Normal Development Research Articles

Cyclin‐dependent kinase 13 is indispensable for normal mouse heart development

AbstractCongenital heart disease (CHD) has an incidence of approximately 1%. Over the last decade, sequencing studies including large cohorts of individuals with CHD have begun to unravel the genetic mechanisms underpinning CHD. This includes the identification of variants in cyclin‐dependent kinase 13 (CDK13), in individuals with syndromic CHD. CDK13 encodes a serine/threonine protein kinase. The cyclin partner of CDK13 is cyclin K; this complex is thought to be important in transcription and RNA processing. Pathogenic variants in CDK13 cause CDK13‐related disorder in humans, characterised by intellectual disability and developmental delay, recognisable facial features, feeding difficulties and structural brain defects, with 35% of individuals having CHD. To obtain a greater understanding for the role that this essential protein kinase plays in embryonic heart development, we have analysed a presumed loss of function Cdk13 transgenic mouse model (Cdk13tm1b). The homozygous mutants were embryonically lethal in most cases by E15.5. X‐gal staining showed Cdk13 expression localised to developing facial regions, heart and surrounding areas at E10.5, whereas at E12.5, it was more widely present. In the E15.5 heart, staining was seen throughout. RT‐qPCR showed significant reduction in Cdk13 transcript expression in homozygous compared with WT and heterozygous hearts at E10.5 and E12.5. Detailed morphological 3D analysis of embryonic and postnatal hearts was performed using high‐resolution episcopic microscopy, which affords a more detailed analysis of structures such as cardiac valve leaflets and endocardial cushions, compared with more traditional histological techniques. We show that both the homozygous and heterozygous Cdk13tm1b mutants exhibit a range of CHD, including ventricular septal defects, bicuspid aortic valve, double outlet right ventricle and atrioventricular septal defects. 100% (n = 4) of homozygous hearts displayed CHD. Differential expression was seen in Cdk13tm1b homozygous mutants for two genes known to be necessary for normal heart development. The types of defects, and the presence of CHD in heterozygous mice (17.02%, n = 8/47), are consistent with the CDK13‐related disorder phenotype in humans. This study provides important insights into the effects of reduced function of CDK13 in the mouse heart and contributes to our understanding of the mechanism behind this disorder as a cause of CHD.

Periodontal and orthodontic management of impacted canines.

The maxillary and mandibular canines are described by many clinicians as the "cornerstone" of the arch. When in their optimal position, they play a critical role in providing a well-balanced occlusal scheme that contributes toward functional as well as neuromuscular stability, harmony, esthetics, and dentofacial balance. When an aberration is noted with the normal eruptive and development process, early diagnosis with strategic intervention is critical and may often require a multidisciplinary approach. A proper diagnosis, risk assessment, and management of the soft tissues, hard tissues, and adjacent structures are vital for a successful outcome. This review highlights the diagnostic and treatment modalities that require consideration for the orthodontic as well as the periodontal management of impacted canines. The reader is guided through the etiology, diagnosis, prevention, and intervention of clinical cases that were managed with different approaches.

Unveiling the Significance of the Androgen Receptor Gene in Disorders of Sex Development

Abstract Disorders of sex development (DSD) encompass a range of congenital conditions where the development of chromosomal, gonadal or anatomical sex is atypical. There are many genes associated with DSD, and one of them is the androgen receptor (AR) gene, which plays a pivotal role in normal sex development. Studies reported numerous genetic variations in the AR gene that lead to 46, XY DSD, including androgen insensitivity syndrome and hypospadias. Identifying and understanding the genetic causes of DSD will aid the healthcare providers design a tailored-made management for DSD patients and optimise patients’ quality of life. This narrative review will explore the significance of the AR gene in DSD while discussing DSD in general.

Transcriptional profiling of the M. complexus in naked neck chickens suggest a direct pleiotropic effect of GDF7 on feathering and reduced hatchability.

