Biology subjects

Jia, S.

Publications and source records attributed to Jia, S..

At least 55 records · Page 3Linked to original sources

bioRxiv2024

Megabase-scale loss of heterozygosity provoked by CRISPR-Cas9 DNA double-strand breaks

Harnessing DNA double-strand breaks (DSBs) is a powerful approach for gene editing, but it may provoke loss of heterozygosity (LOH), which predisposes to tumorigenesis. To interrogate this risk, we developed a two- color flow cytometry-based system (Flo-LOH), detecting LOH in [~]5% of cells following a DSB. After this initial increase, cells with LOH decrease due to a competitive disadvantage with parental cells, but if isolated, they stably propagate. Segmental loss from terminal deletions with de novo telomere addition and nonreciprocal translocations is observed as well as whole chromosome loss, especially following a centromeric DSB. LOH spans megabases distal from the DSB, but also frequently tens of megabases centromere-proximal. Inhibition of microhomology-mediated end joining massively increases LOH, which is synergistically increased with concomitant inhibition of canonical nonhomologous end joining. The capacity for large-scale LOH must therefore be considered when using DSB-based gene editing, especially in conjunction with end joining inhibition.

molecular biology↗

bioRxiv2024

Decoding dynamic visual scenes across the brain hierarchy

Understanding the computational mechanisms that underlie the encoding and decoding of environmental stimuli is a paramount investigation within the domain of neuroscience. Central to this pursuit is the exploration of how the brain represents visual information across its hierarchical architecture. A prominent challenge resides in discerning the neural underpinnings of the processing of dynamic natural visual scenes. Although considerable research efforts have been made to characterize individual components of the visual pathway, a systematic understanding of the distinctive neural coding associated with visual stimuli, as they traverse this hierarchical landscape, remains elusive. In this study, we leverage the comprehensive Allen Visual Coding dataset and utilize the capabilities of deep learning neural network models to study the question of neural coding in response to dynamic natural visual scenes across an expansive array of brain regions. We find that our decoding model adeptly deciphers visual scenes from neural spiking patterns exhibited within each distinct brain area. A compelling observation arises from the comparative analysis of decoding performances, which manifests as a notable encoding proficiency within both the visual cortex and subcortical nuclei, in contrast to a relatively diminished encoding activity within hippocampal neurons. Strikingly, our results reveal a robust correlation between our decoding metrics and well-established anatomical and functional hierarchy indexes. These findings not only corroborate existing knowledge in visual coding using artificial visual stimuli but illuminate the functional role of these deeper brain regions using dynamic natural scenes. Consequently, our results proffer a novel perspective on the utility of decoding neural network models as a metric for quantifying the encoding of dynamic natural visual scenes, thereby advancing our comprehension of visual coding within the complex hierarchy of the brain.

neuroscience↗

bioRxiv2024

Spatiotemporally resolved transcriptome atlas of developing mouse placenta reveals mechanisms of embryonic lethality.

Proper placentation is fundamental to the growth and viability of the maturing embryo. However, a thorough grasp of the spatial organization of cell types, their interactions, and gene expression patterns along the maternal-fetal function during placental development remains incomplete. Here, we utilized Stereo-seq to construct the spatiotemporal transcriptomic atlas of the mouse placenta (STAMP) spanning embryonic (E) days 9.5 to 18.5 at single cell resolution (https://db.cngb.org/stomics/stamp/). This resource delineates spatially resolved cellular dynamics and gene expression patterns across placental and maternal compartments. We identified distinct glycogen trophoblast cell (GC) subclusters, mapped their developmental trajectories, and uncovered transcriptional transitions accompanying their migration from the junctional zone to the maternal decidua from E12.5 onward. In a defective placentation model with perinatal lethality, GCs abnormally persisted at E18.5 with excessive glycogen and reduced degradation metabolites in placenta and fetal liver, indicating impaired glycogen breakdown. Maternal glucose supplementation restored glucose levels and rescued fetal survival, underscoring GC-mediated metabolic support as critical for viability. Together, this study provides a comprehensive spatiotemporal placental atlas and demonstrates that GC-mediated glycogen metabolism is essential for sustaining fetal viability.

developmental biology↗

bioRxiv2024

A high-continuity and annotated reference genome of allotetraploid Siberian wildrye (Elymus sibiricus L., Poaceae: Triticeae)

