Biology subjects

Yoshida, K.

Publications and source records attributed to Yoshida, K..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

A groove brain-music interface for enhancing individual experience of urge to move

When we listen to music, we often feel a pleasurable urge to move to music, known as groove. While previous studies have identified musical features that contribute to the groove experience, such as syncopation and tempo, they also report individual differences in which kinds of music people experience groove. Therefore, recommending groove-eliciting music requires accounting for individual differences. In this study, we aimed to develop a groove brain-music interface (G-BMI) that generates personalized playlists to maximize each individuals groove experience, using a neurofeedback system based on in-ear EEG. Twenty-four participants listened to three high-groove and three low-groove musical excerpts and rated their "urge to move." Using these ratings and the recorded EEG, we trained two LASSO models to build the G-BMI. Model 1 predicted urge to move from acoustic features extracted with VGGish, a pretrained neural network. Model 2 classified EEG data as recorded during listening to high-groove or low-groove music. Using Model 1, we ranked 7,225 candidate songs by predicted groove and assembled one groove-augmenting and one groove-diminishing playlist. Using Models 1 and 2, we created two additional playlists that updated Model 1 and the ranking in real-time based on in-ear EEG. Participants then listened to all four playlists and rated them on items including "urge to move." The groove-augmenting playlist that incorporated EEG achieved the highest "urge to move" ratings. These findings suggest that a personalized neurofeedback system employing EEG can help maximize individual groove experience.

neuroscience↗

bioRxiv2025

Psychological scales in the brain: Trait-linked questionnaire items evoke similar neural patterns in the mPFC

Self-report questionnaires are widely used across psychology and related disciplines, yet the cognitive and neural processes underlying how individuals generate responses to such items remain poorly understood. Here, we investigated whether items from the same psychological scale evoke similar neural activation patterns in the medial prefrontal cortex (mPFC), a region consistently implicated in self-referential processing. While undergoing functional magnetic resonance imaging (fMRI), participants completed a self-reference task in which they judged how well 72 personality-related questionnaire items (e.g., from the Big Five, emotion regulation, and well-being scales) described themselves. Using representational similarity analysis (RSA), we found that items from the same scale elicited more similar multivoxel activation patterns in the mPFC compared to items from different scales. This effect was specific to the self-reference task and was not observed during a semantic judgment control task using the same items. Furthermore, the mPFC encoded not only categorical scale membership but also graded psychological similarity among scales, as reflected in inter-scale behavioral correlations. Importantly, these effects remained significant even after controlling for sentence-level semantic similarity using multiple regression RSA, indicating that the observed neural structure reflects psychological rather than linguistic similarity. These findings suggest that the mPFC integrates internally constructed evidence in a construct-sensitive manner during self-report, and they open new avenues for linking psychological assessment with neural representation. We discuss the implications for understanding self-report as a cognitive process and for future work on neuroimaging-informed scale validation. Significance statementSelf-report questionnaires are widely used across psychology, medicine, and public policy to assess thoughts, feelings, and personality traits. However, little is known about how the brain generates these responses. Using fMRI and a multivariate analysis approach, we found that questionnaire items measuring the same psychological construct evoked similar activity patterns in the medial prefrontal cortex--a region involved in self-reflection. This effect was specific to self-referential judgments and remained significant even after controlling for sentence-level semantic similarity, suggesting that the brain organizes information according to underlying psychological traits rather than linguistic features. These findings offer new insights into how self-report operates at the neural level and may inform future approaches to scale development.

neuroscience↗

bioRxiv2025

Proteomic profiling of bacterial extracellular vesicles for exploring ovarian cancer biomarkers

Extracellular vesicles (EVs) are present in body fluids and act as disease biomarkers. Emerging evidence has proven that EVs are released not only from mammalian cells but also from bacteria. Ovarian cancer has a dismal prognosis because of difficulties in early detection. This study aimed to identify bacterial EV (BEV) proteins associated with ovarian cancer. Fifteen patients with ovarian cancer or benign tumors were recruited, and EVs were isolated from the ascites. BEVs were recovered from seven in vitro-cultured strains of bacteria present in the vaginal microbiota, and LC-MS/MS analysis was performed. The detected peptide data were annotated to both human and bacterial references, and the human data showed that the profiles of cancer EVs were distinct from those of patients with benign tumors. As analyzed by bacterial proteins, P15636_Protease1 was found as the BEV-associated protein highly expressed in patients with cancer. To distinguish patients with cancer, the area under the curve was 0.88 (95% CI, 0.64-1.00). In addition, homology analysis showed that P15636_Protease1 is a unique protein only detected in bacteria. In this study, ovarian cancer-specific bacterial proteins were identified on EVs, and BEVs in bodily fluids are promising in the discovery of disease biomarkers.

