Journal of Developmental Biology最新文献

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Myotube Guidance: Shaping up the Musculoskeletal System. 肌管引导:塑造肌肉骨骼系统。
IF 2.2
Journal of Developmental Biology Pub Date : 2024-09-17 DOI: 10.3390/jdb12030025
Aaron N Johnson
{"title":"Myotube Guidance: Shaping up the Musculoskeletal System.","authors":"Aaron N Johnson","doi":"10.3390/jdb12030025","DOIUrl":"10.3390/jdb12030025","url":null,"abstract":"<p><p>Myofibers are highly specialized contractile cells of skeletal muscles, and dysregulation of myofiber morphogenesis is emerging as a contributing cause of myopathies and structural birth defects. Myotubes are the myofiber precursors and undergo a dramatic morphological transition into long bipolar myofibers that are attached to tendons on two ends. Similar to axon growth cones, myotube leading edges navigate toward target cells and form cell-cell connections. The process of myotube guidance connects myotubes with the correct tendons, orients myofiber morphology with the overall body plan, and generates a functional musculoskeletal system. Navigational signaling, addition of mass and volume, and identification of target cells are common events in myotube guidance and axon guidance, but surprisingly, the mechanisms regulating these events are not completely overlapping in myotubes and axons. This review summarizes the strategies that have evolved to direct myotube leading edges to predetermined tendon cells and highlights key differences between myotube guidance and axon guidance. The association of myotube guidance pathways with developmental disorders is also discussed.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11417883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Roles of the NR2F Family in the Development, Disease, and Cancer of the Lung. NR2F 家族在肺部发育、疾病和癌症中的作用。
IF 2.2
Journal of Developmental Biology Pub Date : 2024-09-10 DOI: 10.3390/jdb12030024
Jiaxin Yang, Wenjing Sun, Guizhong Cui
{"title":"Roles of the NR2F Family in the Development, Disease, and Cancer of the Lung.","authors":"Jiaxin Yang, Wenjing Sun, Guizhong Cui","doi":"10.3390/jdb12030024","DOIUrl":"10.3390/jdb12030024","url":null,"abstract":"<p><p>The NR2F family, including NR2F1, NR2F2, and NR2F6, belongs to the nuclear receptor superfamily. NR2F family members function as transcription factors and play essential roles in the development of multiple organs or tissues in mammals, including the central nervous system, veins and arteries, kidneys, uterus, and vasculature. In the central nervous system, NR2F1/2 coordinate with each other to regulate the development of specific brain subregions or cell types. In addition, NR2F family members are associated with various cancers, such as prostate cancer, breast cancer, and esophageal cancer. Nonetheless, the roles of the NR2F family in the development and diseases of the lung have not been systematically summarized. In this review, we mainly focus on the lung, including recent findings regarding the roles of the NR2F family in development, physiological function, and cancer.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11417824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Evolution and Spatiotemporal Expression of ankha and ankhb in Zebrafish. 斑马鱼ankha和ankhb的进化与时空表达
IF 2.2
Journal of Developmental Biology Pub Date : 2024-09-09 DOI: 10.3390/jdb12030023
Nuwanthika Wathuliyadde, Katherine E Willmore, Gregory M Kelly
{"title":"Evolution and Spatiotemporal Expression of <i>ankha</i> and <i>ankhb</i> in Zebrafish.","authors":"Nuwanthika Wathuliyadde, Katherine E Willmore, Gregory M Kelly","doi":"10.3390/jdb12030023","DOIUrl":"10.3390/jdb12030023","url":null,"abstract":"<p><p>Craniometaphyseal Dysplasia (CMD) is a rare skeletal disorder that can result from mutations in the <i>ANKH</i> gene. This gene encodes progressive anksylosis (ANK), which is responsible for transporting inorganic pyrophosphate (PPi) and ATP from the intracellular to the extracellular environment, where PPi inhibits bone mineralization. When ANK is dysfunctional, as in patients with CMD, the passage of PPi to the extracellular environment is reduced, leading to excess mineralization, particularly in bones of the skull. Zebrafish may serve as a promising model to study the mechanistic basis of CMD. Here, we provide a detailed analysis of the zebrafish Ankh paralogs, Ankha and Ankhb, in terms of their phylogenic relationship with ANK in other vertebrates as well as their spatiotemporal expression patterns during zebrafish development. We found that a closer evolutionary relationship exists between the zebrafish Ankhb protein and its human and other vertebrate counterparts, and stronger promoter activity was predicted for <i>ankhb</i> compared to <i>ankha.