Despite the significant literature about morphological features of limb skeletons involved in tetrapod limb evolution, some questions about carpal and tarsal elements remain. In anurans, the ecomorphological and biomechanical approaches studied long hind limbs (to jump) and forelimbs (to land) and emphasized the role of the long bones in locomotion but disregarded what happens with the nodular elements of the carpus and tarsus. Here, we present a comparative study of nodular elements of the carpus and tarsus in anurans based on whole-mount specimens stained with Alcian Blue (cartilage) and Alizarin Red S (bone and calcified cartilage). The sample comprises 113 species belonging to 33 anuran families and postmetamorphic series in selected species. Further, we analyze the histology of the carpus and tarsus in individuals of nine species. In most anurans, the carpal and tarsal elements are cartilaginous in adult stages. The cartilaginous matrix may present different degrees of calcification. Few taxa present truly ossified carpals and tarsals with marrow cavity, blood cells, and hematopoietic cells. Interpretation of the interspecific variation in the carpus and tarsus skeletons on the most recent anuran phylogeny suggests that the delayed ossification of carpals and tarsals has evolved in derived lineages (e.g. Pelobatoidea and Neobatrachia).
{"title":"A comparative approach to the microstructure in the carpus and tarsus in anurans","authors":"Marissa Fabrezi, Julio César Cruz","doi":"10.1111/dgd.12957","DOIUrl":"10.1111/dgd.12957","url":null,"abstract":"<p>Despite the significant literature about morphological features of limb skeletons involved in tetrapod limb evolution, some questions about carpal and tarsal elements remain. In anurans, the ecomorphological and biomechanical approaches studied long hind limbs (to jump) and forelimbs (to land) and emphasized the role of the long bones in locomotion but disregarded what happens with the nodular elements of the carpus and tarsus. Here, we present a comparative study of nodular elements of the carpus and tarsus in anurans based on whole-mount specimens stained with Alcian Blue (cartilage) and Alizarin Red S (bone and calcified cartilage). The sample comprises 113 species belonging to 33 anuran families and postmetamorphic series in selected species. Further, we analyze the histology of the carpus and tarsus in individuals of nine species. In most anurans, the carpal and tarsal elements are cartilaginous in adult stages. The cartilaginous matrix may present different degrees of calcification. Few taxa present truly ossified carpals and tarsals with marrow cavity, blood cells, and hematopoietic cells. Interpretation of the interspecific variation in the carpus and tarsus skeletons on the most recent anuran phylogeny suggests that the delayed ossification of carpals and tarsals has evolved in derived lineages (e.g. Pelobatoidea and Neobatrachia).</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"67 2","pages":"55-74"},"PeriodicalIF":1.7,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142958284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression, in conjunction with cyclins. The cyclin-CDK system is highly conserved among eukaryotes, and CDK1 is considered essential for progression through the M phase. However, the extent to which cell cycle progression depends on CDK1 varies between cell types. Therefore, a range of cell types must be analyzed to comprehensively elucidate the role of CDK1. Cdk1-knockout mice exhibit lethality at an early developmental stage, specifically before the differentiation of various cell types. The aim of the present study was to characterize the effects of CDK1 deficiency in amphibian newts. Cdk1 was disrupted by injecting fertilized newt eggs with CRISPR/Cas9, and the resulting effects on embryonic development and cell proliferation were then evaluated. In both wild-type and Cdk1-crispant newt embryos, CDK1 protein was either stored in the egg until late embryogenesis or potentially derived from maternal mRNA, which may also be stored during this period. The embryos survived to the hatching stage, during which the cells responsible for forming the basic organs differentiated. To further characterize the long-term effects of Cdk1 knockout, parabiosis experiments were conducted using wild-type embryos and Cdk1 crispants. The results suggested that an endocycle occurred in the crispant larvae, as evidenced by increases in the size of several types of cells. It is anticipated that studies using newts will provide further insights into the role of Cdk1 in regulating the cell cycle.
