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Nonmuscular Troponin-I is required for gastrulation in sea urchin embryos 海胆胚胎的胃形成需要非肌肉型肌钙蛋白-I
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-12-10 DOI: 10.1002/dvdy.680
Mai Kamata, Yuri Taniguchi, Junko Yaguchi, Hiroyuki Tanaka, Shunsuke Yaguchi

Background

Gastrulation is one of the most important events in our lives (Barresi and Gilbert, 2020, Developmental Biology, 12th ed.). The molecular mechanisms of gastrulation in multicellular organisms are not yet fully understood, since many molecular, physical, and chemical factors are involved in the event.

Results

Here, we found that one of muscle components, Troponin-I (TnI), is expressed in future gut cells, which are not muscular cells at all, and regulates gastrulation in embryos of a sea urchin, Hemicentrotus pulcherrimus. When we block the function of TnI, the invagination was inhibited in spite that the gut-cell specifier gene is normally expressed. In addition, blocking myosin activity also induced incomplete gastrulation.

Conclusion

These results strongly suggested that TnI regulates nonmuscular actin–myosin interactions during sea urchin gastrulation. So far, Troponin system is treated as specific only for muscle components, especially for striated muscle, but our data clearly show that TnI is involved in nonmuscular event. It is also reported that recent sensitive gene expression analysis revealed that Troponin genes are expressed in nonmuscular tissues in mammals (Ono et al., Sci Data, 2017;4:170105). These evidences propose the new evolutionary and functional scenario of the involvement of Troponin system in nonmuscular cell behaviors using actin-myosin system in bilaterians including human being.

胃形成是我们生命中最重要的事件之一(Barresi 和 Gilbert,2020 年,《发育生物学》,第 12 版)。多细胞生物胃形成的分子机制尚未完全明了,因为许多分子、物理和化学因素都参与了这一过程。
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引用次数: 0
Elevated Id2 expression causes defective meiosis and spermatogenesis in mice Id2 表达升高导致小鼠减数分裂和精子发生缺陷
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-12-08 DOI: 10.1002/dvdy.676
Zhen He, Rong-Ge Yan, Qin-Bang Shang, Qi-En Yang

Background

Inhibitors of DNA binding (ID) proteins mainly inhibit gene expression and regulate cell fate decisions by interacting with E-proteins. All four ID proteins (ID1–4) are present in the testis, and ID4 has a particularly important role in spermatogonial stem cell fate determination. Several lines of evidence indicate that ID proteins are involved in meiosis; however, functional experiments have not been conducted to validate this observation.

Results

In this study, we report that ID2 is enriched in spermatocytes and that forced ID2 expression in germ cells causes defects in spermatogenesis. A detailed analysis demonstrated that Id2 overexpression (Id2 OE) decreased the total number of spermatogonia and changed the dynamics of meiosis progression. Specifically, spermatocytes were enriched in the zygotene stage, and the proportion of pachytene spermatocytes was significantly decreased, indicating defects in the zygotene–pachytene transition. The number of MLH1-positive foci per cell was decreased in pachytene spermatocytes from Id2 OE testes, suggesting abnormalities in recombination. Transcriptome analysis revealed that forced Id2 expression changed the expression of a list of genes mainly associated with meiosis and spermatid development.

Conclusions

ID2 protein is expressed in spermatocytes, and its genetic ablation in the germline does not affect spermatogenesis, likely due to genetic compensation of its family members. However, forced Id2 expression changes meiosis progression and causes defects in spermiogenesis. These data provide important evidence that ID proteins play pivotal roles in male meiosis and spermatid development.