</i> Furthermore, we noted distinct temporal expression patterns, with <i>ankha</i> more prominently expressed in early development stages, and both paralogs also being expressed at larval growth stages. Whole-mount in situ hybridization was used to compare the spatial expression patterns of each paralog during bone development, and both showed strong expression in the craniofacial region as well as the notochord and somites. Given the substantial overlap in spatiotemporal expression but only subtle patterning differences, the exact roles of these genes remain speculative. In silico analyses predicted that Ankha and Ankhb have the same function in transporting PPi across the membrane. Nevertheless, this study lays the groundwork for functional analyses of each <i>ankh</i> paralog and highlights the potential of using zebrafish to find possible targeted therapies for CMD.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11417794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
From Germ Cells to Implantation: The Role of Extracellular Vesicles. 从生殖细胞到植入:细胞外囊泡的作用
IF 2.2
Journal of Developmental Biology Pub Date : 2024-08-23 DOI: 10.3390/jdb12030022
Anna Fazzio, Angela Caponnetto, Carmen Ferrara, Michele Purrello, Cinzia Di Pietro, Rosalia Battaglia
{"title":"From Germ Cells to Implantation: The Role of Extracellular Vesicles.","authors":"Anna Fazzio, Angela Caponnetto, Carmen Ferrara, Michele Purrello, Cinzia Di Pietro, Rosalia Battaglia","doi":"10.3390/jdb12030022","DOIUrl":"10.3390/jdb12030022","url":null,"abstract":"<p><p>Extracellular vesicles represent a large heterogeneous class of near and long-distance intercellular communication mediators, released by both prokaryotic and eukaryotic cells. Specifically, the scientific community has shown growing interest in exosomes, which are nano-sized vesicles with an endosomal origin. Not so long ago, the physiological goal of exosome generation was largely unknown and required more investigation; at first, it was hypothesized that exosomes are able to remove excess, reject and unnecessary constituents from cells to preserve cellular homeostasis. However, thanks to recent studies, the central role of exosomes in regulating cellular communication has emerged. Exosomes act as vectors in cell-cell signaling by their cargo, proteins, lipids, and nucleic acids, and influence physiological and pathological processes. The findings on exosomes are widespread in a large spectrum of biomedical applications from diagnosis and prognosis to therapies. In this review, we describe exosome biogenesis and the current methods for their isolation and characterization, emphasizing the role of their cargo in female reproductive processes, from gametogenesis to implantation, and the potential involvement in human female disorders.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11417829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lowered GnT-I Activity Decreases Complex-Type N-Glycan Amounts and Results in an Aberrant Primary Motor Neuron Structure in the Spinal Cord. GnT-I 活性降低会减少复合型 N-糖的数量,导致脊髓中的初级运动神经元结构异常。
IF 2.2
Journal of Developmental Biology Pub Date : 2024-08-16 DOI: 10.3390/jdb12030021
Cody J Hatchett, M Kristen Hall, Abel R Messer, Ruth A Schwalbe