The locus for naked neck (Na) in chickens reduces feather coverage and leads to increased heat dissipation from the body surface resulting in better adaptability to hot conditions. However, the Na gene is linked to significantly lower hatchability due to an increased late embryonic mortality. It has been argued that the causative gene GDF7 may have a direct pleiotropic effect on hatchability via its effect on muscle development. Thus, the study presented here analyses the transcriptome of the hatching muscle (M. complexus) and shows how GDF7 impacts development leading to reduced hatching rates in Na chickens. Using 12 chicken embryos (6 x wildtype (Wt) and 6 x Na) RNA was extracted from the M. complexus of each embryo and sequenced. The resulting differential expression analyses led to the discovery of 461 differentially expressed (DE) genes in the M. complexus of the experimental group. Among those, 77 genes were of uncertain function (LOC symbols), with 31 were classified as uncharacterised. The regulation of a number of pathways involved in normal embryonic development, were found to be negatively influenced by the Na genotype. Further pathways involved in cell-cell adhesion, cell signalling pathways, and amino acid (AA) metabolism/transport were also observed. GDF7 (alias BMP12), whose localised overexpression in the neck skin causes the Na/Na phenotype, was significantly overexpressed in the M. complexus of Na/Na embryos, and shows a significant increase in the number of binding sites for the transcription factor PITX2 was also observed. In Na chickens, GDF7 is under the control of a mutated cis-regulatory element, whose actions are known to suppress the development and distribution of feathers through the sensitizing action of retinoic acid. In this study, a number of DE genes with over 10 retinoic acid response elements (RAREs) in close proximity were observed, indicating changes to the retinol metabolism. With the understanding that the Na/Na mutation leads to increased retinoic acid activity, this indicates a high likelihood of GDF7 excerpting a direct pleiotropic effect, not just in the observed reduction in feather patterning, but also impacting the development of the M.complexus, and consequently leading to the reduced hatchability observed in birds with the Na/Na genotype. Furthermore, the enrichment of PITX2 binding sites in proximity to DE genes in the M. complexus, also indicates that muscle development is still ongoing in Na embryos. This suggests that the M. complexus is not yet fully developed, further increasing the potential for late embryonic mortality in Na chicks at hatching.

Pseudo-trajectory inference for identifying essential regulations and molecules in cell fate decisions.

Cell fate decision is crucial in biological development and plays fundamental roles in normal development and functional maintenance of organisms. By identifying key regulatory interactions and molecules involved in these fate decisions, we can shed light on the intricate mechanisms underlying the cell fates. This understanding ultimately reveals the fundamental principles driving biological development and the origins of various diseases. In this study, we present an overarching framework which integrates pseudo-trajectory inference and differential analysis to determine critical regulatory interactions and molecules during cell fate transitions. To demonstrate feasibility and reliability of the approach, we employ the differentiation networks of hepatobiliary system and embryonic stem cells as representative model systems. By applying pseudo-trajectory inference to biological data, we aim to identify critical regulatory interactions and molecules during the cell fate transition processes. Consistent with experimental observations, the approach can allow us to infer dynamical cell fate decision processes and gain insights into the underlying mechanisms which govern cell state decisions.

Lactate dehydrogenase a-like 6B is not essential for spermatogenesis and male fertility in mice.

Lactate is recognized as a principal energy substrate for male germ cells. Lactate dehydrogenases (LDHs) catalyze the reversible conversion between pyruvate and lactate, which are required for male fertility. Among them, lactate dehydrogenase A-like 6B (Ldhal6b) has been identified as a testis-specific LDH gene. However, its precise roles in spermatogenesis remain to be elucidated. In this study, we used a Ldhal6b knockout mouse model to assess its impact on spermatogenesis. Our findings reveal that Ldhal6b knockout mice exhibit normal development and no significant alterations in male fertility. Further, LDHAL6B is localized to mitochondria and closely associated with germ granules. Nevertheless, its depletion does not result in significant abnormalities in mitochondria, germ granules or impact piRNA biogenesis. We also observed alterations in the abundance of proteins related to mitochondrial metabolism in sperm from Ldhal6b knockout mice, align with its specific localization to mitochondria. Overall, our results indicate that Ldhal6b is dispensable for both mouse development and spermatogenesis under normal laboratory conditions.