DNA结合抑制蛋白(ID)主要通过与E蛋白相互作用来抑制基因表达和调节细胞命运决定。所有四种ID蛋白(ID1-4)都存在于睾丸中,其中ID4在精原干细胞命运决定中起着特别重要的作用。一些证据表明,ID 蛋白参与了减数分裂过程;然而,尚未进行功能实验来验证这一观察结果。
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引用次数: 0
Editorial highlights 社论强调。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-12-01 DOI: 10.1002/dvdy.679
Paul A. Trainor
<p>Every organism is a model organism for understanding development, evolution, disease, and regeneration, and we have only begun to scratch the surface of the interdisciplinary genetic, molecular, cellular, and developmental mechanisms that regulate these biological processes. These “Highlights” denote exciting advances recently reported in <i>Developmental Dynamics</i> that illustrate the complex dynamics of developmental biology.</p><p><b>Xenopus Ectoderm Patterning.</b> “The sulfotransferase XB5850668.L is required to apportion embryonic ectodermal domains’ by Alexander Marchak, Karen Neilson, Himani Majumdar, Kiyoshi Yamauchi, Steven Klein and Sally Moody; <i>DevDyn</i> 252:12, https://doi.org/10.1002/dvdy.648. Six1 is a transcription factor required for patterning the embryonic ectoderm into neural plate, neural crest, preplacodal and epidermal domains, and mutations in <i>SIX1</i> in humans are causative for Branchio-oto-renal (BOR), and Deafness, autosomal dominant 23 (DFNA23) syndromes. In this study, screening for Six1 targets identified a previously uncharacterized sulfotransferase. Sulfotransferases, catalyze the transfer of a sulfuryl (SO3) group from a donor to a substrate, and have been studied extensively in adult tissues where they play important roles in detoxifying compounds and metabolizing drugs. Loss, and gain-of-function analyses in <i>Xenopus</i> embryos reveals for the first time that sulfotransferases play regulate early craniofacial development by balancing the proportional specifical of the embryonic ectoderm into presumptive neural plate versus neural crest and cranial placode tissues. Variants in Sulfotransferase genes could therefore be potential new candidates for BOR and DFNA23 syndromes.</p><p><b>Pharyngeal Development</b> “Foxi3GFP and Foxi3CreER mice allow identification and lineage labeling of pharyngeal arch ectoderm and endoderm, and tooth and hair placodes” by Harinarayana Ankamreddy, Ankita Thawani, Onur Birol, Hongyuan Zhang, and Andrew Groves, <i>DevDyn</i> 252:12; https://doi.org/10.1002/dvdy.645. Pharyngeal arches are transient embryonic structures that give rise to many craniofacial structures including the lower jaw, middle and external ears, and endoderm derived organs such as the thymus, thyroid and parathyroid. FOXI3 is a forkhead family transcription factor that is expressed in the progenitors of craniofacial placodes, epidermal placodes, and the ectoderm and endoderm of the pharyngeal arch region. This study generated new Foxi3GFP and Foxi3CreER genetic tools for studying pharyngeal development. Foxi3GFP mice recapitulate the expression patterns of Foxi3 mRNA, and Foxi3CreER mice can trace the derivatives of pharyngeal arch ectoderm and endoderm, the pharyngeal pouches and clefts that separate each arch, and the derivatives of hair and tooth placodes.</p><p><b>Zebrafish Metalloproteases</b> “Dynamic and Broad Expression of adamts9 in Developing and Adult Zebrafish” by Yuanfa He, Jonathan Carver,
每一种生物都是理解发育、进化、疾病和再生的模式生物,而我们才刚刚开始触及调节这些生物过程的跨学科遗传、分子、细胞和发育机制的表面。这些“亮点”表示最近在《发育动力学》上报道的令人兴奋的进展,这些进展说明了发育生物学的复杂动力学。爪蟾外胚层图案。“硫转移酶XB5850668。Alexander Marchak、Karen Neilson、Himani Majumdar、Kiyoshi Yamauchi、Steven Klein和Sally Moody的研究表明,L是分配胚胎外胚层域所必需的;DevDyn 252:12, https://doi.org/10.1002/dvdy.648。Six1是胚胎外胚层形成神经板、神经嵴、胎盘前区和表皮结构域所需的转录因子,人类Six1的突变可导致耳肾支(BOR)、耳聋、常染色体显性23 (DFNA23)综合征。在这项研究中,筛选Six1靶点发现了一种以前未被表征的硫转移酶。硫基转移酶,催化硫基(SO3)基团从供体转移到底物,在成人组织中被广泛研究,它们在解毒化合物和代谢药物中起重要作用。非洲爪蟾胚胎的功能缺失和功能获得分析首次揭示了硫转移酶通过平衡胚胎外胚层形成神经板、神经嵴和颅板组织的比例特异性来调节早期颅面发育。因此,硫转移酶基因的变异可能是BOR和DFNA23综合征的潜在新候选者。Harinarayana Ankamreddy, Ankita Thawani, Onur Birol, Hongyuan Zhang, Andrew Groves,《Foxi3GFP和Foxi3CreER小鼠允许对咽前外表皮和内表皮以及牙齿和毛发基板进行鉴定和谱系标记》,DevDyn, 52:12;https://doi.org/10.1002/dvdy.645。咽弓是一种短暂的胚胎结构,可发育为许多颅面结构,包括下颌、中耳和外耳,以及内胚层衍生器官,如胸腺、甲状腺和甲状旁腺。FOXI3是叉头家族转录因子,在颅面基板、表皮基板以及咽弓区外胚层和内胚层的祖细胞中表达。本研究为研究咽发育提供了新的fox3gfp和fox3creer遗传工具。fox3gfp小鼠概括了fox3mrna的表达模式,fox3creer小鼠可以追踪咽部弓外胚层和内胚层的衍生物,咽部弓的囊袋和间隙,以及毛发和牙齿基板的衍生物。何元发,Jonathan Carver, Timothy Erickson, Pierre Le Pabic,朱勇,“发育和成年斑马鱼中adamts9的动态和广泛表达”;DevDyn 252:12, https://doi.org/10.1002/dvdy.643。金属蛋白酶在形态发生、组织重塑、细胞迁移和细胞信号传导等方面发挥着重要作用。本研究报道了一种新的转基因斑马鱼报告系Tg(adamts9:EGFP)的产生和表征,以在细胞水平上可视化adamts9的活性。adamts9在胚胎和成人中的表达模式表明,进化保守的金属蛋白酶参与眼睛、脊髓和卵巢发育、生理功能和病理生理过程。
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引用次数: 0
Exploring the role of mechanical forces on tendon development using in vivo model: A scoping review 使用体内模型探索机械力在肌腱发育中的作用:范围界定综述。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-11-10 DOI: 10.1002/dvdy.673
Yuna Usami, Hirotaka Iijima, Takanori Kokubun

