{"title":"社论要点。","authors":"Paul A. Trainor","doi":"10.1002/dvdy.718","DOIUrl":null,"url":null,"abstract":"<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>Mechanical Forces in Development</b> “Exploring the Role of Mechanical Forces on Tendon Development Using in vivo Model: A Scoping Review,” by Yuna Usami, Hirotaka Iijima, Takanori Kokubun; <i>DevDyn</i> 253:6, pp. 550-565. https://doi.org/10.1002/dvdy.673. Tendons comprise connective tissue that transmits muscle contraction forces to bones and drives joint movement throughout life. Interestingly, however, mechanical forces also regulate and control key cellular and molecular responses during musculoskeletal tissue development, differentiation, and growth. Scleraxis (Scx), a basic helix–loop–helix (bHLH) transcription factor, is the most representative marker of tendon development and most studies have focused on the loss of muscle, muscle dysfunction, and weight-bearing regulation, but few investigated the effect of increased mechanical force. This review summarizes our current knowledge about animal models and approaches for modulating mechanical forces on tendon development; defines the role of mechanical force through the activity of Scx and other tendon development-associated factors; and raises important questions and directions for the field to address in the future.</p><p><b>Zebrafish Fin Development</b> “wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis” by Erica Benard, Ismail Küçükaylak, Julia Hatzold, Kilian Berendes, Thomas J. Carney, Filippo Beleggia, and Matthias Hammerschmidt; <i>DevDyn</i> 253:6, pp. 566-592. https://doi.org/10.1002/dvdy.672.</p><p>Wnt signaling regulates critical cell-to-cell interactions in multiple developmental processes during embryogenesis and in the homeostasis of adult tissues. Mutations in human <i>WNT10A</i> are associated with odonto-ectodermal dysplasia syndromes, which are primarily characterized by severe oligodontia of permanent teeth, and skin anomalies. In this study, the authors generate <i>wnt10a</i> mutant zebrafish embryos, which display impaired tooth development and a collapsing median fin fold (MFF), making them a good model for odonto-onycho-dermal dysplasia. Focusing on the MFF, <i>dlx2a</i> activity was found to be decreased in the distal-most cells, together with perturbed expression of <i>col1a1a</i> and other extracellular matrix proteins encoding genes. Consequently, positioning of actinotrichia within the cleft of distal MFF cells become compromised, coinciding with actinotrichia shrinkage and MFF collapse. Rescue experiments demonstrate that wnt10a is essential for MFF maintenance, both during embryogenesis and later metamorphosis. The mechanism is strikingly similar to the proposed molecular etiology and cellular pathogenesis mechanisms underlying the teeth defects caused by Wnt10 loss-of-function in fish and mammals.</p><p><b>Meiosis and Spermatogenesis in Mammals</b> “Elevated Id2 Expression Causes Defective Meiosis and Spermatogenesis in Mice” by Zhen He, Rong-Ge Yan, Qin-Bang Shang, and Qi-En Yang; <i>DevDyn</i> 253:6, pp. 593-605. https://doi.org/10.1002/dvdy.676.</p><p>Meiosis during germ cell development generates genetic diversity via recombination and redistribution of homologous chromosomes. In the male germline, spermatogonia are the most primitive germ cells, and they arise from gonocytes (or prespermatogonia) shortly after birth. Spermatogonia are capable of entering meiosis prophase I after several rounds of division, but defects in their development and errors in meiosis often lead to infertility or aneuploidy in humans. Although meiotic progression can be driven by cyclin-CDK (cyclin-dependent kinase) complexes, the proteins that govern this process remain to be fully elucidated. Inhibitors of DNA binding/differentiation (ID