Elymus sibiricus L. (Siberian wildrye, Es), a species belonging to the wheat tribe, is extensively employed as forage and for the reclamation of degraded grasslands within the Qinghai-Tibet Plateau (QTP). This study provides a high-quality reference genome assembly for the allotetraploid Es, which is composed of 14 pseudomolecules with the total genome size of 6.57 Gb. Our finding suggest that large-scale bursts of retrotransposons are critical for the genome expansion of Es. We discovered a translocation event between the Es4H and Es6H chromosomes with a low frequency of combination. Phylogenetic analyses of 90 Es accessions and 25 diploid accessions representing proposed ancestors from various habitats revealed the existence of four distinct populations. We further provided support for the hypothesis that the QTP is the center of origin and genetic diversity for Es. Collectively, our study offers valuable insights into the evolution of Es, as well as providing genomic resources for genetic enhancement in the Elymus genus and wheat tribe.

genomics↗

bioRxiv2024

Gray Matters: An Efficient Vision Transformer GAN Framework for Predicting Functional Network Connectivity Biomarkers from Brain Structure

The field of brain connectivity research has under-gone revolutionary changes thanks to state-of-the-art advancements in neuroimaging, particularly regarding structural and functional magnetic resonance imaging (MRI). To navigate the intricate neural dynamics, one must possess a keen comprehension of the interdependent links between structure and function. Such relationships are understudied as they are complex and likely nonlinear. To address this, we created a new generative deep learning architecture using a conditional efficient vision transformer generative adversarial network (cEViTGAN) to capture the distinct information in structural and functional MRI of the human brain. Our model generates functional network connectivity (FNC) matrices directly from three-dimensional sMRI data. Two pioneering innovations are central to our approach. First, we use a novel linear embedding method for structural MRI (sMRI) data that retains the 3D spatial detail. This embedding is best for representative learning, and when used on a consistent dataset, and shows that it is good at upstream classification assignments. To estimate neural biomarkers, we need to process much smaller patches using ViT-based architectures, which usually makes the computations more difficult because of the self-attention operations. We present a new, lightweight self-attention mechanism to address this challenge. Our mechanism not only overcomes computational shortcomings of traditional softmax self-attention but also surpasses pure linear self-attention models in accuracy and performance. This optimization enables us to analyze even the tiniest neuroanatomical details with exceptional precision. Our model allows for the identification of functional network connectivity (FNC) with 74.2% accuracy and also predicts subject differences in FNC for schizophrenia patients versus controls. The results are intriguing and suggest the links between gray matter volume and brain function may be stronger than previously considered.

neuroscience↗

bioRxiv2023

DNA nicks in both leading and lagging strand templates can trigger break-induced replication

Encounters between replication forks and unrepaired single-strand DNA breaks (SSBs) generate single-ended double-strand breaks (seDSBs) that can later become double-ended (deDSBs) through fork convergence. seDSBs can be repaired by break-induced replication (BIR), which is a highly mutagenic pathway that is thought to be repsonsible for many of the mutations and genome rearrangements that drive cancer development. However, the frequency of BIRs deployment and its ability to be triggered by both leading and lagging template strand SSBs was unclear. Using site- and strand-specific SSBs generated by nicking enzymes, including CRISPR-Cas9n, we demonstrate that leading and lagging template strand SSBs in fission yeast are typically converted into deDSBs that are repaired primarily by error-free homologous recombination. However, both types of SSB can also trigger BIR, and the frequency of these events increases when the converging fork is delayed and the non-homologous end joining protein Ku70 is deleted.

molecular biology↗

bioRxiv2023

Single-cell transcriptomic profiling of the neonatal oviduct and uterus reveals new insights into upper M&uumlllerian duct regionalization