Tendons transmit the muscle contraction forces to bones and drive joint movement throughout life. While extensive research have indicated the essentiality of mechanical forces on tendon development, a comprehensive understanding of the fundamental role of mechanical forces still needs to be impaerted. This scoping review aimed to summarize the current knowledge about the role of mechanical forces during the tendon developmental phase. The electronic database search using PubMed, performed in May 2023, yielded 651 articles, of which 16 met the prespecified inclusion criteria. We summarized and divided the methods to reduce the mechanical force into three groups: loss of muscle, muscle dysfunction, and weight-bearing regulation. In contrast, there were few studies to analyze the increased mechanical force model. Most studies suggested that mechanical force has some roles in tendon development in the embryo to postnatal phase. However, we identified species variability and methodological heterogeneity to modulate mechanical force. To establish a comprehensive understanding, methodological commonality to modulate the mechanical force is needed in this field. Additionally, summarizing chronological changes in developmental processes across animal species helps to understand the essence of developmental tendon mechanobiology. We expect that the findings summarized in the current review serve as a groundwork for future study in the fields of tendon developmantal biology and mechanobiology.

肌腱将肌肉收缩力传递给骨骼,并在一生中驱动关节运动。尽管广泛的研究表明了机械力对肌腱发育的重要性,但对机械力的基本作用仍需全面了解。本范围综述旨在总结目前关于肌腱发育阶段机械力作用的知识。2023年5月,使用PubMed进行的电子数据库搜索共产生651篇文章,其中16篇符合预先指定的纳入标准。我们总结并将减少机械力的方法分为三组:肌肉损失、肌肉功能障碍和负重调节。相比之下,很少有研究来分析增加的机械力模型。大多数研究表明,机械力在胚胎至出生后阶段的肌腱发育中起着一定作用。然而,我们发现了调节机械力的物种变异性和方法学异质性。为了建立全面的理解,在该领域需要调节机械力的方法通用性。此外,总结动物物种发育过程的时间变化有助于理解发育肌腱机械生物学的本质。我们希望本综述中总结的发现为肌腱发育生物学和机械生物学领域的未来研究奠定基础。
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引用次数: 0
Editorial highlights 编辑亮点。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-11-01 DOI: 10.1002/dvdy.675
Paul A. Trainor
<p>Every organism is a model organism for understanding development, evolution, disease, and regeneration, and we have only begun to scratch the surface of the interdisciplinary genetic, molecular, cellular, and developmental mechanisms that regulate these biological processes. These “Highlights” denote exciting advances recently reported in <i>Developmental Dynamics</i> that illustrate the complex dynamics of developmental biology.</p><p><b>Zebrafish Neurogenesis.</b> “Plexina4 and cell survival in the developing zebrafish hindbrain” by Zachary Nurcombe, Carrie Lynn Hehr, and Sarah McFarlane; DevDyn 252:11, pp. 1323–1337, https://doi.org/10.1002/dvdy.633. Apoptosis plays a fundamental role in normal embryo development and tissue homeostasis. For example, during nervous system development, neurons are initially overproduced but then pruned through programmed cell death. Plexins (PLXNs) are transmembrane receptors for a class of guidance proteins known as Semaphorins (SEMAs) and control the directed movements of migrating neurons and extending axons. But what about proliferation? <i>plxna4</i> is dynamically expressed within the developing embryonic brain, including the hindbrain, and in this paper CRISPR mediated gene editing of zebrafish demonstrates that <i>plxna4</i> plays a critical role in neuronal survival during zebrafish hindbrain development. This has implications for neurodegenerative disorders since <i>PLXNA4</i> is implicated in Alzheimer’s Disease.