{"title":"Lowered GnT-I Activity Decreases Complex-Type N-Glycan Amounts and Results in an Aberrant Primary Motor Neuron Structure in the Spinal Cord.","authors":"Cody J Hatchett, M Kristen Hall, Abel R Messer, Ruth A Schwalbe","doi":"10.3390/jdb12030021","DOIUrl":"10.3390/jdb12030021","url":null,"abstract":"<p><p>The attachment of sugar to proteins and lipids is a basic modification needed for organismal survival, and perturbations in glycosylation cause severe developmental and neurological difficulties. Here, we investigated the neurological consequences of N-glycan populations in the spinal cord of Wt AB and <i>mgat1b</i> mutant zebrafish. Mutant fish have reduced N-acetylglucosaminyltransferase-I (GnT-I) activity as <i>mgat1a</i> remains intact. GnT-I converts oligomannose N-glycans to hybrid N-glycans, which is needed for complex N-glycan production. MALDI-TOF MS profiles identified N-glycans in the spinal cord for the first time and revealed reduced amounts of complex N-glycans in mutant fish, supporting a lesion in <i>mgat1b</i>. Further lectin blotting showed that oligomannose N-glycans were more prevalent in the spinal cord, skeletal muscle, heart, swim bladder, skin, and testis in mutant fish relative to WT AB, supporting lowered GnT- I activity in a global manner. Developmental delays were noted in hatching and in the swim bladder. Microscopic images of caudal primary (CaP) motor neurons of the spinal cord transiently expressing EGFP in mutant fish were abnormal with significant reductions in collateral branches. Further motor coordination skills were impaired in mutant fish. We conclude that identifying the neurological consequences of aberrant N-glycan processing will enhance our understanding of the role of complex N-glycans in development and nervous system health.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11348029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Canonical and Non-Canonical Wnt Signaling Generates Molecular and Cellular Asymmetries to Establish Embryonic Axes. 典型和非典型 Wnt 信号产生分子和细胞不对称,从而建立胚轴
IF 2.2
Journal of Developmental Biology Pub Date : 2024-08-02 DOI: 10.3390/jdb12030020
De-Li Shi
{"title":"Canonical and Non-Canonical Wnt Signaling Generates Molecular and Cellular Asymmetries to Establish Embryonic Axes.","authors":"De-Li Shi","doi":"10.3390/jdb12030020","DOIUrl":"10.3390/jdb12030020","url":null,"abstract":"<p><p>The formation of embryonic axes is a critical step during animal development, which contributes to establishing the basic body plan in each particular organism. Wnt signaling pathways play pivotal roles in this fundamental process. Canonical Wnt signaling that is dependent on β-catenin regulates the patterning of dorsoventral, anteroposterior, and left-right axes. Non-canonical Wnt signaling that is independent of β-catenin modulates cytoskeletal organization to coordinate cell polarity changes and asymmetric cell movements. It is now well documented that components of these Wnt pathways biochemically and functionally interact to mediate cell-cell communications and instruct cellular polarization in breaking the embryonic symmetry. The dysfunction of Wnt signaling disrupts embryonic axis specification and proper tissue morphogenesis, and mutations of Wnt pathway genes are associated with birth defects in humans. This review discusses the regulatory roles of Wnt pathway components in embryonic axis formation by focusing on vertebrate models. It highlights current progress in decoding conserved mechanisms underlying the establishment of asymmetry along the three primary body axes. By providing an in-depth analysis of canonical and non-canonical pathways in regulating cell fates and cellular behaviors, this work offers insights into the intricate processes that contribute to setting up the basic body plan in vertebrate embryos.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11348223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Genes Related to Frontonasal Malformations Are Regulated by miR-338-5p, miR-653-5p, and miR-374-5p in O9-1 Cells O9-1细胞中与前鼻孔畸形有关的基因受miR-338-5p、miR-653-5p和miR-374-5p调控
IF 2.2
Journal of Developmental Biology Pub Date : 2024-07-06 DOI: 10.3390/jdb12030019
C. Iwaya, Sunny Yu, J. Iwata