The upper Mullerian duct (MD) is patterned and specified into two morphologically and functionally distinct organs, the oviduct and uterus. It is known that this regionalization process is instructed by inductive signals from the adjacent mesenchyme. However, the interaction landscape between epithelium and mesenchyme during upper MD development remains largely unknown. Here, we performed single-cell transcriptomic profiling of mouse neonatal oviducts and uteri at the initiation of MD epithelial differentiation (postnatal day 3). We identified major cell types including epithelium, mesenchyme, pericytes, mesothelium, endothelium, and immune cells in both organs with established markers. Moreover, we uncovered region-specific epithelial and mesenchymal subpopulations and then deduced region-specific ligand-receptor pairs mediating mesenchymal-epithelial interactions along the craniocaudal axis. Unexpectedly, we discovered a mesenchymal subpopulation marked by neurofilaments with specific localizations at the mesometrial pole of both the neonatal oviduct and uterus. Lastly, we analyzed and revealed organ-specific signature genes of pericytes and mesothelial cells. Taken together, our study enriches our knowledge of upper Mullerian duct development, and provides a manageable list of potential genes, pathways, and region-specific cell subtypes for future functional studies.

developmental biology↗

bioRxiv2023

Systematic comparison of sequencing-based spatial transcriptomic methods

Recent advancements of sequencing-based spatial transcriptomics (sST) have catalyzed significant advancements by facilitating transcriptome-scale spatial gene expression measurement. Despite this progress, efforts to comprehensively benchmark different platforms are currently lacking. The extant variability across technologies and datasets poses challenges in formulating standardized evaluation metrics. In this study, we established a collection of reference tissues and regions characterized by well-defined histological architectures, and used them to generate data to compare six sST methods. We highlighted molecular diffusion as a variable parameter across different methods and tissues, significantly impacting the effective resolutions. Furthermore, we observed that spatial transcriptomic data demonstrate unique attributes beyond merely adding a spatial axis to single-cell data, including an enhanced ability to capture patterned rare cell states along with specific markers, albeit being influenced by multiple factors including sequencing depth and resolution. Our study assists biologists in sST platform selection, and helps foster a consensus on evaluation standards and establish a framework for future benchmarking efforts that can be used as a gold standard for the development and benchmarking of computational tools for spatial transcriptomic analysis.

genomics↗

bioRxiv2023

PPARγ controls ESCRT-dependent fibroblast-like synoviocyte exosome biogenesis and Alleviates Chondrocyte Osteoarthritis Mediated by Exosomal ANXA1

Osteoarthritis (OA) is characterized by synovitis, cartilage degeneration and exercise therapy has been recognized as first line therapy. The exercise related exosome involved in the interaction between fibroblast-like synoviocytes (FLSs) and chondrocytes could be a novel promising strategy for treating OA. In this study, PPAR{gamma} was upregulated in FLSs under exercise by single cell transcriptome sequencing. Then, we investigated the underlying mechanisms of PPAR{gamma}-treated FLSs derived exosome on OA in vivo and vitro. Our data revealed that overexpression PPAR{gamma} FLSs derived exosome could ameliorate the OA severity in vivo and vitro. But knockdown PPAR{gamma} FLSs derived exosome aggravate OA. Moreover, we found PPAR{gamma} controls the endosomal sorting complex required for the transport (ESCRT)-dependent exosome biogenesis pathway. Annexin A1 (ANXA1) was enriched in OE-PPAR{gamma} exosome by quantitative proteomics. By Chip-qPCR and Co-IP methods, PPAR{gamma} and its coactivator -1 (PGC-1) acts with ESCRT subunits including HRS, STAM1, TSG101, CHMP7 and promotes their association to cargo ANXA1. As a therapeutic cargo, exosomal ANXA1 was confirmed be internalization by chondrocyte via exosome labeled experiment and ANXA1 could inhibit the phospharylation of ERK to activate the autophagy and decrease chondrocyte apoptosis. While the ANXA1 receptor blocker BOC-2 could reverse the therapic effect. In conclusion, PPAR{gamma}/ESCRT - FLSs exosomal ANXA1 - ERK axis provides a deeper theoretical basis for exercise therapy of OA and a new idea for the clinical transformation of exosomes into OA therapy.

cell biology↗

bioRxiv2023

A resource for probing influences of perinatal factors on neurodevelopment in 3-10-years-old Chinese children

Adverse perinatal factors can disrupt the normal development of the brain, with potential long-term impacts on childrens overall development. Currently, the neuropathological mechanisms by which these factors lead to various neurodevelopmental disorders (NDDs) remain largely unknown. An open resource that integrate perinatal factors with brain and mental health development is essential for investigating NDD-related aetiology. In this Data Descriptor, we introduce a multicentre database containing information on perinatal factors that influence childrens brain-mind development, namely, periCBD, that combines neuroimaging and behavioural phenotypes with perinatal factors associated with a high incidence of NDDs at county/region/central district hospitals. PeriCBD was designed to establish a platform for the investigation of individual differences in brain-mind development among children aged 3-10 years are associated with perinatal factors. Ultimately, our goal was to develop an early prediction and screening model for NDDs that leverages normative data to facilitate NDD aetiology research. Herein, we provide a systematic overview of the data acquisition/cleaning/quality control/sharing, processes of periCBD and present preliminary brain-mind associations.