</p><p><b>Retina Development</b> “A framework to identify functional interactors that contribute to disrupted early retinal development in Vsx2 ocular retardation J mice” by Amanda Leung, Mahesh Rao, Nathan Raju, Minh Chung, Allison Klinger, DiAnna Rowe, Xiaodong Li, and Edward Levine; DevDyn 252:11, pp. 1338–1362, https://doi.org/10.1002/dvdy.629. <i>The Visual System Homeobox</i> 2 (<i>Vsx2</i>) gene is initially expressed in retinal progenitor cells where it regulates retinal neurogenesis before ultimately resolving to bipolar cells and Müller glia. Mutations in <i>VSX2</i> in humans cause bilateral congenital microphthalmia, disrupted retinal architecture, and lifelong blindness. The recessive loss-of-function ocular retardation J allele encodes a premature stop codon in the mouse Vsx2 homeodomain. Combining <i>in vivo</i> and <i>ex vivo</i> testing with transcriptome analysis revealed interactions between Vsx2, Mitf, RXR, and gamma-Secretase activities during retinal development, and provides a platform that could be adapted to other gene mutations with complex phenotypes.</p><p><b>Cartilage Development and Evolution</b> “Common features of cartilage maturation are not conserved in an amphibian model” by Jason Nguyen, Patsy Gómez-Picos, Yiwen Liu, Katie Ovens, and B. Frank Eames; DevDyn 252:11, pp. 1375–1390, https://doi.org/10.1002/dvdy.594. Cartilage is a flexible connective tissue made up of specialized cells called chondrocytes. It is replaced by bone in many parts of the body thro
每一种生物都是理解发育、进化、疾病和再生的模式生物,而我们才刚刚开始触及调节这些生物过程的跨学科遗传、分子、细胞和发育机制的表面。这些“亮点”表示最近在《发育动力学》上报道的令人兴奋的进展,这些进展说明了发育生物学的复杂动力学。斑马鱼神经发生。Zachary Nurcombe、Carrie Lynn Hehr和Sarah McFarlane的《斑马鱼后脑发育中的神经丛和细胞存活》;DevDyn 252:11, pp. 1323-1337, https://doi.org/10.1002/dvdy.633。细胞凋亡在正常胚胎发育和组织稳态中起着重要作用。例如,在神经系统发育过程中,神经元最初产生过多,但随后通过程序性细胞死亡而被修剪。丛蛋白(PLXNs)是一类被称为信号蛋白(SEMAs)的指导蛋白的跨膜受体,并控制迁移神经元和延伸轴突的定向运动。但是核扩散呢?plxna4在发育中的胚胎脑包括后脑内是动态表达的,本文通过CRISPR介导的斑马鱼基因编辑证实了plxna4在斑马鱼后脑发育过程中对神经元存活起着关键作用。这对神经退行性疾病有影响,因为PLXNA4与阿尔茨海默病有关。由Amanda Leung、Mahesh Rao、Nathan Raju、Minh Chung、Allison Klinger、DiAnna Rowe、Xiaodong Li和Edward Levine撰写的《识别Vsx2眼发育迟滞小鼠早期视网膜发育中断的功能相互作用的框架》;DevDyn 252:11, pp. 1338-1362, https://doi.org/10.1002/dvdy.629。Visual System Homeobox 2 (Vsx2)基因最初在视网膜祖细胞中表达,在那里它调节视网膜神经发生,然后最终分化到双极细胞和神经胶质细胞。人类VSX2基因突变可导致双侧先天性小眼症、视网膜结构破坏和终身失明。隐性功能障碍J等位基因在小鼠Vsx2同源结构域中编码一个过早停止密码子。结合体内和体外测试和转录组分析,揭示了Vsx2、Mitf、RXR和γ -分泌酶在视网膜发育过程中的相互作用,并为适应其他复杂表型的基因突变提供了一个平台。“软骨成熟的共同特征在两栖动物模型中并不保守”,作者:Jason Nguyen, Patsy Gómez-Picos, Yiwen Liu, Katie Ovens和B. Frank Eames;DevDyn 252:11, pp. 1375-1390, https://doi.org/10.1002/dvdy.594。软骨是一种灵活的结缔组织,由称为软骨细胞的特殊细胞组成。通过软骨内成骨的过程,它在身体的许多部位被骨头取代。我们对骨骼发育的大部分知识来自于对鸡和小鼠模型的研究,在这些模型中,软骨在软骨内成骨过程中的成熟是一个渐进的过程。本研究验证了在热带水陆两栖动物中软骨成熟的标准过程是保守的假设。尽管长骨软骨形成遵循一个相对保守的成熟过程,但幼虫头部软骨,如角鼻软骨,在时间和基因表达上与软骨成熟的标准过程有显著差异。这些在两栖动物身上的发现具有进化和健康意义。
{"title":"Editorial highlights","authors":"Paul A. Trainor","doi":"10.1002/dvdy.675","DOIUrl":"10.1002/dvdy.675","url":null,"abstract":"&lt;p&gt;Every organism is a model organism for understanding development, evolution, disease, and regeneration, and we have only begun to scratch the surface of the interdisciplinary genetic, molecular, cellular, and developmental mechanisms that regulate these biological processes. These “Highlights” denote exciting advances recently reported in &lt;i&gt;Developmental Dynamics&lt;/i&gt; that illustrate the complex dynamics of developmental biology.