cancer biology↗

bioRxiv2025

Enhancing CAR-T cell activity prediction via fine-tuning protein language models with generated CAR sequences

Chimeric antigen receptor (CAR)-T cell therapy has shown remarkable success in treating hematological malignancies; however, several challenges remain, including limited efficacy against solid tumors, T cell exhaustion, and lack of T cell persistence, which have restricted its clinical efficacy across various indications. Sequence optimization of CAR constructs offers a promising strategy to enhance therapeutic efficacy of CAR-T cells. Recent advances in machine learning, especially protein language models (PLMs), enable prediction of mutational effects based on sequence representations. Nevertheless, applying PLMs to CARs is challenging due to the artificial nature of CARs and the absence of comprehensive CAR sequence databases. In this study, we developed a computational framework to predict CAR-T cell activity by fine-tuning ESM-2 with the CAR sequences generated using sequence augmentation. These CAR sequences were constructed by recombining homologous domains of CARs, enabling task-specific adaptation of the model. To evaluate prediction performance, we experimentally assessed the cytotoxicity of CAR-T cells expressing mutated CAR variants and compared these results with model predictions. Our results demonstrated that fine-tuned ESM-2 significantly improves prediction performance of CAR-T cell activity. Furthermore, we showed that training parameters--such as sequence diversity, number of training steps, and model size--substantially influence prediction performance. This work highlights the potential of combining sequence augmentation with fine-tuning PLMs to advance data-driven CAR-T cell design.

bioinformatics↗

bioRxiv2025

Chronic social defeat causes dysregulation of systemic glucose metabolism via the cerebellar fastigial nucleus

Chronic psychological stress leads to hyperglycemia through the endocrine and sympathetic nervous systems, which contributes to the development of type II diabetes mellitus (T2DM). Higher plasma corticosteroids after stress is one well-established driver of insulin resistance in peripheral tissues. However, previous studies have indicated that only a fraction of patients with depression and post-traumatic disorder (PTSD) who develop T2DM exhibit hypocortisolism, so corticosteroids do not fully explain psychological stress-induced T2DM. Here, we find that chronic social defeat stress (CSDS) in mice enhances gluconeogenesis, which is accompanied by a decrease in plasma insulin, an increase in plasma catecholamines, and a drop in plasma corticosterone levels. We further reveal that these metabolic and endocrinological changes are mediated by the activation of neurons projecting from the cerebellar fastigial nucleus (FN) to the medullary parasolitary nucleus (PSol). These neurons are crucial in shifting the bodys primary energy source from glucose to lipids. Additionally, data from patients with depression reveal correlations between the presence of cerebellar abnormalities and both worsening depressive symptoms and elevated HbA1c levels. These findings highlight a previously unappreciated role of the cerebellum in metabolic regulation and its importance as a potential therapeutic target in depression, PTSD, and similar psychological disorders.

neuroscience↗

bioRxiv2025

Visual Influence Networks in Walking Crowds

Collective motion in human crowds has been understood as a self-organizing phenomenon that is generated from local visual interactions between neighboring pedestrians. To analyze these interactions, we introduce an approach that estimates local influences in observational data on moving human crowds and represents them as spatially-embedded dynamic networks (visual influence networks). We analyzed data from a human "swarm" experiment (N = 10, 16, 20) in which participants were instructed to walk about the tracking area while staying together as a group. We reconstructed the network every 0.5 seconds using Time-Dependent Delayed Correlation (TDDC). Using novel network measures of local and global leadership (direct influence and branching influence), we find that both measures strongly depend on an individuals spatial position within the group, yielding similar but distinctive leadership gradients from the front to the back. There was also a strong linear relationship between individual influence and front-back position in the crowd. The results reveal that influence is concentrated in specific positions in a crowd, a fact that could be exploited by individuals seeking to lead collective crowd motion.