neuroscience↗

bioRxiv2023

Shape-changing electrode array for minimally invasive large-scale intracranial brain activity mapping

Large-scale brain activity mapping is important for understanding the neural basis of behaviour. Electrocorticograms (ECoGs) have high spatiotemporal resolution, bandwidth, and signal quality. However, the invasiveness and surgical risks of electrode array implantation limit its application scope. We developed an ultrathin, flexible shape-changing electrode array (SCEA) for large-scale ECoG mapping with minimal invasiveness. SCEAs were inserted into cortical surfaces in compressed states through small openings in the skull or dura and fully expanded to cover large cortical areas. MRI and histological studies on rats proved the minimal invasiveness of the implantation process and the high chronic biocompatibility of the SCEAs. High-quality micro-ECoG activities mapped with SCEAs from rodent brains during seizures and canine brains during the emergence period revealed the spatiotemporal organization of different brain states with resolution and bandwidth that cannot be achieved using existing noninvasive techniques. The biocompatibility and ability to map large-scale physiological and pathological cortical activities with high spatiotemporal resolution, bandwidth, and signal quality in a minimally invasive manner offer SCEAs as a superior tool for applications ranging from fundamental brain research to brain-machine interfaces.

neuroscience↗

bioRxiv2023

Genetically Encodable in situ Gelation Redox-Responsive Collagen-Like Protein Hydrogel for Accelerating Diabetic Wound Healing

Genetically encoded collagen-like protein-based hydrogels have demonstrated remarkable efficacy in promoting the healing process in diabetic patients. However, the current methods for preparing these hydrogels pose significant challenges due to harsh reaction conditions and the reliance on chemical crosslinkers. In this study, we present a genetically encoded approach that allows for the creation of protein hydrogels without the need for chemical additives. Our design involves the genetic encoding of paired-cysteine residues at the C- and N-terminals of a meticulously engineered collagen-like recombination protein. The protein-based hydrogel undergoes a gel-sol transition in response to redox stimulation, achieving a sol-gel transition. We provide evidence that the co-incubation of the protein hydrogel with 3T3 cells not only enhances cell viability but also promotes cell migration. Moreover, the application of the protein hydrogel significantly accelerates the healing of diabetic wounds by upregulating the expression of COL-1 and CK-14, while simultaneously reducing oxidant stress in the wound microenvironment. Our study highlights a straightforward and chemical-free strategy for the preparation of redox-responsive protein hydrogels. Importantly, our findings underscore the potential of this hydrogel system for effectively treating diabetic wounds, offering a promising avenue for future therapeutic applications.

bioengineering↗

bioRxiv2023

N6-methyladenosine demethylase FTO serves as an indicator for predicting prognosis and immunotherapy response in individuals with gastric cancer