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Zebrafish Neurogenesis.&lt;/b&gt; “Plexina4 and cell survival in the developing zebrafish hindbrain” by Zachary Nurcombe, Carrie Lynn Hehr, and Sarah McFarlane; DevDyn 252:11, pp. 1323–1337, https://doi.org/10.1002/dvdy.633. Apoptosis plays a fundamental role in normal embryo development and tissue homeostasis. For example, during nervous system development, neurons are initially overproduced but then pruned through programmed cell death. Plexins (PLXNs) are transmembrane receptors for a class of guidance proteins known as Semaphorins (SEMAs) and control the directed movements of migrating neurons and extending axons. But what about proliferation? &lt;i&gt;plxna4&lt;/i&gt; is dynamically expressed within the developing embryonic brain, including the hindbrain, and in this paper CRISPR mediated gene editing of zebrafish demonstrates that &lt;i&gt;plxna4&lt;/i&gt; plays a critical role in neuronal survival during zebrafish hindbrain development. This has implications for neurodegenerative disorders since &lt;i&gt;PLXNA4&lt;/i&gt; is implicated in Alzheimer’s Disease.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Retina Development&lt;/b&gt; “A framework to identify functional interactors that contribute to disrupted early retinal development in Vsx2 ocular retardation J mice” by Amanda Leung, Mahesh Rao, Nathan Raju, Minh Chung, Allison Klinger, DiAnna Rowe, Xiaodong Li, and Edward Levine; DevDyn 252:11, pp. 1338–1362, https://doi.org/10.1002/dvdy.629. &lt;i&gt;The Visual System Homeobox&lt;/i&gt; 2 (&lt;i&gt;Vsx2&lt;/i&gt;) gene is initially expressed in retinal progenitor cells where it regulates retinal neurogenesis before ultimately resolving to bipolar cells and Müller glia. Mutations in &lt;i&gt;VSX2&lt;/i&gt; in humans cause bilateral congenital microphthalmia, disrupted retinal architecture, and lifelong blindness. The recessive loss-of-function ocular retardation J allele encodes a premature stop codon in the mouse Vsx2 homeodomain. Combining &lt;i&gt;in vivo&lt;/i&gt; and &lt;i&gt;ex vivo&lt;/i&gt; testing with transcriptome analysis revealed interactions between Vsx2, Mitf, RXR, and gamma-Secretase activities during retinal development, and provides a platform that could be adapted to other gene mutations with complex phenotypes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Cartilage Development and Evolution&lt;/b&gt; “Common features of cartilage maturation are not conserved in an amphibian model” by Jason Nguyen, Patsy Gómez-Picos, Yiwen Liu, Katie Ovens, and B. Frank Eames; DevDyn 252:11, pp. 1375–1390, https://doi.org/10.1002/dvdy.594. Cartilage is a flexible connective tissue made up of specialized cells called chondrocytes. It is replaced by bone in many parts of the body thro","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"252 11","pages":"1322"},"PeriodicalIF":2.5,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71421582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Kdm7a expression is spatiotemporally regulated in developing Xenopus laevis embryos, and its overexpression influences late retinal development Kdm7a的表达在发育中的非洲爪蟾胚胎中受到时空调控,其过表达影响视网膜发育后期。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-11-01 DOI: 10.1002/dvdy.670
Davide Martini, Matteo Digregorio, Ilaria Anna Pia Voto, Giuseppe Morabito, Andrea Degl'Innocenti, Guido Giudetti, Martina Giannaccini, Massimiliano Andreazzoli