proteins) are master regulators of cell cycle progression and cell differentiation, and gene expression analyses of spermatogenic cells identified ID2 as a potentially important regulator of meiosis in mice. ID2 is expressed in spermatogonia, spermatocytes, and Sertoli. In this study, the authors generated conditional <i>Id2</i> knockout and transgenic <i>Id2</i> overexpressing mouse lines to dissect the function of ID2 in spermatogenesis. Although a germ cell-specific knockout of Id2 did not affect spermatogenesis, most likely due to functional compensation with other Id proteins, in contrast, overexpression of Id2 in germ cells led to decreased testis size and severe meiotic defects. Thus, ID2 is functionally important for zygotene to pachytene transition during meiosis in male germ cells during mammalian development.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"253 6","pages":"548-549"},"PeriodicalIF":2.0000,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.718","citationCount":"0","resultStr":"{\"title\":\"Editorial highlights\",\"authors\":\"Paul A. Trainor\",\"doi\":\"10.1002/dvdy.718\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<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>Mechanical Forces in Development</b> “Exploring the Role of Mechanical Forces on Tendon Development Using in vivo Model: A Scoping Review,” by Yuna Usami, Hirotaka Iijima, Takanori Kokubun; <i>DevDyn</i> 253:6, pp. 550-565. https://doi.org/10.1002/dvdy.673. Tendons comprise connective tissue that transmits muscle contraction forces to bones and drives joint movement throughout life. Interestingly, however, mechanical forces also regulate and control key cellular and molecular responses during musculoskeletal tissue development, differentiation, and growth. Scleraxis (Scx), a basic helix–loop–helix (bHLH) transcription factor, is the most representative marker of tendon development and most studies have focused on the loss of muscle, muscle dysfunction, and weight-bearing regulation, but few investigated the effect of increased mechanical force. This review summarizes our current knowledge about animal models and approaches for modulating mechanical forces on tendon development; defines the role of mechanical force through the activity of Scx and other tendon development-associated factors; and raises important questions and directions for the field to address in the future.</p><p><b>Zebrafish Fin Development</b> “wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis” by Erica Benard, Ismail Küçükaylak, Julia Hatzold, Kilian Berendes, Thomas J. Carney, Filippo Beleggia, and Matthias Hammerschmidt; <i>DevDyn</i> 253:6, pp. 566-592. https://doi.org/10.1002/dvdy.672.</p><p>Wnt signaling regulates critical cell-to-cell interactions in multiple developmental processes during embryogenesis and in the homeostasis of adult tissues. Mutations in human <i>WNT10A</i> are associated with odonto-ectodermal dysplasia syndromes, which are primarily characterized by severe oligodontia of permanent teeth, and skin anomalies. In this study, the authors generate <i>wnt10a</i> mutant zebrafish embryos, which display impaired tooth development and a collapsing median fin fold (MFF), making them a good model for odonto-onycho-dermal dysplasia. Focusing on the MFF, <i>dlx2a</i> activity was found to be decreased in the distal-most cells, together with perturbed expression of <i>col1a1a</i> and other extracellular matrix proteins encoding genes. Consequently, positioning of actinotrichia within the cleft of distal MFF cells become compromised, coinciding with actinotrichia shrinkage and MFF collapse. Rescue experiments demonstrate that wnt10a is essential for MFF maintenance, both during embryogenesis and later metamorphosis. The mechanism is strikingly similar to the proposed molecular etiology and cellular pathogenesis mechanisms underlying the teeth defects caused by Wnt10 loss-of-function in fish and mammals.