BackgroundN6-methyladenosine (m6A) RNA methylation is the most common chemical decoration in mammalian RNAs which exerts vital effects on numerous cellular processes. Recently, m6A regulators have been validated to participate in promoting immune evasion and act as prognostic factors in various cancers. Nevertheless, the predictive abilities of m6A regulators for the prognosis and immunotherapy response in gastric cancer (GC) remain indistinct. MethodsHerein, The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) database, The Human Protein Atlas (HPA), and a clinical GC cohort were applied for differential expression analysis, correlation analysis, survival analysis, and hazard model construction. Consensus clustering analysis was performed to authenticate the PD-L1 (CD274) expression, stemness features, immune cell infiltration, and tumor microenvironment (TME) in GC individuals. Furthermore, protein-protein interaction, immunotherapy response prediction, and drug susceptibility prediction were performed, respectively. Additionally, tissue microarray (TMA), immunohistochemical staining, western blot assay, Transwell assay, and flow cytometry assay were adopted to evaluate the protein expression, the prognostic value, and the influence of FTO on GC malignant phenotypes as well as the expression of PD-L1. ResultsIn agreement with the majority of m6A regulators, FTO was overexpressed and predicted poor prognosis in GC. Based on consensus clustering analysis, two independent subgroups (G1/G2) were identified. Notably, FTO was upregulated in the G1 subgroup. Meanwhile, the infiltration level of CD8+ T cells was strikingly decreased while the stemness features were enhanced in the G1 subgroup. More importantly, FTO was negatively correlated with microsatellite instability (MSI) and tumor mutation burden (TMB). Furthermore, immune checkpoint blockade (ICB) response prediction indicated that patients with upregulated FTO showed high tumor immune dysfunction and exclusion (TIDE) scores. Subsequently, FTO was confirmed to be related to multiple immune checkpoints, particularly PD-L1. Specifically, FTO was dramatically upregulated in GC cell lines and clinical cancer samples. Functional experiments illustrated that FTO acted as an oncogene to facilitate malignant phenotypes. Notably, PD-L1 was remarkably downregulated after RNA interference-mediated knockdown of FTO. ConclusionFTO can aggravate GC malignant phenotypes. More importantly, it could be utilized to predict the long-term prognosis and the immunotherapy response in GC individuals. However, larger trials should be performed to verify the prediction accuracy.

cancer biology↗

bioRxiv2023

Neural Extracellular Matrix Remodeling Signatures in Genetic and Acquired Mouse Models of Epilepsy

Epilepsies are multifaceted neurological disorders characterized by abnormal brain activity, e.g., caused by imbalanced synaptic excitation and inhibition. The neural extracellular matrix (ECM) is dynamically modulated by physiological and pathophysiological activity and critically involved in controlling the brains excitability. We used different epilepsy models, i.e. mice lacking the presynaptic scaffolding protein Bassoon at excitatory, inhibitory or all synapse types as genetic models for rapidly generalizing early-onset epilepsy, and intra-hippocampal kainate injection, a model for acquired temporal lobe epilepsy, to study the relationship between epileptic seizures and ECM composition. Electroencephalogram recordings revealed Bassoon deletion at excitatory or inhibitory synapses having diverse effects on epilepsy-related phenotypes. While constitutive Bsn mutants and GABAergic neuron-specific knockouts (BsnDlx5/6cKO) displayed severe epilepsy with more and stronger seizures than kainate-injected animals, mutants lacking Bassoon solely in excitatory forebrain neurons (BsnEmx1cKO) showed only mild impairments. By semiquantitative immunoblotting and immunohistochemistry we show model-specific patterns of neural ECM remodeling, and we also demonstrate significant upregulation of the ECM receptor CD44 in null and BsnDlx5/6cKO mutants. ECM-associated WFA-binding chondroitin sulfates were strongly augmented in seizure models. Strikingly, Brevican, Neurocan, Aggrecan and link protein Hapln1 levels reliably predicted seizure properties across models, suggesting a link between ECM state and epileptic phenotype.

neuroscience↗

bioRxiv2023

Insm1 regulates the development of mTECs and immune tolerance

The Insm1 gene encodes a zinc finger protein with known functions in neuroendocrine cells and neurons. Here we characterized the expression and function of Insm1 in medullary thymic epithelial cells (mTECs). Insm1 is co-expressed with Aire in majority of Insm1 or Aire positive cells, while a few Insm1 positive cells did not express Aire. Mutation of Insm1 impair the expression of Aire and the generation of normal numbers of Aire-expressing mTECs during development. We detected downregulation of genes that expressed specifically in Aire-expressing mTEC and mimetic cells in Insm1 mutant mTECs. Conversely, when Insm1 was overexpressed in thymic epithelial cells in vivo, the size of the mTECs compartment was enlarged and the expression of Aire and genes expressed specifically in the neuroendocrine mimetic cells were increased. Mechanistically, Insm1 bound DNA in mTECs and the majority of the Insm1 binding sites were co-occupied by Aire. These Insm1 binding sites were enriched on super-enhancer regions and thus may contributed to remoted regulation. Both, mice with a thymus-specific mutation in Insm1 or nude mice transplanted with Insm1 mutant thymus, displayed autoimmune responses in multiple peripheral tissues. Together, our data demonstrate a role of Insm1 in development of mTECs and immune tolerance.