Association between narrow palate and respiratory function in children: a literature review

Changes in the airways and dentoalveolar system are one of the most challenging aspects of modern practical and theoretical dentistry. Nasal breathing is essential for the normal development of the maxillofacial area. During a child’s growth, the respiratory tract and facial skull development are closely linked. The main stage of dentoalveolar system development occurs during preschool and elementary school years. Nasal breathing disorders are currently widespread in this age group. Dental professionals are frequently the first to detect these disorders. A dental professional can then inform parents on the potential causes and consequences of habitual mouth breathing, justify the need for treatment and prevention of this pathology, and refer a child to an ENT specialist. The review examines the association between narrow palate and respiratory function in children. Domestic and international studies addressing the association between dentoalveolar system pathologies and respiratory patterns and functional parameters were analyzed. The studies present a variety of opinions: some authors confirm the association between narrow palate and mouth breathing, while others refute it. Moreover, changes in respiratory function parameters following rapid palatal expansion have been analyzed, emphasizing the importance of timely orthodontic treatment to improve breathing.

Exploring the influences of resource limitation and plant aging on pollen development in Azorella nivalis Phil. (Apiaceae), a long-lived high-Andean cushion plant.

Angiosperm pollen, the male gametophyte, plays a crucial role in facilitating fertilization by protecting and transporting male sperm cells to the female pistil. Despite their seemingly simple structure, pollen grains undergo intricate development to produce viable sperm cells capable of fertilizing the egg cell. Factors such as resource limitation and plant aging can disrupt normal pollen development and affect pollen performance. We investigated the influence of plant resources and aging on pollen developmental failure in Azorella nivalis Phil., an exceptionally long-lived high-Andean species that grows in a stressful alpine environment. Leveraging the modular nature of plants, we aimed to identify intra-individual sources of variation in pollen developmental failure. By using pollen viability and variation in viable pollen grain size as indicators of pollen developmental performance, we assessed whether proxies of plant resource availability and aging influenced these pollen traits at the inter-individual, inter-flower and intra-flower levels. Our findings revealed decreased pollen viability in putative resource-depleted flowers and in shoots that experienced higher levels of meristematic divisions from the zygote (i.e., greater cell depth). Additionally, we observed increased variability in the size of viable pollen grains in resource-depleted anthers. Our study suggests that resource availability and shoot aging are critical determinants shaping pollen development in long-lived plants at the intra-individual level. These findings contribute to our understanding of how differences in male fitness can arise in plants, with implications for their evolutionary trajectory.

Relating normal human cardiac development to the anatomical findings in the congenitally malformed heart.

A proper appreciation of cardiac development can now provide the necessary background to understand the anatomical findings in the congenitally malformed heart. We recently presented an account of human cardiac development based on reconstructions of histological datasets from human embryos aged between 3.5 and 8 weeks subsequent to conception. In this review, we summarize the changes observed relative to the findings when the heart is congenitally malformed. Beginning at the stage when it is first possible to recognize the primary heart tube, we describe the looping of its ventricular component, which occurs in the 5th week. We proceed with discussion of the formation of the atrial and ventricular chambers in the 6th week. The phases are successive, albeit partially overlapping. Separation of the circulations at the venous pole is completed at stage 17, equivalent to almost 6 weeks of development. During stages representing the 7th week of development, we concentrate on the remodeling of the outflow tract. This involves initially septation, but then separation of the developing circulations. The changes involve incorporation of the proximal outflow tract into the ventricles, with formation of the arterial roots in its middle part, and addition of a distal non-myocardial component to produce the intrapericardial arterial trunks. We pay particular attention to the changes occurring during remodeling of the interventricular foramen. We show that an understanding of this process provides the basis for understanding the functionally univentricular heart, as well as the arrangement found in double outlet right ventricle.