{"title":"Effect of Cdk1 gene disruption on cell cycle progression in newt cells","authors":"Yuta Nakao, Kazuko Okamoto, Ichiro Tazawa, Tatsuro Nishijima, Nobuaki Furuno, Tetsushi Sakuma, Takashi Yamamoto, Takashi Takeuchi, Toshinori Hayashi","doi":"10.1111/dgd.12958","DOIUrl":"10.1111/dgd.12958","url":null,"abstract":"<p>Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression, in conjunction with cyclins. The cyclin-CDK system is highly conserved among eukaryotes, and CDK1 is considered essential for progression through the M phase. However, the extent to which cell cycle progression depends on CDK1 varies between cell types. Therefore, a range of cell types must be analyzed to comprehensively elucidate the role of CDK1. <i>Cdk1</i>-knockout mice exhibit lethality at an early developmental stage, specifically before the differentiation of various cell types. The aim of the present study was to characterize the effects of CDK1 deficiency in amphibian newts. <i>Cdk1</i> was disrupted by injecting fertilized newt eggs with CRISPR/Cas9, and the resulting effects on embryonic development and cell proliferation were then evaluated. In both wild-type and <i>Cdk1</i>-crispant newt embryos, CDK1 protein was either stored in the egg until late embryogenesis or potentially derived from maternal mRNA, which may also be stored during this period. The embryos survived to the hatching stage, during which the cells responsible for forming the basic organs differentiated. To further characterize the long-term effects of <i>Cdk1</i> knockout, parabiosis experiments were conducted using wild-type embryos and <i>Cdk1</i> crispants. The results suggested that an endocycle occurred in the crispant larvae, as evidenced by increases in the size of several types of cells. It is anticipated that studies using newts will provide further insights into the role of <i>Cdk1</i> in regulating the cell cycle.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"67 2","pages":"85-93"},"PeriodicalIF":1.7,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142958322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
From September 16 to 19, 2024, an international symposium to celebrate the centennial of the discovery of the gastrula organizer by Hans Spemann and Hilde Mangold, was held at the University of Freiburg, Germany, where they studied embryology. There were 41 plenary lectures, 11 short talks, and 182 poster presentations, with more than 300 participants from 23 countries. The symposium covered research topics broadly related to developmental, cell, genome, and evolutionary biology, mainly focused on early animal development. In addition to in vivo studies on topics such as gastrulation, embryonic patterning, cell polarity, and morphogenesis, recent studies using gastruloids and organoids, which recapitulate embryogenesis and organogenesis in in vitro cell culture, were also presented at this symposium, entitled Self-Organization in Biology. Most of the reported studies used vertebrate models such as mice, frogs, and zebrafish; however, evolutionary studies involving invertebrate and plant models were also presented. Presentations employing traditional methods such as cell transplantation and phenotype screening, and state-of-the-art technologies such as single-cell omics, high-resolution imaging, and computational analysis showed that experimental embryology has a long history, to which studies of the organizer have contributed significantly. Here we discuss memorable aspects of the symposium in the hope that this report will encourage young scientists to actively participate in face-to-face international conferences.
{"title":"Meeting report about self-organization in biology: Freiburg Spemann–Mangold Centennial Symposium","authors":"Satoshi Kuwana, Yuuri Yasuoka","doi":"10.1111/dgd.12954","DOIUrl":"10.1111/dgd.12954","url":null,"abstract":"<p>From September 16 to 19, 2024, an international symposium to celebrate the centennial of the discovery of the gastrula organizer by Hans Spemann and Hilde Mangold, was held at the University of Freiburg, Germany, where they studied embryology. There were 41 plenary lectures, 11 short talks, and 182 poster presentations, with more than 300 participants from 23 countries. The symposium covered research topics broadly related to developmental, cell, genome, and evolutionary biology, mainly focused on early animal development. In addition to in vivo studies on topics such as gastrulation, embryonic patterning, cell polarity, and morphogenesis, recent studies using gastruloids and organoids, which recapitulate embryogenesis and organogenesis in in vitro cell culture, were also presented at this symposium, entitled Self-Organization in Biology. Most of the reported studies used vertebrate models such as mice, frogs, and zebrafish; however, evolutionary studies involving invertebrate and plant models were also presented. Presentations employing traditional methods such as cell transplantation and phenotype screening, and state-of-the-art technologies such as single-cell omics, high-resolution imaging, and computational analysis showed that experimental embryology has a long history, to which studies of the organizer have contributed significantly. Here we discuss memorable aspects of the symposium in the hope that this report will encourage young scientists to actively participate in face-to-face international conferences.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"67 2","pages":"36-42"},"PeriodicalIF":1.7,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/dgd.12954","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142958324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
5′Hox genes regulate pattern formation along the axes of the limb. Previously, we showed that Hoxa13/Hoxd13 double-mutant newts lacked all digits of the forelimbs during development and regeneration, showing that newt Hox13 is necessary for digit formation in development and regeneration. In addition, we found another unique phenotype. Some of the Hox13 crispant newts showed hindlimb defects, in which whole or almost whole hindlimbs were lost, suggesting a novel function of Hox13 in limb development. Using germline mutants, we showed that mutation in Hox13 led to hindlimb defects. The limb buds of Hox13 crispants formed, however, did not show outgrowth. Expression of Fgf10 and Tbx4, which are involved in limb outgrowth, decreased in the hindlimb buds of Hox13 crispants. In addition, hindlimb defects were observed in both Fgf10 and Tbx4 crispant newts. Finally, Fgf10 and Tbx4 interacted with Hox13 genetically. Our results revealed a novel function of Hox13 in regulating the outgrowth of the newt hindlimb bud through interaction with Fgf10 and Tbx4.