animal behavior and cognition↗

bioRxiv2025

IL-21-STAT3 axis negatively regulates LAIR1 expression in B cells

LAIR1 is an inhibitory receptor broadly expressed on human immune cells, including B cells. LAIR1 has been shown to modulate BCR signaling, however, it is still unclear whether its suppressive activity can be a negative regulator for autoreactivity. In this study, we demonstrate the LAIR1 expression profile on human B cells and prove its regulatory function and relationships to B cell autoreactivity. We show that both the frequency and level of LAIR1 expression decreases during B cell differentiation. LAIR1 expressing (LAIR1+) switched memory (SWM) B cells have a transcriptional profile less differentiated toward a plasma cell (PC) phenotype, harbor more autoreactive B cells and exhibit less PC differentiation in vitro than the LAIR1 negative (LAIR1-) counterpart. These data suggests that LAIR1 functions as a B cell tolerance checkpoint. We confirm previous data showing that patients with systemic lupus erythematosus (SLE) express less LAIR1 on B cells, implying a breakdown of the checkpoint, consistent with the enhanced PC differentiation seen in SLE. We further demonstrate that LAIR1 expression is down-regulated through the IL-21/STAT3 pathway which is known to be upregulated in SLE. These data suggest therapeutic targets that might decrease the aberrant PC differentiation observed in SLE.

immunology↗

bioRxiv2024

How does immediate auditory feedback coupled to locomotion influence the spontaneous actions of rats?

Sense of agency is a subjective experience that is difficult to examine in animals and preverbal infants. In animals and infants, the sensory monitoring of self-motion, which is the basis of this sense, and the contingency between self-motion and sensory feedback are investigated. Here, we performed experiments on rats using locomotor movements and auditory feedback of pulsed sounds with real-time changes in pulse interval corresponding to the velocity of locomotion, and tested whether rats change their locomotion depending on the degree of contingency between locomotion and auditory feedback. The results showed that rats increased their locomotion distance when the pulse interval of sound changed in accordance with the velocity of locomotion. However, this effect was not long-lasting. This study provides a simple and convenient method to examine the awareness of the contingency between self-motion and auditory feedback in a wide range of animal species without long-term training, and is expected to be a useful tool for comparisons with humans.

animal behavior and cognition↗

bioRxiv2024

SOQ1 functions as a methionine sulfoxide reductase in the chloroplast lumen for regulation of photoprotective qH in Arabidopsis

Photosynthetic organisms must balance light absorption and energy dissipation to prevent photo-oxidative damage. Non-photochemical quenching (NPQ) dissipates excess light energy as heat, with the quenching component qH providing sustained photoprotection. However, the molecular mechanism underlying qH induction remains unclear. Our study focuses on the thylakoid membrane protein SUPPRESSOR OF QUENCHING 1 (SOQ1) and its inhibition of qH through interaction with LIPOCALIN IN THE PLASTID (LCNP) in Arabidopsis thaliana. Structural homology of SOQ1 lumenal domains with bacterial disulfide bond protein D suggested potential thiol-disulfide exchange activity. In vitro assays determined that both SOQ1 thioredoxin-like (Trx-like) and C-terminal (CTD) domains contain a redox-active cysteine pair and evidenced electron transfer from Trx-like to CTD. Importantly, we found that SOQ1 lumenal domains exhibit methionine sulfoxide reductase (Msr) activity converting oxidized methionine residues in LCNP back to methionine, which thereby inactivates LCNP and prevents qH formation. Mutational analyses identified cysteine residues in SOQ1-CTD and methionine residues in LCNP as critical for qH suppression, supporting their role in redox regulation. Additionally, we found that the redox state of SOQ1 in vivo is light-dependent, shifting from reduced to oxidized under stress conditions, indicating a dynamic regulation of its activity. We conclude that the Trx-like domain of SOQ1 provides reducing power to its CTD displaying Msr activity. SOQ1 is therefore an unusual example of a protein possessing both a disulfide reductase and Msr domain in tandem. Our findings elucidate the redox-regulation mechanism of qH involving SOQ1-mediated methionine reduction of LCNP, providing insights into the intricate control of photoprotective processes in chloroplasts and enhancing our understanding of plant resilience under environmental stress.

plant biology↗

bioRxiv2024

Distinct classes of antidepressants commonly act to shape pallidal structure and function in mice