Rescuable sleep and synaptogenesis phenotypes in a Drosophila model of O-GlcNAc transferase intellectual disability.

O-GlcNAcylation is an essential intracellular protein modification mediated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Recently, missense mutations in OGT have been linked to intellectual disability, indicating that this modification is important for the development and functioning of the nervous system. However, the processes that are most sensitive to perturbations in O-GlcNAcylation remain to be identified. Here, we uncover quantifiable phenotypes in the fruit fly Drosophila melanogaster carrying a patient-derived OGT mutation in the catalytic domain. Hypo-O-GlcNAcylation leads to defects in synaptogenesis and reduced sleep stability. Both these phenotypes can be partially rescued by genetically or chemically targeting OGA, suggesting that a balance of OGT/OGA activity is required for normal neuronal development and function.

A large-scale screening identifies receptor-like kinases with common features in kinase domains that are potentially related to disease resistance in planta

IntroductionThe plant genome encodes a plethora of proteins with structural similarity to animal receptor protein kinases, collectively known as receptor-like protein kinases (RLKs), which predominantly localize to the plasma membrane where they activate their kinase domains to convey extracellular signals to the interior of the cell, playing crucial roles in various signaling pathways. Despite the large number of members within the RLK family, to date, only a few have been identified as pattern-recognition receptors (PRRs), leaving many potential RLKs that could play roles in plant immunity undiscovered.MethodsIn this study, a recombinant strategy was initially employed to screen the kinase domains of 133 RLKs in the Arabidopsis genome to determine their involvement in the pathogen-triggered immunity (PTI) pathway. Subsequently, 6 potential immune-related recombinant RLKs (rRLKs) were selected for the creation of transgenic materials and underwent functional characterization analysis. Finally, a sequence analysis was conducted on the kinase domains of these 133 RLKs as well as the known immune RLK receptor kinase domains from other species.ResultsIt was found that 24 rRLKs activated the PTI response in Arabidopsis fls2 mutant protoplasts following flg22 treatment. Consistently, when 6 of these rRLKs were individually expressed in fls2 background, they exhibited diverse PTI signal transduction capabilities via different pathways while all retained membrane localization. Intriguingly, sequence analysis revealed multiple conserved amino acid sites within kinase domains of these experimentally identified immune-related RLKs in Arabidopsis. Importantly, these patterns are also preserved in RLKs involved in PTI in other species.DiscussionThis study, on one hand, identifies common features that theoretically can enhance our understanding of immune-related RLKs and facilitate the discovery of novel immune-related RLKs in the future. On the other hand, it provides experimental evidence for the use of recombinant technique to develop diverse rRLKs for molecular breeding, thereby conferring high resistance to plants without compromising their normal growth and development.

Rasmussen Encephalitis: Clinical Features, Pathophysiology, and Management Strategies—A Comprehensive Literature Review

Rasmussen encephalitis (RE) is a rare and progressive form of chronic encephalitis that typically affects one hemisphere of the brain and primarily occurs in pediatric individuals. The current study aims to narratively review the literature about RE, including historical information, pathophysiology, and management of this condition. RE often occurs in individuals with normal development, and it is estimated that only a few new cases are identified each year in epilepsy centers. Approximately 10% of cases also occur in adolescents and adults. The hallmark feature of RE is drug-resistant focal seizures that can manifest as epilepsia partialis continua. Also, patients with RE usually develop motor and cognitive impairment throughout the years. Neuroimaging studies show progressive damage to the affected hemisphere, while histopathological examination reveals T-cell-dominated encephalitis with activated microglial cells and reactive astrogliosis. The current therapy guidelines suggest cerebral hemispherotomy is the most recommended treatment for seizures in RE, although significant neurological dysfunction can occur. Another option is pharmacological management with antiseizure medications and immunomodulatory agents. No significant progress has been made in understanding the pathophysiology of this condition in the last decades, especially regarding genetics. Notably, RE diagnosis still depends on the criteria established by Bien et al., and the accuracy can be limited and include genetically different individuals, leading to unexpected responses to management.