{"title":"Novel function of Hox13 in regulating outgrowth of the newt hindlimb bud through interaction with Fgf10 and Tbx4","authors":"Sayo Tozawa, Haruka Matsubara, Fumina Minamitani, Yasuhiro Kamei, Misako Saida, Momoko Asao, Ken-ichi T. Suzuki, Masatoshi Matsunami, Shuji Shigenobu, Toshinori Hayashi, Gembu Abe, Takashi Takeuchi","doi":"10.1111/dgd.12952","DOIUrl":"10.1111/dgd.12952","url":null,"abstract":"<p>5′<i>Hox</i> genes regulate pattern formation along the axes of the limb. Previously, we showed that <i>Hoxa13/Hoxd13</i> double-mutant newts lacked all digits of the forelimbs during development and regeneration, showing that newt <i>Hox13</i> is necessary for digit formation in development and regeneration. In addition, we found another unique phenotype. Some of the <i>Hox13</i> crispant newts showed hindlimb defects, in which whole or almost whole hindlimbs were lost, suggesting a novel function of <i>Hox13</i> in limb development. Using germline mutants, we showed that mutation in <i>Hox13</i> led to hindlimb defects. The limb buds of <i>Hox13</i> crispants formed, however, did not show outgrowth. Expression of <i>Fgf10</i> and <i>Tbx4</i>, which are involved in limb outgrowth, decreased in the hindlimb buds of <i>Hox13</i> crispants. In addition, hindlimb defects were observed in both <i>Fgf10</i> and <i>Tbx4</i> crispant newts. Finally, <i>Fgf10</i> and <i>Tbx4</i> interacted with <i>Hox13</i> genetically. Our results revealed a novel function of <i>Hox13</i> in regulating the outgrowth of the newt hindlimb bud through interaction with <i>Fgf10</i> and <i>Tbx4.</i></p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"67 1","pages":"10-22"},"PeriodicalIF":1.7,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Transcription factors collaborate with epigenetic regulatory factors to orchestrate cardiac differentiation for heart development, but the underlying mechanism is not fully understood. Here, we report that GATA-6 induces cardiac differentiation but peroxisome proliferator-activated receptor α (PPARα) reverses GATA-6-induced cardiac differentiation, possibly because GATA-6/PPARα recruits the polycomb protein complex containing EZH2/Ring1b/BMI1 to the promoter of the cardiac-specific α-myosin heavy chain (α-MHC) gene and suppresses α-MHC expression, which ultimately inhibits cardiac differentiation. Furthermore, Ring1b ubiquitylates PPARα and GATA-6. By overexpression and knockout of EZH2/BMI1, it was demonstrated that the polycomb protein complex inhibits cardiac differentiation induced by GATA-6 and PPARα. Together, our results demonstrate that the polycomb protein complex interacts with GATA-6/PPARα to inhibit cardiac differentiation, a finding that could facilitate the development of new therapies for congenital heart disease.