{"title":"Genes Related to Frontonasal Malformations Are Regulated by miR-338-5p, miR-653-5p, and miR-374-5p in O9-1 Cells","authors":"C. Iwaya, Sunny Yu, J. Iwata","doi":"10.3390/jdb12030019","DOIUrl":"https://doi.org/10.3390/jdb12030019","url":null,"abstract":"Frontonasal malformations are caused by a failure in the growth of the frontonasal prominence during development. Although genetic studies have identified genes that are crucial for frontonasal development, it remains largely unknown how these genes are regulated during this process. Here, we show that microRNAs, which are short non-coding RNAs capable of targeting their target mRNAs for degradation or silencing their expression, play a crucial role in the regulation of genes related to frontonasal development in mice. Using the Mouse Genome Informatics (MGI) database, we curated a total of 25 mouse genes related to frontonasal malformations, including frontonasal hypoplasia, frontonasal dysplasia, and hypotelorism. MicroRNAs regulating the expression of these genes were predicted through bioinformatic analysis. We then experimentally evaluated the top three candidate miRNAs (miR-338-5p, miR-653-5p, and miR-374c-5p) for their effect on cell proliferation and target gene regulation in O9-1 cells, a neural crest cell line. Overexpression of these miRNAs significantly inhibited cell proliferation, and the genes related to frontonasal malformations (Alx1, Lrp2, and Sirt1 for miR-338-5p; Alx1, Cdc42, Sirt1, and Zic2 for miR-374c-5p; and Fgfr2, Pgap1, Rdh10, Sirt1, and Zic2 for miR-653-5p) were directly regulated by these miRNAs in a dose-dependent manner. Taken together, our results highlight miR-338-5p, miR-653-5p, and miR-374c-5p as pathogenic miRNAs related to the development of frontonasal malformations.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141671551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Getting to the Core: Exploring the Embryonic Development from Notochord to Nucleus Pulposus 深入核心:探索从脊索到核浆的胚胎发育过程
IF 2.2
Journal of Developmental Biology Pub Date : 2024-07-03 DOI: 10.3390/jdb12030018
L. Ambrosio, Jordy Schol, C. Ruiz-Fernández, Shota Tamagawa, Kieran Joyce, Akira Nomura, Elisabetta de Rinaldis, Daisuke Sakai, R. Papalia, G. Vadalà, Vincenzo Denaro
{"title":"Getting to the Core: Exploring the Embryonic Development from Notochord to Nucleus Pulposus","authors":"L. Ambrosio, Jordy Schol, C. Ruiz-Fernández, Shota Tamagawa, Kieran Joyce, Akira Nomura, Elisabetta de Rinaldis, Daisuke Sakai, R. Papalia, G. Vadalà, Vincenzo Denaro","doi":"10.3390/jdb12030018","DOIUrl":"https://doi.org/10.3390/jdb12030018","url":null,"abstract":"The intervertebral disc (IVD) is the largest avascular organ of the human body and plays a fundamental role in providing the spine with its unique structural and biomechanical functions. The inner part of the IVD contains the nucleus pulposus (NP), a gel-like tissue characterized by a high content of type II collagen and proteoglycans, which is crucial for the disc’s load-bearing and shock-absorbing properties. With aging and IVD degeneration (IDD), the NP gradually loses its physiological characteristics, leading to low back pain and additional sequelae. In contrast to surrounding spinal tissues, the NP presents a distinctive embryonic development since it directly derives from the notochord. This review aims to explore the embryology of the NP, emphasizing the pivotal roles of key transcription factors, which guide the differentiation and maintenance of the NP cellular components from the notochord and surrounding sclerotome. Through an understanding of NP development, we sought to investigate the implications of the critical developmental aspects in IVD-related pathologies, such as IDD and the rare malignant chordomas. Moreover, this review discusses the therapeutic strategies targeting these pathways, including the novel regenerative approaches leveraging insights from NP development and embryology to potentially guide future treatments.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.2,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141683857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Rho-Associated Protein Kinase Activity Is Required for Tissue Homeostasis in the Xenopus laevis Ciliated Epithelium 章鱼纤毛上皮细胞的组织稳态需要 Rho 相关蛋白激酶的活性
IF 2.7
Journal of Developmental Biology Pub Date : 2024-06-11 DOI: 10.3390/jdb12020017
Fayhaa Khan, L. Pitstick, Jessica Lara, Rosa Ventrella