Background

Post-translational histone modifications are among the most common epigenetic modifications that orchestrate gene expression, playing a pivotal role during embryonic development and in various pathological conditions. Among histone lysine demethylases, KDM7A, also known as KIAA1718 or JHDM1D, catalyzes the demethylation of H3K9me1/2 and H3K27me1/2, leading to transcriptional regulation. Previous data suggest that KDM7A plays a central role in several biological processes, including cell proliferation, commitment, differentiation, apoptosis, and maintenance. However, information on the expression pattern of KDM7A in whole organisms is limited, and its functional role is still unclear.

Results

In Xenopus development, kdm7a is expressed early, undergoing spatiotemporal regulation in various organs and tissues, including the central nervous system and the eye. Focusing on retinal development, we found that kdm7a overexpression does not affect the expression of genes critically involved in early neural development and eye-field specification, whereas unbalances the distribution of neural cell subtypes in the mature retina by disfavoring the development of ganglion cells while promoting that of horizontal cells.

Conclusions

Kdm7a is dynamically expressed during embryonic development, and its overexpression influences late retinal development, suggesting a potential involvement in the molecular machinery regulating the spatiotemporally ordered generation of retinal neuronal subtypes.

背景:翻译后组蛋白修饰是协调基因表达的最常见的表观遗传学修饰之一,在胚胎发育和各种病理条件下发挥着关键作用。在组蛋白赖氨酸去甲基化酶中,KDM7A,也称为KIAA1718或JHDM1D,催化H3K9me1/2和H3K27me1/2的去甲基化,导致转录调控。先前的数据表明,KDM7A在几个生物学过程中发挥着核心作用,包括细胞增殖、分化、凋亡和维持。然而,关于KDM7A在整个生物体中的表达模式的信息有限,其功能作用尚不清楚。结果:在爪蟾的发育过程中,kdm7a早期表达,在包括中枢神经系统和眼睛在内的各种器官和组织中经历时空调控。关注视网膜发育,我们发现kdm7a过表达不会影响与早期神经发育和视野规范密切相关的基因的表达,而通过不利于神经节细胞的发育而促进水平细胞的发育,从而不平衡神经细胞亚型在成熟视网膜中的分布。结论:Kdm7a在胚胎发育过程中动态表达,其过表达影响视网膜发育后期,表明其可能参与调节视网膜神经元亚型时空有序生成的分子机制。
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引用次数: 0
wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis wnt10a是斑马鱼中鳍折叠维持和成年非成对鳍变态所必需的。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-10-23 DOI: 10.1002/dvdy.672
Erica L. Benard, Ismail Küçükaylak, Julia Hatzold, Kilian U. W. Berendes, Thomas J. Carney, Filippo Beleggia, Matthias Hammerschmidt

Background

Mutations of human WNT10A are associated with odonto-ectodermal dysplasia syndromes. Here, we present analyses of wnt10a loss-of-function mutants in the zebrafish.

Results

wnt10a mutant zebrafish embryos display impaired tooth development and a collapsing median fin fold (MFF). Rescue experiments show that wnt10a is essential for MFF maintenance both during embryogenesis and later metamorphosis. The MFF collapse could not be attributed to increased cell death or altered proliferation rates of MFF cell types. Rather, wnt10a mutants show reduced expression levels of dlx2a in distal-most MFF cells, followed by compromised expression of col1a1a and other extracellular matrix proteins encoding genes. Transmission electron microscopy analysis shows that although dermal MFF compartments of wnt10a mutants initially are of normal morphology, with regular collagenous actinotrichia, positioning of actinotrichia within the cleft of distal MFF cells becomes compromised, coinciding with actinotrichia shrinkage and MFF collapse.

Conclusions

MFF collapse of wnt10a mutant zebrafish is likely caused by the loss of distal properties in the developing MFF, strikingly similar to the proposed molecular pathomechanisms underlying the teeth defects caused by the loss of Wnt10 in fish and mammals. In addition, it points to thus fur unknown mechanisms controlling the linear growth and stability of actinotrichia and their collagen fibrils.

背景:人类WNT10A突变与齿外胚层发育不良综合征有关。在这里,我们对斑马鱼的wnt10a功能缺失突变体进行了分析。结果:wnt10a突变斑马鱼胚胎显示出牙齿发育受损和中鳍折叠(MFF)塌陷。拯救实验表明,wnt10a在胚胎发生和后期变态过程中对MFF的维持至关重要。MFF崩溃不能归因于细胞死亡增加或MFF细胞类型的增殖率改变。相反,wnt10a突变体在最远端的MFF细胞中显示出dlx2a的表达水平降低,随后col1a1a和其他细胞外基质蛋白编码基因的表达受损。透射电子显微镜分析显示,尽管wnt10a突变体的真皮MFF区室最初具有正常形态,具有规则的胶原放线三丝,但放线三线在远端MFF细胞间隙内的定位会受到影响,与放线三纤维收缩和MFF塌陷相吻合。结论:wnt10a突变斑马鱼的MFF崩溃可能是由发育中的MFF远端特性的丧失引起的,与鱼类和哺乳动物中Wnt10缺失引起的牙齿缺陷的分子病理机制惊人地相似。此外,它还指出了控制放线菌及其胶原原纤维线性生长和稳定性的未知机制。
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引用次数: 0
Specific CaMKIIs mediate convergent extension cell movements in early zebrafish development 特异性CaMKII介导斑马鱼早期发育过程中的会聚延伸细胞运动。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-10-20 DOI: 10.1002/dvdy.665
Jamie J. McLeod, Sarah C. Rothschild, Ludmila Francescatto, Haerin Kim, Robert M. Tombes

Background

Noncanonical Wnts are morphogens that can elevate intracellular Ca2+, activate the Ca2+/calmodulin-dependent protein kinase, CaMKII, and promote cell movements during vertebrate gastrulation.

Results

Zebrafish express seven CaMKII genes during embryogenesis; two of these, camk2b1 and camk2g1, are necessary for convergent extension (CE) cell movements. CaMKII morphant phenotypes were observed as early as epiboly. At the 1–3 somite stage, neuroectoderm and paraxial cells remained unconverged in both morphants. Later, somites lacked their stereotypical shape and were wider, more closely spaced, and body gap angles increased. At 24hpf, somite compression and notochord undulation coincided with a shorter and broader body axis. A camk2b1 crispant was generated which phenocopied the camk2b1 morphant. The levels of cell proliferation, apoptosis and paraxial and neuroectodermal markers were unchanged in morphants. Hyperactivation of CaMKII during gastrulation by transient pharmacological intervention (thapsigargin) also caused CE defects. Mosaically expressed dominant-negative CaMKII recapitulated these phenotypes and showed significant midline bifurcation. Finally, the introduction of CaMKII partially rescued Wnt11 morphant phenotypes.