Antidepressants including selective serotonin reuptake inhibitors, ketamine, and psilocybin are all effective for treating depression despite their distinct primary mechanisms. We hypothesized that these drugs may share a common mechanism that underlies their therapeutic actions. We treated mice with one of the following: escitalopram, R-/S-/RS-ketamine, or psilocin. Additionally, groups exposed to electroconvulsive stimulation and a saline control were included. Following treatment, fixed brains underwent structural magnetic resonance imaging, and voxel-based morphometry was performed to evaluate brain-wide volumetric changes. Compared with control treatment, we observed greater volumes in the nucleus accumbens, ventral pallidum, and external globus pallidus across all antidepressant treatments, and a smaller volume in the mediodorsal thalamus. Specifically, R-ketamine, RS-ketamine, and psilocin induced more pronounced hypertrophy of the ventral pallidum, whereas selective serotonin reuptake inhibitors and S-ketamine predominantly increased the volume of the external globus pallidus. Further analyses using super-resolution microscopy and imaging mass spectrometry revealed corresponding microstructural and molecular changes. Greater pallidal volume was associated with striatal medium spiny neuron terminal hypertrophy and elevated {gamma}-aminobutyric acid (GABA) levels. Interestingly, all antidepressants were also associated with higher striatal dopamine content. Moreover, striatal vesicular GABA transporter overexpression reproduced the medium spiny neuron terminal hypertrophy and increased pallidal GABA content, and was associated with a reduction in innate anxiety. These findings indicate that despite their pharmacological diversity, antidepressant treatments lead to shared pallidum-centered structural and molecular changes. We propose that these shared changes may potentiate the striato-pallidal inhibitory circuit, thereby contributing to the overall antidepressant effect.

neuroscience↗

bioRxiv2024

Dual roles of EGO-1 and RRF-1 in regulating germline exo-RNAi efficiency in Caenorhabditis elegans

RNA interference (RNAi) is widely used in life science research and is critical for diverse biological processes, such as germline development and antiviral defense. In Caenorhabditis elegans, RNA-dependent RNA polymerases, with redundant involvement of EGO-1 and RRF-1, facilitate small RNA amplification in germline exogenous RNAi (exo-RNAi). However, their coordination during the regulation of exo-RNAi processes in the germline remains unclear. Here, we examined non-null mutants of the ego-1 gene and found that ego-1(S1198L) animals exhibited germline exo-RNAi defects with normal fertility, abnormalities in germ granules, and synthetic temperature-dependent sterility with rrf-1. The exo-RNAi defects in ego-1(S1198L) were partially restored by inhibiting hrde-1, cde-1, and znfx-1. Similar defects were observed in wild-type and ego-1(S1198L) heterozygous descendants derived from ego-1(S1198L), but these were suppressed by ancestral inhibition of rrf-1. These data reveal a dual role for EGO-1 in the positive regulation of germline exo-RNAi: it not only mediates target silencing through its RNA-dependent RNA polymerase activity, but also fine-tunes germ granule function or downstream processes, which are antagonized by RRF-1.

developmental biology↗

bioRxiv2024

Endemic demographics of the Jomon people estimated based on complete mitogenomes reveal their regional diversity

The Jomon culture that spread across Japanese archipelago began about 16,000 years ago and lasted for over 10,000 years. The genetic diversity of the Jomon people, prehistoric hunter-gatherers bearing the Jomon culture, is of great interest in understanding prehistoric East Eurasians. Until now, their demographic history has been estimated using archaeological sites and present-day genomes, but detailed studies using Jomon genomes have been insufficient. To investigate the Jomon demography, we determined the complete mitochondrial genome (mitogenome) sequences from 13 Jomon individuals and conducted population genetic analysis on 40 Jomon genomes including previously published data. Our results revealed an effective population size increase during the Incipient - Initial phase of the Jomon period, which had not been observed in analysis of mitogenome sequences from present-day Japanese populations. This endemic demographic pattern is pronounced in the eastern part of the archipelago, under the assumption of no gene flow between the Eastern and Western Jomon.