The Relationship between Intensity of Gadget Use and Speech and Language Development in Toddlers

Background : The alpha generation are those born after 2010, who are claimed to be the smartest generation because they were born and grew up in an era of rapid technological and internet development. So that we can find many toddlers who are familiar with gadgets. However, excessive use of gadgets will reduce toddler interaction with the environment and toddlers rarely communicate with people around them, this naturally disrupts the process of toddler speech and language development. Objective: This study aims to analyze the relationship between the intensity of gadget use and the development of speech and language aspects in toddlers in Wameo Village, Baubau City. Method: This study is an observational analytic type with a cross sectional approach. This study used 77 samples taken using purposive sampling technique which were then measured using a questionnaire. Result: The results showed that toddlers who used gadgets with mild intensity experienced normal speech and language development, 10.4% of toddlers who used gadgets with moderate intensity experienced delays, and 33.8% who used gadgets with severe intensity experienced delays. Hypothesis testing using the Chi-Square Test obtained a p-velue value of 0.000 (P <0.05). Conclusion: In conclusion, there is a significant relationship between the intensity of gadget use and delayed speech and language development in toddlers in Wameo Village, Baubau City.

Abstract 4143267: Bicaudal-C Homolog 1 Plays a Significant Role in Cardiac Development and Congenital Heart Defects

Background: Congenital heart defects (CHDs) are the most common birth defects globally and often require palliative surgical interventions with limited long-term effectiveness. Prenatal detection of CHDs is challenging due to the absence of heart failure signs in most fetuses. Thus, early detection methods and therapeutic drugs to correct abnormal heart development are crucial. We have discovered that the RNA-binding protein Bicaudal-C homolog 1 (Bicc1) influences normal and abnormal heart development. Bicc1 is involved in post-transcriptional regulation and interacts with RNA interference (RNAi) components. While its role in left-right patterning, kidney development, and the interaction with PKD genes ( Pkd1 and Pkd2 ) is documented, the role of Bicc1 and its expression in heart development and whether it relies on interaction with Pkd1/Pkd2 are not understood. Methods and Results: To start addressing these knowledge gaps, we used a transgenic mouse line with an in-frame fusion of Bicc1 and the LacZ reporter gene to perform β-galactosidase staining, RNAscope and immunostaining to identify the cardiac cell types expressing Bicc1 . High Bicc1 expression was observed in embryonic and neonatal hearts, particularly in the ventricles, atria, and endothelial cells of blood vessels. Expression decreased in adulthood but persisted at basal levels. We observed that Bicc1 knockout (KO) developed heterotaxy of the heart and enlarged atria. Next, to elucidate the gene and miRNA regulatory networks involved in cardiac development disrupted by the absence of Bicc1, we carried out RNA- and miRNA-seq on hearts from wild-type and Bicc1 KO embryonic hearts at different developmental stages. Several genes and miRNAs associated with ciliopathy and heterotaxy, including miR-196 , Hand1 , and Lefy2, were significantly altered in Bicc1 KO mice. Moreover, as reported for the kidney, Pkd2 mRNA expression was altered in Bicc1 KO mice, while Pkd1 expression remained unchanged. Finally, we detected changes linked to lipid metabolism and related pathways, such as members of aldehyde dehydrogenase ( Adlh1a ) and cytochrome P450 family ( Cyp5a1 ), that were altered in the absence of Bicc1 . Conclusions: Our study reveals additional role(s) for Bicc1 in heart development suggesting its involvement in regulating heart metabolism in fetuses. These findings provide a conceptual basis for future investigations into the function of Bicc1 in heart development and how its disruption contributes to CHDs.