{"title":"The polycomb protein complex interacts with GATA-6/PPARα to inhibit α-MHC expression","authors":"Fei-Fei Dai, Jing Chen, Zhen Ma, Ming-Hui Yang, Tong Sun, Juan Ma, Meng-Jiao Zhou, Zhi-Ru Wei, Yunzeng Zou, Shoutao Zhang, Ming-Xi Zang","doi":"10.1111/dgd.12953","DOIUrl":"10.1111/dgd.12953","url":null,"abstract":"<p>Transcription factors collaborate with epigenetic regulatory factors to orchestrate cardiac differentiation for heart development, but the underlying mechanism is not fully understood. Here, we report that GATA-6 induces cardiac differentiation but peroxisome proliferator-activated receptor α (PPARα) reverses GATA-6-induced cardiac differentiation, possibly because GATA-6/PPARα recruits the polycomb protein complex containing EZH2/Ring1b/BMI1 to the promoter of the cardiac-specific α-myosin heavy chain (α-MHC) gene and suppresses α-MHC expression, which ultimately inhibits cardiac differentiation. Furthermore, Ring1b ubiquitylates PPARα and GATA-6. By overexpression and knockout of EZH2/BMI1, it was demonstrated that the polycomb protein complex inhibits cardiac differentiation induced by GATA-6 and PPARα. Together, our results demonstrate that the polycomb protein complex interacts with GATA-6/PPARα to inhibit cardiac differentiation, a finding that could facilitate the development of new therapies for congenital heart disease.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"67 1","pages":"23-32"},"PeriodicalIF":1.7,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>The 83rd Annual Meeting of the Society for Developmental Biology (SDB) (https://www.sdbonline.org/2024mtg) was held in Atlanta, where the Japanese Society of Developmental Biologists (JSDB) participated as the guest society. To promote societal interactions, three researchers from Japan and gave invited talks in the SDB meeting as representatives of JSDB. On the other hand, four researchers from SDB gave invited talks and also participated in the Diversity Committee's Luncheon Seminar that I organized in the JSDB meeting (https://pub.confit.atlas.jp/en/event/jsdb2024). These scientific exchanges are aimed at fostering collaboration between developmental biologists in the United States and Japan and promoting mutual research advancements. The hope is that these initiatives will continue to build a long-term cooperative framework between both parties. Notably, this year, SDB President Dr. Ken Cho attended the JSDB meeting in Kyoto and played a significant role in facilitating our visit, underscoring the importance of mutual exchange.</p><p>I had the privilege of attending the Society for Developmental Biology (SDB) Annual Meeting for the first time in 2024. The 2024 SDB Annual Meeting took place at the Signia by Hilton, a newly opened venue in downtown Atlanta, Georgia (Figure 1). The hotel location offers excellent access to key landmarks such as the Mercedes-Benz Stadium and the Georgia World Congress Center. The city of Atlanta, with a population of approximately 500,000 as of 2022, is one of the major urban centers of the southern United States and is notable for hosting the 1996 Summer Olympics for our generations. The hotel provided an ideal setting for networking and engaging with colleagues, which complemented the productive scientific sessions held throughout the meeting.</p><p>The SDB meeting delivered a broad range of topics in developmental biology, and the sessions offered excellent opportunities for exchanging ideas and discussing the latest research advances. As a participant, I found the meeting to be highly valuable for staying updated with cutting-edge discoveries and methodologies, as well as for establishing new collaborations within the developmental biology community.</p><p>The scheduling format included a Presidential Symposium in the evening of day 1, with concurrent sessions and symposia in the morning, and plenary sessions after dinner. The invited speakers delivered outstanding presentations, both in terms of research content and presentation skills. The presentation by Dr. Zeba Wunderlich and her team from Boston University explored the functional significance of shadow enhancers, a critical yet enigmatic element in gene regulation. Using Drosophila embryos, they demonstrated how shadow enhancers, which bind distinct sets of transcription factors, ensure robust gene expression even under stress conditions. A particularly surprising finding came from their experiments with “squish” enhancers, where the endogenous DNA b