Conclusions

Overall, these data support a model whereby cyclically activated CaMKII encoded from two genes enables cell migration during the process of CE.

背景:非经典Wnts是在脊椎动物原肠胚形成过程中能够升高细胞内Ca2+、激活Ca2+/钙调蛋白依赖性蛋白激酶CaMKII并促进细胞运动的形态发生素。结果:斑马鱼在胚胎发生过程中表达7个CaMKII基因;其中两个,camk2b1和camk2g1,是会聚延伸(CE)细胞运动所必需的。早在epiboly时就观察到CaMKII变体表型。在1-3 体节期、神经外胚层和轴旁细胞在两种形态中均未融合。后来,体节失去了它们的定型形状,变得更宽,间隔更近,身体间隙角增加。在24hpf时,体节压缩和脊索起伏与较短和较宽的体轴一致。生成了camk2b1脆化剂,该脆化剂对camk2b1变体进行了表型复制。变形体的细胞增殖、凋亡以及轴旁和神经外胚层标志物的水平没有变化。原肠胚形成过程中CaMKII通过瞬时药物干预(thapsigargin)的过度激活也导致CE缺陷。多数表达显性阴性的CaMKII概括了这些表型,并显示出显著的中线分叉。最后,CaMKII的引入部分挽救了Wnt11变体表型。结论:总的来说,这些数据支持一个模型,即由两个基因编码的循环激活的CaMKII能够在CE过程中实现细胞迁移。
{"title":"Specific CaMKIIs mediate convergent extension cell movements in early zebrafish development","authors":"Jamie J. McLeod,&nbsp;Sarah C. Rothschild,&nbsp;Ludmila Francescatto,&nbsp;Haerin Kim,&nbsp;Robert M. Tombes","doi":"10.1002/dvdy.665","DOIUrl":"10.1002/dvdy.665","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Noncanonical Wnts are morphogens that can elevate intracellular Ca<sup>2+</sup>, activate the Ca<sup>2+</sup>/calmodulin-dependent protein kinase, CaMKII, and promote cell movements during vertebrate gastrulation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Zebrafish express seven CaMKII genes during embryogenesis; two of these, <i>camk2b1</i> and <i>camk2g1</i>, are necessary for convergent extension (CE) cell movements. CaMKII morphant phenotypes were observed as early as epiboly. At the 1–3 somite stage, neuroectoderm and paraxial cells remained unconverged in both morphants. Later, somites lacked their stereotypical shape and were wider, more closely spaced, and body gap angles increased. At 24hpf, somite compression and notochord undulation coincided with a shorter and broader body axis. A <i>camk2b1</i> crispant was generated which phenocopied the <i>camk2b1</i> morphant. The levels of cell proliferation, apoptosis and paraxial and neuroectodermal markers were unchanged in morphants. Hyperactivation of CaMKII during gastrulation by transient pharmacological intervention (thapsigargin) also caused CE defects. Mosaically expressed dominant-negative CaMKII recapitulated these phenotypes and showed significant midline bifurcation. Finally, the introduction of CaMKII partially rescued Wnt11 morphant phenotypes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Overall, these data support a model whereby cyclically activated CaMKII encoded from two genes enables cell migration during the process of CE.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"253 4","pages":"390-403"},"PeriodicalIF":2.5,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.665","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49675495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Is African non-annual killifish Fundulopanchax gardneri (Teleostei; Cyprinodontiformes; Nothobranchiidae) true non-annual? 非洲非年生圆底溪鱼真的是非年生的吗?
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-10-19 DOI: 10.1002/dvdy.668
Vasily Borisov, Fedor Shkil, Dmitry Seleznev, Sergei Smirnov

Background

Annual or seasonal killifishes (Cyprinodontiformes: Nothobranchiidae) are unique among fish in their ability to enter into developmental arrests (diapauses: DI, DII, and DIII). They have a short lifespan and their embryos are exceptionally tolerant to a variety of environmental stresses. These traits make them a popular model for studying vertebrate diapause, aging, stress tolerance, genome adaptation, and evolution. In such issues, in a comparative evolutionary framework, Fundulopanchax gardneri, a popular aquarium fish from Africa, is commonly used as a representative non-annual model though its development is not studied in detail and whether it includes diapauses remains uncertain.

Results

We described in detail for the first time embryonic development of F. gardneri and revealed it to resemble that in the undoubtedly annual Austrofundulus limnaeus killifish in displaying two developmental depressions. However, if compared with A. limnaeus, these developmental states look like “less intense” versions of DII and DIII rather than true diapauses.