CNSC-10. WHEN GOOD THINGS GO OFF TRK: THE INTERSECTION OF NEUROSCIENCE & ONCOLOGY

Abstract How and why do processes and molecular players that were once an integral part of normal neurodevelopment go awry in pathological conditions, such as cancer? Embryogenesis, and neurodevelopment in particular, comprise an elegant and well-orchestrated series of tightly regulated events, culminating in an organized and highly functioning organism. Cancer, on the other hand, can often be viewed as an uncontrolled, unrestrained, genetically chaotic disease, lacking the precise spatial and temporal rigidity associated with normal development. While appearing to be on opposite sides of the organizational spectrum, the similarities between early neurodevelopment and oncogenesis are numerous. The link between developmental signaling and cancer initiation, maintenance, and metastasis has long been known for several members of the Wnt, Hedgehog, and Notch pathways and years of gene-level analyses have provided a wealth of knowledge and mechanistic insight. As advances in next generation sequencing allow for deeper characterization of genetic programs, it is increasingly possible to explore various isoforms of cancer associated genes. It is widely known that neurotrophins and their receptors (TrkA, TrkB, TrkC) are instrumental for neurodevelopment and that they remain critical for proper neuronal functioning throughout life. Our work highlights a previously unidentified role for an alternatively spliced neurotrophin receptor in neurodevelopment, embryogenesis, transformation, and oncogenesis across multiple tumor types in humans and mice. This specific isoform, TrkB.T1, is the predominant NTRK2 isoform across embryonic organogenesis, and forced overexpression of this embryonic pattern causes multiple solid and nonsolid tumors in mice. TrkB.T1 also emerges as the predominant NTRK isoform expressed in a wide range of adult and pediatric tumors, including those harboring various NTRK fusions. This work hopes to address the fundamental question of how neurodevelopmental processes can go awry in cancer, while seeking to better characterize the role of TRKs, in normal developmental processes and oncogenesis.

Integrated Profiling Identifies Long-Term Molecular Consequences of Prenatal Dexamethasone Treatment in the Rat Brain-Potential Triggers of Depressive Phenotype and Cognitive Impairment.

Prenatal excess of glucocorticoids (GCs) is considered to be one of the highly impacting factors contributing to depression development. Although GCs are crucial for normal fetal development and their administration (mainly dexamethasone, DEX) is a life-saving procedure for those at risk of preterm delivery, exposure to excess levels of GCs during pregnancy can yield detrimental consequences. Therefore, we aimed to systematically investigate the brain molecular alterations triggered by prenatal DEX administration. We used a rat model of depression based on prenatal exposure to DEX and performed integrative multi-level methylomic, transcriptomic, and proteomic analyses of adult rats' brains (i.e., frontal cortex (FCx) and hippocampus (Hp)) to identify the outcomes of DEX action. Each of the investigated levels was significantly affected by DEX in the long-term manner. Particularly, we found 200 CpG islands to be differentially methylated in the FCx and 200 in the Hp of prenatally DEX-treated rats. Global transcriptomic analysis uncovered differential expression of transcripts mostly in FCx (271) and 1 in Hp, while proteomic study identified 146 differentially expressed proteins in FCx and 123 in Hp. Among the identified enriched molecular networks, we found altered pathways involved in synaptic plasticity (i.e., cAMP, calcium, and Wnt signaling pathways or tight junctions and adhesion molecules), which may contribute to cognitive impairment, observed in DEX-treated animals. Moreover, in the FCx, DEX administration in the prenatal period downregulates the expression of ribosome protein genes associated both with large and small ribosomal subunit assembly which can lead to a global decrease in translation and protein synthesis processes and, indirectly, alterations in the neurotransmission process.