{"title":"Meeting report: Society for Developmental Biology 83rd annual meeting","authors":"Shunsuke Yaguchi","doi":"10.1111/dgd.12950","DOIUrl":"10.1111/dgd.12950","url":null,"abstract":"<p>The 83rd Annual Meeting of the Society for Developmental Biology (SDB) (https://www.sdbonline.org/2024mtg) was held in Atlanta, where the Japanese Society of Developmental Biologists (JSDB) participated as the guest society. To promote societal interactions, three researchers from Japan and gave invited talks in the SDB meeting as representatives of JSDB. On the other hand, four researchers from SDB gave invited talks and also participated in the Diversity Committee's Luncheon Seminar that I organized in the JSDB meeting (https://pub.confit.atlas.jp/en/event/jsdb2024). These scientific exchanges are aimed at fostering collaboration between developmental biologists in the United States and Japan and promoting mutual research advancements. The hope is that these initiatives will continue to build a long-term cooperative framework between both parties. Notably, this year, SDB President Dr. Ken Cho attended the JSDB meeting in Kyoto and played a significant role in facilitating our visit, underscoring the importance of mutual exchange.</p><p>I had the privilege of attending the Society for Developmental Biology (SDB) Annual Meeting for the first time in 2024. The 2024 SDB Annual Meeting took place at the Signia by Hilton, a newly opened venue in downtown Atlanta, Georgia (Figure 1). The hotel location offers excellent access to key landmarks such as the Mercedes-Benz Stadium and the Georgia World Congress Center. The city of Atlanta, with a population of approximately 500,000 as of 2022, is one of the major urban centers of the southern United States and is notable for hosting the 1996 Summer Olympics for our generations. The hotel provided an ideal setting for networking and engaging with colleagues, which complemented the productive scientific sessions held throughout the meeting.</p><p>The SDB meeting delivered a broad range of topics in developmental biology, and the sessions offered excellent opportunities for exchanging ideas and discussing the latest research advances. As a participant, I found the meeting to be highly valuable for staying updated with cutting-edge discoveries and methodologies, as well as for establishing new collaborations within the developmental biology community.</p><p>The scheduling format included a Presidential Symposium in the evening of day 1, with concurrent sessions and symposia in the morning, and plenary sessions after dinner. The invited speakers delivered outstanding presentations, both in terms of research content and presentation skills. The presentation by Dr. Zeba Wunderlich and her team from Boston University explored the functional significance of shadow enhancers, a critical yet enigmatic element in gene regulation. Using Drosophila embryos, they demonstrated how shadow enhancers, which bind distinct sets of transcription factors, ensure robust gene expression even under stress conditions. A particularly surprising finding came from their experiments with “squish” enhancers, where the endogenous DNA b","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"67 1","pages":"6-9"},"PeriodicalIF":1.7,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/dgd.12950","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142774347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the embryonic neuroepithelium (NE), neural progenitor cells undergo cell cycle-dependent interkinetic nuclear migration (IKNM) along the apicobasal axis. Extensive IKNM supports increasing cell production rates per unit apical surface, as typically observed in the mammalian telencephalic NE. Apical nucleokinesis during the G2 phase is an essential premitotic event, but its occurrence has not yet been quantitatively analyzed at a large 3D-scale with sufficient spatiotemporal resolution. Here, we comprehensively analyzed apically migrating nuclei/somata in reference to their surroundings from embryonic day (E)11 to E13 in the mouse telencephalon. The velocity of apical nucleokinesis decreased, with more frequent nuclear pausing occurring at E12 and E13, whereas the nuclear density in the middle NE zone (20–40-μm deep) increased. This result, together with the results of Shh-mediated overproliferation experiments in which the nuclear density was increased in vivo at E11, suggests that apical nucleokinesis is physically influenced by the surrounding nuclei. Mean square displacement analysis for nuclei being passed by the apically migrating nuclei via horizontal sectioning in toto-recorded movies revealed that the “tissue fluidity” or physical permissiveness of the NE to apical nucleokinesis gradually decreased (E11 > E12 > E13). To further investigate the spatial relationship between preexisting mitoses and subsequent premitotic apical nucleokinesis, the horizontal distribution of mitoses was cumulatively (~3 hr) analyzed under in toto monitoring. The four-dimensional cumulative apical mitoses presented a “random”, not “clustered” or “regular”, distribution pattern throughout the period examined. These methodologies provide a basis for future comparative studies of interspecies differences.