</p><p><b>Meiosis and Spermatogenesis in Mammals</b> “Elevated Id2 Expression Causes Defective Meiosis and Spermatogenesis in Mice” by Zhen He, Rong-Ge Yan, Qin-Bang Shang, and Qi-En Yang; <i>DevDyn</i> 253:6, pp. 593-605. https://doi.org/10.1002/dvdy.676.</p><p>Meiosis during germ cell development generates genetic diversity via recombination and redistribution of homologous chromosomes. In the male germline, spermatogonia are the most primitive germ cells, and they arise from gonocytes (or prespermatogonia) shortly after birth. Spermatogonia are capable of entering meiosis prophase I after several rounds of division, but defects in their development and errors in meiosis often lead to infertility or aneuploidy in humans. Although meiotic progression can be driven by cyclin-CDK (cyclin-dependent kinase) complexes, the proteins that govern this process remain to be fully elucidated. Inhibitors of DNA binding/differentiation (ID proteins) are master regulators of cell cycle progression and cell differentiation, and gene expression analyses of spermatogenic cells identified ID2 as a potentially important regulator of meiosis in mice. ID2 is expressed in spermatogonia, spermatocytes, and Sertoli. In this study, the authors generated conditional <i>Id2</i> knockout and transgenic <i>Id2</i> overexpressing mouse lines to dissect the function of ID2 in spermatogenesis. Although a germ cell-specific knockout of Id2 did not affect spermatogenesis, most likely due to functional compensation with other Id proteins, in contrast, overexpression of Id2 in germ cells led to decreased testis size and severe meiotic defects. 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引用次数: 0
摘要
每种生物都是了解发育、进化、疾病和再生的模式生物,而我们对调节这些生物过程的跨学科遗传、分子、细胞和发育机制的研究才刚刚起步。这些 "亮点 "指出了《发育生物学》最近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态:由 Yuna Usami、Hirotaka Iijima、Takanori Kokubun 撰写的 "利用体内模型探索机械力对肌腱发育的作用:范围综述";DevDyn 253:6,第 550-565 页。https://doi.org/10.1002/dvdy.673。肌腱由结缔组织组成,可将肌肉收缩力传递到骨骼,并在整个生命过程中驱动关节运动。但有趣的是,机械力还能在肌肉骨骼组织的发育、分化和生长过程中调节和控制关键的细胞和分子反应。Scleraxis(Scx)是一种碱性螺旋-环-螺旋(bHLH)转录因子,是肌腱发育过程中最具代表性的标志物,大多数研究都集中在肌肉损失、肌肉功能障碍和负重调节方面,但很少有研究对机械力增加的影响进行调查。这篇综述总结了我们目前对动物模型和调节机械力对肌腱发育影响的方法的了解;界定了机械力通过 Scx 和其他肌腱发育相关因子的活性所发挥的作用;并提出了该领域未来需要解决的重要问题和方向。斑马鱼鳍的发育》(Zebrafish Fin Development):"wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis" 作者:Erica Benard, Ismail Küçükaylak, Julia Hatzold, Kilian Berendes, Thomas J. Carney, Filippo Beleggia, and Matthias Hammerschmidt; DevDyn 253:6, pp. https://doi.org/10.1002/dvdy.672。.Wnt信号在胚胎发生过程中的多个发育过程和成体组织的稳态中调节细胞间的关键相互作用。人类 WNT10A 基因突变与颅骨外胚层发育不良综合征有关,该综合征的主要特征是严重的恒牙缺失和皮肤畸形。在这项研究中,作者生成了 wnt10a 突变体斑马鱼胚胎,它们显示出牙齿发育受损和中鳍褶皱(MFF)塌陷,使其成为骨-髁-皮发育不良的良好模型。以中鳍褶为研究重点,发现最远端细胞中的 dlx2a 活性降低,同时 col1a1a 和其他细胞外基质蛋白编码基因的表达也受到干扰。因此,放线菌在 MFF 远端细胞裂隙内的定位受到影响,同时放线菌萎缩和 MFF 崩溃。拯救实验证明,无论是在胚胎发生过程中还是在后来的变态过程中,wnt10a 对于 MFF 的维持都是必不可少的。该机制与鱼类和哺乳动物中 Wnt10 功能缺失导致的牙齿缺陷的分子病因学和细胞发病机制惊人地相似。哺乳动物的减数分裂和精子发生 "Elevated Id2 Expression Causes Defective Meiosis and Spermatogenesis in Mice" by Zhen He, Rong-Ge Yan, Qin-Bang Shang, and Qi-En Yang; DevDyn 253:6, pp. https://doi.org/10.1002/dvdy.676.生殖细胞发育过程中的减数分裂通过同源染色体的重组和重新分配产生遗传多样性。在男性生殖细胞中,精原细胞是最原始的生殖细胞,它们在出生后不久由生殖腺细胞(或前精原细胞)产生。精原细胞经过几轮分裂后能够进入减数分裂原期 I,但其发育缺陷和减数分裂过程中的错误往往会导致人类不育或非整倍体。尽管减数分裂的进展可由细胞周期蛋白-CDK(细胞周期蛋白依赖性激酶)复合物驱动,但支配这一过程的蛋白质仍有待完全阐明。DNA结合/分化抑制蛋白(ID蛋白)是细胞周期进展和细胞分化的主要调节因子,对精原细胞的基因表达分析发现,ID2可能是小鼠减数分裂的重要调节因子。ID2 在精原细胞、精母细胞和 Sertoli 中均有表达。在这项研究中,作者产生了条件性Id2基因敲除和转基因Id2过表达小鼠品系,以研究ID2在精子发生中的功能。生精细胞特异性敲除Id2并不影响精子发生,这很可能是由于Id2与其他Id蛋白的功能补偿作用;相反,在生精细胞中过表达Id2会导致睾丸体积减小和严重的减数分裂缺陷。因此,在哺乳动物的发育过程中,Id2对雄性生殖细胞减数分裂过程中的合子到幼子的转变具有重要功能。
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 Developmental Dynamics that illustrate the complex dynamics of developmental biology.