Conclusions

To determine whether developmental depressions in F. gardneri represent “true” diapauses or only their functional equivalents, detailed studies of embryonic development of different killifish both annual and non-annual are needed. Before that, acceptance of F. gardneri as a representative non-annual fish seems premature.

背景:在鱼类中,年生或季节性的killifish(Cyprinodontiformes:Nothobranchiidae)在进入发育停滞(滞育:DI、DII和DIII)的能力方面是独特的。它们的寿命很短,而且它们的胚胎对各种环境压力都特别耐受。这些特征使它们成为研究脊椎动物滞育、衰老、应激耐受、基因组适应和进化的流行模型。在这些问题上,在一个比较进化的框架中,来自非洲的一种受欢迎的水族馆鱼类gardneri,通常被用作一种具有代表性的非年度模型,尽管它的发展没有得到详细研究,是否包括滞育仍不确定。结果:我们首次详细描述了F.gardneri的胚胎发育,并发现它与毫无疑问的年度鲎鱼的胚胎发育相似,表现出两种发育抑制。然而,如果与林蛙相比,这些发育状态看起来像是DII和DIII的“不那么强烈”版本,而不是真正的滞育。结论:为了确定F.gardneri的发育凹陷是否代表“真正的”滞育,或者只是它们的功能等价物,需要对不同的年生和非年生基利鱼的胚胎发育进行详细研究。在此之前,人们似乎还为时过早地接受加德奈里作为一种具有代表性的非年度鱼类。
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引用次数: 0
Maternal exposure to hyperbaric oxygen at the preimplantation stages increases apoptosis and ectopic Cdx2 expression and decreases Oct4 expression in mouse blastocysts via Nrf2-Notch1 upregulation and Nf2 downregulation 母体在植入前阶段暴露于高压氧可通过Nrf2-Notch1上调和Nf2下调增加小鼠胚泡中的细胞凋亡和异位Cdx2表达,并降低Oct4表达。
IF 2.5 3区 生物学 Q2 ANATOMY & MORPHOLOGY Pub Date : 2023-10-18 DOI: 10.1002/dvdy.671
Yu-Ming Li, Yu Lang Chung, Yung-Fu Wu, Chien-Kuo Wang, Chieh-Min Chen, Yi-Hui Chen

Background

The environmental oxygen tension has been reported to impact the blastocyst quality and cell numbers in the inner cell mass (ICM) during human and murine embryogenesis. While the molecular mechanisms leading to increased ICM cell numbers and pluripotency gene expression under hypoxia have been deciphered, it remains unknown which regulatory pathways caused the underweight fetal body and overweight placenta after maternal exposure to hyperbaric oxygen (HBO).

Results

The blastocysts from the HBO-exposed pregnant mice revealed significantly increased signals of reactive oxygen species (ROS) and nuclear Nrf2 staining, decreased Nf2 and Oct4 expression, increased nuclear Tp53bp1 and active caspase-3 staining, and ectopic nuclear signals of Cdx2, Yap, and the Notch1 intracellular domain (N1ICD) in the ICM. In the ICM of the HBO-exposed blastocysts, both Nf2 cDNA microinjection and Nrf2 shRNA microinjection significantly decreased the ectopic nuclear expression of Cdx2, Tp53bp1, and Yap whereas increased Oct4 expression, while Nrf2 shRNA microinjection also significantly decreased Notch1 mRNA levels and nuclear expression of N1ICD and active caspase-3.

Conclusion

We show for the first time that maternal exposure to HBO at the preimplantation stage induces apoptosis and impairs ICM cell specification via upregulating Nrf2-Notch1-Cdx2 expression and downregulating Nf2-Oct4 expression.

背景:据报道,在人类和小鼠胚胎发生过程中,环境氧张力会影响胚泡质量和内部细胞团(ICM)中的细胞数量。虽然在低氧条件下导致ICM细胞数量和多能性基因表达增加的分子机制已经被破译,目前尚不清楚是哪些调节途径导致母体暴露于高压氧(HBO)后胎儿体重不足和胎盘超重。结果:暴露于HBO的妊娠小鼠的胚泡显示活性氧(ROS)和核Nrf2染色信号显著增加,Nf2和Oct4表达降低,增加细胞核Tp53bp1和活性胱天蛋白酶3染色,以及ICM中Cdx2、Yap和Notch1细胞内结构域(N1ICD)的异位核信号。在暴露于HBO的胚泡的ICM中,Nf2 cDNA微注射和Nrf2 shRNA微注射均显著降低了Cdx2、Tp53bp1和Yap的异位核表达,而增加了Oct4的表达,而Nrf2-shRNA微注射也显著降低了Notch1mRNA水平以及N1ICD和活性胱天蛋白酶3的核表达。结论:我们首次表明,母体在植入前暴露于HBO通过上调Nrf2-Notch1-Cdx2表达和下调Nf2-Oct4表达来诱导细胞凋亡并损害ICM细胞的特异性。
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引用次数: 0
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Developmental Dynamics
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