genomics↗

bioRxiv2024

A biological model of nonlinear dimensionality reduction

Obtaining appropriate low-dimensional representations from high-dimensional sensory inputs in an unsupervised manner is essential for straightforward downstream processing. Although nonlinear dimensionality reduction methods such as t-distributed stochastic neighbor embedding (t-SNE) have been developed, their implementation in simple biological circuits remains unclear. Here, we develop a biologically plausible dimensionality reduction algorithm compatible with t-SNE, which utilizes a simple three-layer feedforward network mimicking the Drosophila olfactory circuit. The proposed learning rule, described as three-factor Hebbian plasticity, is effective for datasets such as entangled rings and MNIST, comparable to t-SNE. We further show that the algorithm could be working in olfactory circuits in Drosophila by analyzing the multiple experimental data in previous studies. We finally suggest that the algorithm is also beneficial for association learning between inputs and rewards, allowing the generalization of these associations to other inputs not yet associated with rewards.

neuroscience↗

bioRxiv2024

TRPC6 is a mechanosensitive channel essential for ultrasound neuromodulation in mammalian brain

Ultrasound neuromodulation has become an innovative technology that enables non-invasive intervention in mammalian brain circuits with high spatiotemporal precision. Despite the expanding utility of ultrasound neuromodulation in the neuroscience research field and clinical applications, the molecular and cellular mechanisms by which ultrasound impacts neural activity in the brain are still largely unknown. Here, we report that transient receptor potential canonical 6 (TRPC6), a mechanosensitive non-selective cation channel, is essential for ultrasound neuromodulation of mammalian neurons in vitro and in vivo. We first demonstrated that ultrasound irradiation elicited rapid and robust Ca2+ transients mediated via extracellular Ca2+ influx in cultured mouse cortical and hippocampal neurons. Ultrasound-induced neuronal responses were massively diminished by blocking either the generation of action potential or synaptic transmission. Importantly, both pharmacological inhibition and genetic deficiency of TRPC6 almost completely abolished neuronal responses to ultrasound. Furthermore, we found that intracerebroventricular administration of a TRPC6 blocker significantly attenuated the population of neuronal firings in the cerebral cortex evoked by transcranial ultrasound irradiation in mice. Our findings indicate that TRPC6 is an indispensable molecule of ultrasound neuromodulation in the intact mammalian brains, providing fundamental understanding of biophysical molecular mechanisms of ultrasound neuromodulation as well as insight into its future feasibility in neuroscience and translational researches in humans.

neuroscience↗

bioRxiv2023

Zinc-finger (ZiF) fold secreted effectors form a functionally diverse family across lineages of the blast fungus Magnaporthe oryzae.

Filamentous plant pathogens deliver effector proteins into host cells to suppress host defence responses and manipulate metabolic processes to support colonization. Understanding the evolution and molecular function of these effectors provides knowledge about pathogenesis and can suggest novel strategies to reduce damage caused by pathogens. However, effector proteins are highly variable, share weak sequence similarity and, although they can be grouped according to their structure, only a few structurally conserved effector families have been functionally characterized to date. Here, we demonstrate that Zinc-finger fold (ZiF) secreted proteins form a functionally diverse effector family in the blast fungus Magnaporthe oryzae. This family relies on the Zinc-finger motif for protein stability and is ubiquitously present, forming different effector tribes in blast fungus lineages infecting 13 different host species. Homologs of the canonical ZiF effector, AVR-Pii from rice infecting isolates, are present in multiple M. oryzae lineages, and the wheat infecting strains of the fungus, for example, possess an allele that also binds host Exo70 proteins and activates the immune receptor Pii. Furthermore, ZiF tribes vary in the host Exo70 proteins they bind, indicating functional diversification and an intricate effector/host interactome. Altogether, we uncovered a new effector family with a common protein fold that has functionally diversified in lineages of M. oryzae. This work expands our understanding of the diversity of M. oryzae effectors, the molecular basis of plant pathogenesis and may ultimately facilitate the development of new sources for pathogen resistance. Author SummaryDiseases caused by filamentous plant pathogens impact global food production, leading to severe economic and humanitarian consequences. These pathogens secrete hundreds of effectors inside the host to alter cellular processes and to promote infection and disease. Effector proteins have weak or no sequence similarity but can be grouped in structural families based on conserved protein folds. However, very few conserved effector families have been functionally characterized. We have identified a family of effectors with a shared Zinc-finger protein fold (ZiF) that is present in lineages of the blast fungus Magnaporthe oryzae that can, collectively, infect 13 different grasses. We characterized the binding of a sub-set of these proteins to putative Exo70 host targets and showed they can be recognized by the plant immune system. Furthermore, we show that other ZiF effectors do not bind Exo70 targets, suggesting functional specialization within this effector family for alternative interactors. These findings shed light on the diversity of effectors and their molecular functions, as well as potentially leading to the development of new sources of blast disease resistance in the future.