immunology↗

bioRxiv2022

The dark kinase STK32A regulates hair cell planar polarity opposite of EMX2 in the developing mouse inner ear

The vestibular maculae of the inner ear contain sensory receptor hair cells that detect linear acceleration, contribute to equilibrioception, and thereby coordinate posture and ambulatory movements. These hair cells are divided between two groups, separated by a line of polarity reversal (LPR), with oppositely oriented planar-polarized stereociliary bundles that detect motion in opposite directions. The transcription factor EMX2 is known to establish this planar polarized organization by regulating the distribution of the transmembrane receptor GPR156 at the hair cell surface in one group of cells, however those genes regulated by EMX2 in this context were previously not known. We have identified the serine threonine kinase STK32A as a downstream effector negatively regulated by EMX2. Stk32a is expressed in hair cells on one side of the LPR in a pattern complementary to Emx2 due to transcriptional repression. Stk32a is necessary to align the intrinsic polarity of the bundle with the core planar cell polarity (PCP) proteins in EMX2-negative regions, and is sufficient to reorient bundles when ectopically expressed in neighboring EMX2-positive regions. We demonstrate that STK32a reinforces LPR formation by regulating the apical localization of GPR156. These observations support a model in which bundle orientation is determined through separate mechanisms in hair cells on opposite sides of the LPR, with EMX2-mediated repression of Stk32a determining the position of the LPR. HighlightsO_LISTK32A is a planar polarity effector that is negatively regulated by the transcription factor EMX2 C_LIO_LIStk32a is necessary and sufficient to determine vestibular hair cell stereociliary bundle orientation C_LIO_LISTK32A contributes to the post-translational regulation of GPR156, preventing GPR156 localization in the absence of EMX2 C_LI

developmental biology↗

bioRxiv2022

Aberrant DNA repair is a vulnerability in histone H3.3-mutant brain tumors

Pediatric high-grade gliomas (pHGG) are devastating and incurable brain tumors with recurrent mutations in histone H3.3. These mutations promote oncogenesis by dysregulating gene expression through alterations of histone modifications. We identify aberrant DNA repair as an independent oncogenic mechanism, which fosters genome instability and tumor cell growth in H3.3 mutant pHGG, thus opening new therapeutic options. The two most frequent H3.3 mutations in pHGG, K27M and G34R, drive aberrant repair of replication-associated damage by non-homologous end joining (NHEJ). Aberrant NHEJ is mediated by the DNA repair enzyme Polynucleotide Kinase 3-Phosphatase (PNKP), which shows increased association with mutant H3.3 at damaged replication forks. PNKP sustains the proliferation of cells bearing H3.3 mutations, thus conferring a molecular vulnerability, specific to mutant cells, with potential for therapeutic targeting.

cancer biology↗

bioRxiv2022

Evolution of m6A related genes in insects and function of METTL3 in embryonic development of silkworm.

N6-methyladenosine (m6A), the most prevalent modification in eukaryotic RNAs, plays a key role in biological processes. However, the evolutionary relationships and function of m6A related genes in insects are still largely unknown. Here, we analyzed the phylogenetics of m6A related genes among 207 insects and find that m6A related genes are evolutionarily conserved in insects. We apply the lepidopteran model insect Bombyx. mori as a study system. Subcellular localization experiments in BmN cells confirmed that YTHDF3 localizes in the cytoplasm, METTL3, METTL14 and YTHDC localize in the nucleus, while FL2D localizes in both nucleus and cytoplasm. We also detected expression pattern of m6A related genes during the embryonic development of B. mori and found that m6A related genes expression pattern is temporally specific. To elucidate the function of METTL3 during embryonic stage, RNA sequencing was performed to measure differential expressions of mRNA from silkworm eggs after METTL3 knockdown, and METTL3-overexpressing BmN cells. The global transcriptional pattern showed that METTL3 knockdown affected multiple cellular processes, including oxidoreductase activity, transcription regulator activity, cation binding and fundamental many metabolism processes, such as carbon metabolism, purine metabolism, biosynthesis of amino acids, and the citrate cycle, were affected. In addition, METTL3 knockdown significantly affected Wnt and Toll/Imd pathways in embryonic stage. The results suggest that METTL3 plays an important role during the embryonic development of B. mori. This study deepens our understanding of the function of m6A related genes in insects.

evolutionary biology↗