EPCO-06. DIFFUSE MIDLINE GLIOMAS: FROM CELL CYCLE TO THERAPEUTIC OPPORTUNITIES

Abstract The fatal Diffuse Midline Gliomas (DMG) are characterized by an undruggable H3K27M mutation in H3.1 or H3.3. K27M impairs normal development by stalling of differentiation. As replication timing influences gene expression, cell fate, and cellular response to therapeutics, we undertook a multi-omics approach (Repli-seq, cell cycle RNA-seq, single cell RNA-seq) in DMG cells (H3.1K27M and H3.3K27M subgroups) and tumors in comparison to normal brain to gain an appreciation for targetable pathways in DMG. DMG cells presented differential replication timing in each subgroup, which, in turn, correlated with significant differential gene expression including the cholesterol biosynthesis pathway. Consistent with these findings, DMG tumors presented high replication stress and cholesterol biosynthesis pathway signatures. Moreover, DMG cells were specifically vulnerable to an inhibitor of the cholesterol pathway and to a replication stress therapy, singly and in combination. In conclusion, this combinatorial genomics approach revealed insights into therapeutic opportunities for this incurable disease.

Reconstructing the regulatory programs underlying the phenotypic plasticity of neural cancers

Nervous system cancers exhibit diverse transcriptional cell states influenced by normal development, injury response, and growth. However, the understanding of these states’ regulation and pharmacological relevance remains limited. Here we present “single-cell regulatory-driven clustering” (scregclust), a method that reconstructs cellular regulatory programs from extensive collections of single-cell RNA sequencing (scRNA-seq) data from both tumors and developing tissues. The algorithm efficiently divides target genes into modules, predicting key transcription factors and kinases with minimal computational time. Applying this method to adult and childhood brain cancers, we identify critical regulators and suggest interventions that could improve temozolomide treatment in glioblastoma. Additionally, our integrative analysis reveals a meta-module regulated by SPI1 and IRF8 linked to an immune-mediated mesenchymal-like state. Finally, scregclust’s flexibility is demonstrated across 15 tumor types, uncovering both pan-cancer and specific regulators. The algorithm is provided as an easy-to-use R package that facilitates the exploration of regulatory programs underlying cell plasticity.

Research on Equity in Early Childhood Education in Western China: A Case Study of Sichuan Province

Abstract: This article investigates the issue of equity in early childhood education in Western China through interviews with ten kindergarten principals from the region. The study reveals several factors impacting educational fairness, including a vague understanding of the concept of educational equity, a lack of equitable practices in education, and the inability to ensure equal educational opportunities. Furthermore, the region faces a severe shortage of early childhood educational resources, instability within the teaching staff, difficulty in maintaining educational quality, and a lack of communication and cooperation among kindergartens. These issues contribute significantly to the imbalance of educational opportunities, severely affecting the normal development of children and the overall quality of preschool education. To address these challenges, the article recommends enhancing policy support to improve resource allocation and optimization, increasing professional training and compensation for teachers to strengthen the practice of equity in education, and raising societal awareness about the importance of educational equity. These measures are crucial for promoting equitable and high-quality education for every child in Western China, ensuring that all children have access to equal and quality educational opportunities.

Alteration of Cytoskeletal Proteins Leads to Retinal Degeneration in Drosophila.

The eye holds a special fascination for many neuroscientists because of its meticulously organized structure. Vertebrates typically possess a simple camera-type eye, whereas the compound eye structure is predominantly observed in arthropods including model organism Drosophila melanogaster. Cell shape, cell polarization, and tissue integrity are the cell biological processes crucial for shaping the eye, which directly or indirectly depends on the cytoskeleton. Henceforth the cytoskeleton, specifically actin microfilaments, essentially has a dynamic role in the normal development and growth of eye structure. This review provides insight into the roles played by the actin cytoskeleton during the development and maintenance of the Drosophila eye.