{"title":"Rho-Associated Protein Kinase Activity Is Required for Tissue Homeostasis in the Xenopus laevis Ciliated Epithelium","authors":"Fayhaa Khan, L. Pitstick, Jessica Lara, Rosa Ventrella","doi":"10.3390/jdb12020017","DOIUrl":"https://doi.org/10.3390/jdb12020017","url":null,"abstract":"Lung epithelial development relies on the proper balance of cell proliferation and differentiation to maintain homeostasis. When this balance is disturbed, it can lead to diseases like cancer, where cells undergo hyperproliferation and then can undergo migration and metastasis. Lung cancer is one of the deadliest cancers, and even though there are a variety of therapeutic approaches, there are cases where treatment remains elusive. The rho-associated protein kinase (ROCK) has been thought to be an ideal molecular target due to its role in activating oncogenic signaling pathways. However, in a variety of cases, inhibition of ROCK has been shown to have the opposite outcome. Here, we show that ROCK inhibition with y-27632 causes abnormal epithelial tissue development in Xenopus laevis embryonic skin, which is an ideal model for studying lung cancer development. We found that treatment with y-27632 caused an increase in proliferation and the formation of ciliated epithelial outgrowths along the tail edge. Our results suggest that, in certain cases, ROCK inhibition can disturb tissue homeostasis. We anticipate that these findings could provide insight into possible mechanisms to overcome instances when ROCK inhibition results in heightened proliferation. Also, these findings are significant because y-27632 is a common pharmacological inhibitor used to study ROCK signaling, so it is important to know that in certain in vivo developmental models and conditions, this treatment can enhance proliferation rather than lead to cell cycle suppression.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141355421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Harderian Gland Development and Degeneration in the Fgf10- Deficient Heterozygous Mouse Fgf10 基因缺陷杂合子小鼠硬腺的发育和退化
IF 2.7
Journal of Developmental Biology Pub Date : 2024-06-03 DOI: 10.3390/jdb12020016
Shiori Ikeda, Keita Sato, Hirofumi Fujita, Hitomi Ono-Minagi, Satoru Miyaishi, Tsutomu Nohno, Hideyo Ohuchi
{"title":"Harderian Gland Development and Degeneration in the Fgf10- Deficient Heterozygous Mouse","authors":"Shiori Ikeda, Keita Sato, Hirofumi Fujita, Hitomi Ono-Minagi, Satoru Miyaishi, Tsutomu Nohno, Hideyo Ohuchi","doi":"10.3390/jdb12020016","DOIUrl":"https://doi.org/10.3390/jdb12020016","url":null,"abstract":"The mouse Harderian gland (HG) is a secretory gland that covers the posterior portion of the eyeball, opening at the base of the nictitating membrane. The HG serves to protect the eye surface from infection with its secretions. Mice open their eyelids at about 2 weeks of age, and the development of the HG primordium mechanically opens the eye by pushing the eyeball from its rear. Therefore, when HG formation is disturbed, the eye exhibits enophthalmos (the slit-eye phenotype), and a line of Fgf10+/− heterozygous loss-of-function mice exhibits slit-eye due to the HG atrophy. However, it has not been clarified how and when HGs degenerate and atrophy in Fgf10+/− mice. In this study, we observed the HGs in embryonic (E13.5 to E19), postnatal (P0.5 to P18) and 74-week-old Fgf10+/− mice. We found that more than half of the Fgf10+/− mice had markedly degenerated HGs, often unilaterally. The degenerated HG tissue had a melanized appearance and was replaced by connective tissue, which was observed by P10. The development of HGs was delayed or disrupted in the similar proportion of Fgf10+/− embryos, as revealed via histology and the loss of HG-marker expression. In situ hybridization showed Fgf10 expression was observed in the Harderian mesenchyme in wild-type as well as in the HG-lacking heterozygote at E19. These results show that the Fgf10 haploinsufficiency causes delayed or defective HG development, often unilaterally from the unexpectedly early neonatal period.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141269102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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