Mechanical Forces in Development “Exploring the Role of Mechanical Forces on Tendon Development Using in vivo Model: A Scoping Review,” by Yuna Usami, Hirotaka Iijima, Takanori Kokubun; DevDyn 253:6, pp. 550-565. https://doi.org/10.1002/dvdy.673. Tendons comprise connective tissue that transmits muscle contraction forces to bones and drives joint movement throughout life. Interestingly, however, mechanical forces also regulate and control key cellular and molecular responses during musculoskeletal tissue development, differentiation, and growth. Scleraxis (Scx), a basic helix–loop–helix (bHLH) transcription factor, is the most representative marker of tendon development and most studies have focused on the loss of muscle, muscle dysfunction, and weight-bearing regulation, but few investigated the effect of increased mechanical force. This review summarizes our current knowledge about animal models and approaches for modulating mechanical forces on tendon development; defines the role of mechanical force through the activity of Scx and other tendon development-associated factors; and raises important questions and directions for the field to address in the future.
Zebrafish Fin Development “wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis” by Erica Benard, Ismail Küçükaylak, Julia Hatzold, Kilian Berendes, Thomas J. Carney, Filippo Beleggia, and Matthias Hammerschmidt; DevDyn 253:6, pp. 566-592. https://doi.org/10.1002/dvdy.672.
Wnt signaling regulates critical cell-to-cell interactions in multiple developmental processes during embryogenesis and in the homeostasis of adult tissues. Mutations in human WNT10A are associated with odonto-ectodermal dysplasia syndromes, which are primarily characterized by severe oligodontia of permanent teeth, and skin anomalies. In this study, the authors generate wnt10a mutant zebrafish embryos, which display impaired tooth development and a collapsing median fin fold (MFF), making them a good model for odonto-onycho-dermal dysplasia. Focusing on the MFF, dlx2a activity was found to be decreased in the distal-most cells, together with perturbed expression of col1a1a and other extracellular matrix proteins encoding genes. Consequently, positioning of actinotrichia within the cleft of distal MFF cells become compromised, coinciding with actinotrichia shrinkage and MFF collapse. Rescue experiments demonstrate that wnt10a is essential for MFF maintenance, both during embryogenesis and later metamorphosis. The mechanism is strikingly similar to the proposed molecular etiology and cellular pathogenesis mechanisms underlying the teeth defects caused by Wnt10 loss-of-function in fish and mammals.
Meiosis and Spermatogenesis in Mammals “Elevated Id2 Expression Causes Defective Meiosis and Spermatogenesis in Mice” by Zhen He, Rong-Ge Yan, Qin-Bang Shang, and Qi-En Yang; DevDyn 253:6, pp. 593-605. https://doi.org/10.1002/dvdy.676.
Meiosis during germ cell development generates genetic diversity via recombination and redistribution of homologous chromosomes. In the male germline, spermatogonia are the most primitive germ cells, and they arise from gonocytes (or prespermatogonia) shortly after birth. Spermatogonia are capable of entering meiosis prophase I after several rounds of division, but defects in their development and errors in meiosis often lead to infertility or aneuploidy in humans. Although meiotic progression can be driven by cyclin-CDK (cyclin-dependent kinase) complexes, the proteins that govern this process remain to be fully elucidated. Inhibitors of DNA binding/differentiation (ID proteins) are master regulators of cell cycle progression and cell differentiation, and gene expression analyses of spermatogenic cells identified ID2 as a potentially important regulator of meiosis in mice. ID2 is expressed in spermatogonia, spermatocytes, and Sertoli. In this study, the authors generated conditional Id2 knockout and transgenic Id2 overexpressing mouse lines to dissect the function of ID2 in spermatogenesis. Although a germ cell-specific knockout of Id2 did not affect spermatogenesis, most likely due to functional compensation with other Id proteins, in contrast, overexpression of Id2 in germ cells led to decreased testis size and severe meiotic defects. Thus, ID2 is functionally important for zygotene to pachytene transition during meiosis in male germ cells during mammalian development.
期刊介绍:
Developmental Dynamics, is an official publication of the American Association for Anatomy. This peer reviewed journal provides an international forum for publishing novel discoveries, using any model system, that advances our understanding of development, morphology, form and function, evolution, disease, stem cells, repair and regeneration.