plant biology↗

bioRxiv2023

Production of Infectious Reporter Murine Norovirus by VP2 trans-Complementation

Human norovirus (HuNoV) causes gastroenteritis, a disease with no effective therapy or vaccine. Murine norovirus (MNV) easily replicates in cell culture and small animals and has often been used as a model to elucidate the structural and functional characteristics of HuNoV. A MNV plasmid-based reverse genetics system was developed to produce modified recombinant virus. In this study, we attempted to construct the recombinant virus by integrating a foreign gene into MNV ORF3 that encodes the minor structural protein VP2. We found that deletion of VP2 expression abolished infectious particles from MNV cDNA clones, and supplying exogenous VP2 to the cells rescued the infectivity of cDNA clones without VP2 expression. In addition, we found that the coding sequence of C-terminal ORF3 was essential for cDNA clones compensated with VP2 to produce infectious particles. Further, the recombinant virus with exogenous reporter genes in place of the dispensable ORF3 coding region was able to propagate when VP2 was constitutively supplied. Our findings indicate that foreign genes can be transduced into the norovirus ORF3 region when VP2 is supplied and that successive propagation of modified recombinant norovirus could lead to the development of norovirus-based vaccines or therapeutics. IMPORTANCEIn this study, we revealed that some of the coding regions of ORF3 could be replaced by foreign gene and infectious virus could be produced under conditions with VP2 supplied. Propagation of this virus depended on VP2 being supplied in trans, indicating that this virus could infect only once. Our findings help to elucidate the functions of VP2 in virus lifecycle and to the development of other caliciviral vectors for recombinant attenuated live enteric virus vaccines or therapeutics.

microbiology↗

bioRxiv2023

Engineering a highly durable adeno-associated virus receptor for analytical applications

Adeno-associated virus (AAV) is a major viral vector used in gene therapy. There are multiple AAV serotypes, and many engineered AAV serotypes with modified capsids altering tissue tropism are enthusiastically being developed. The universal AAV receptor (AAVR) is an essential receptor for multiple AAV infections. Since most AAV serotypes used in gene therapy infect cells via interaction with AAVR, the quantification of the vector-binding ability of AAV to AAVR could be an important quality check for therapeutic AAV vectors. To enable a steady evaluation of the AAV-AAVR interaction, we created an engineered AAVR through mutagenesis. Engineered AAVR showed high durability against acid while retaining its AAV-binding activity and an affinity chromatography column with engineered AAVR was also developed. This column enabled repeated binding and acid dissociation measurements of AAVR with various AAV serotypes. Our data showed that the binding affinities of AAV to AAVR were diverse among serotypes, providing insight into the relationship with the infection efficiency of AAV vectors. Thus, this affinity column can be used in process development for quality checks, quantitating capsid titers, and affinity purification of AAV vectors. Furthermore, this column may work for a useful tool of novel AAV vector capsid engineering.

bioengineering↗

bioRxiv2022

Epidermal growth factor receptor signaling protects epithelia from morphogenetic instability and tissue damage in Drosophila

Dying cells in the epithelia communicate with neighboring cells to initiate coordinated cell removal to maintain epithelial integrity. Naturally occurring apoptotic cells are mostly extruded basally and engulfed by macrophages. Here, we investigated the role of Epidermal growth factor (EGF) receptor (EGFR) signaling in the maintenance of epithelial homeostasis. In Drosophila embryos, epithelial tissues undergoing groove formation preferentially enhanced extracellular signal-regulated kinases (ERK) signaling. In EGFR mutant embryos at stage 11, sporadic apical cell extrusion in the head initiates a cascade of apical extrusions of apoptotic and non-apoptotic cells that sweeps the entire ventral body wall. Here, we showed that clustered apoptosis, groove formation, and wounding sensitized EGFR mutant epithelia to initiate massive tissue disintegration. We further showed that tissue detachment from the vitelline membrane, which frequently occurs during morphogenetic processes, is a key trigger for the EGFR mutant phenotype. These findings indicate that, in addition to cell survival, EGFR plays a role in maintaining epithelial integrity, which is essential for protecting tissues from transient instability caused by morphogenetic movement and damage.

developmental biology↗