility, and epithelial-mesenchymal transition (EMT), as well as promising potential for embryo implantation. As such, WOI assembloids hold great promise as a platform to unravel the intricate mechanisms governing the regulation of endometrial receptivity, maternal-fetal interactions, and associated pathologies, ultimately driving impactful advancements in the field.

cell biology↗