{"title":"Quantitative in toto live imaging analysis of apical nuclear migration in the mouse telencephalic neuroepithelium","authors":"Tsukasa Shimamura, Takaki Miyata","doi":"10.1111/dgd.12949","DOIUrl":"10.1111/dgd.12949","url":null,"abstract":"<p>In the embryonic neuroepithelium (NE), neural progenitor cells undergo cell cycle-dependent interkinetic nuclear migration (IKNM) along the apicobasal axis. Extensive IKNM supports increasing cell production rates per unit apical surface, as typically observed in the mammalian telencephalic NE. Apical nucleokinesis during the G2 phase is an essential premitotic event, but its occurrence has not yet been quantitatively analyzed at a large 3D-scale with sufficient spatiotemporal resolution. Here, we comprehensively analyzed apically migrating nuclei/somata in reference to their surroundings from embryonic day (E)11 to E13 in the mouse telencephalon. The velocity of apical nucleokinesis decreased, with more frequent nuclear pausing occurring at E12 and E13, whereas the nuclear density in the middle NE zone (20–40-μm deep) increased. This result, together with the results of Shh-mediated overproliferation experiments in which the nuclear density was increased in vivo at E11, suggests that apical nucleokinesis is physically influenced by the surrounding nuclei. Mean square displacement analysis for nuclei being passed by the apically migrating nuclei via horizontal sectioning in toto-recorded movies revealed that the “tissue fluidity” or physical permissiveness of the NE to apical nucleokinesis gradually decreased (E11 > E12 > E13). To further investigate the spatial relationship between preexisting mitoses and subsequent premitotic apical nucleokinesis, the horizontal distribution of mitoses was cumulatively (~3 hr) analyzed under in toto monitoring. The four-dimensional cumulative apical mitoses presented a “random”, not “clustered” or “regular”, distribution pattern throughout the period examined. These methodologies provide a basis for future comparative studies of interspecies differences.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"66 9","pages":"462-474"},"PeriodicalIF":1.7,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/dgd.12949","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142717545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Avian species are essential resources for human society, with their preservation and utilization heavily dependent on primordial germ cells (PGCs). However, efficient methods for isolating live PGCs from embryos remain elusive in avian species beyond chickens, and even in chickens, existing techniques have shown limited efficiency. In this study, we present a rapid, simple, and cost-effective method for labeling and sorting circulating-stage PGCs across various avian species, including Carinatae and Ratitae, using Lycopersicon Esculentum (Tomato) lectin (LEL). Notably, this method demonstrates high sorting efficiency by identifying a wide range of PGC subtypes while preserving the proliferative and migratory potential of chicken PGCs. This approach is anticipated to significantly contribute to the conservation, research, and agricultural industries related to avian species globally.
禽类是人类社会的重要资源,其保存和利用在很大程度上依赖于原始生殖细胞(PGCs)。然而,在鸡以外的禽类物种中,从胚胎中分离活的 PGCs 的有效方法仍然难以找到,即使在鸡中,现有技术也显示出有限的效率。在本研究中,我们提出了一种快速、简单且经济有效的方法,利用番茄凝集素(LEL)对不同禽类物种(包括鲤科和鼠科)的循环期 PGCs 进行标记和分拣。值得注意的是,这种方法既能识别多种 PGC 亚型,又能保留鸡 PGC 的增殖和迁移潜能,因此具有很高的分拣效率。预计这种方法将为全球禽类物种的保护、研究和农业产业做出重大贡献。
{"title":"Labeling and sorting of avian primordial germ cells utilizing Lycopersicon Esculentum lectin","authors":"Hiroko Iikawa, Aika Nishina, Mizuki Morita, Yuji Atsuta, Yoshiki Hayashi, Daisuke Saito","doi":"10.1111/dgd.12948","DOIUrl":"10.1111/dgd.12948","url":null,"abstract":"<p>Avian species are essential resources for human society, with their preservation and utilization heavily dependent on primordial germ cells (PGCs). However, efficient methods for isolating live PGCs from embryos remain elusive in avian species beyond chickens, and even in chickens, existing techniques have shown limited efficiency. In this study, we present a rapid, simple, and cost-effective method for labeling and sorting circulating-stage PGCs across various avian species, including Carinatae and Ratitae, using <i>Lycopersicon Esculentum</i> (Tomato) lectin (LEL). Notably, this method demonstrates high sorting efficiency by identifying a wide range of PGC subtypes while preserving the proliferative and migratory potential of chicken PGCs. This approach is anticipated to significantly contribute to the conservation, research, and agricultural industries related to avian species globally.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"66 9","pages":"452-461"},"PeriodicalIF":1.7,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/dgd.12948","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142632048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiovascular disease is the leading cause of mortality worldwide. Myocardial injury resulting from ischemia can be fatal because of the limited regenerative capacity of adult myocardium. Mammalian cardiomyocytes rapidly lose their proliferative capacities, with only a small fraction of adult myocardium remaining proliferative, which is insufficient to support post-injury recovery. Recent investigations have revealed that this decline in myocardial proliferative capacity is closely linked to perinatal metabolic shifts. Predominantly glycolytic fetal myocardial metabolism transitions towards mitochondrial fatty acid oxidation postnatally, which not only enables efficient production of ATP but also causes a dramatic reduction in cardiomyocyte proliferative capacity. Extensive research has elucidated the mechanisms behind this metabolic shift, as well as methods to modulate these metabolic pathways. Some of these methods have been successfully applied to enhance metabolic reprogramming and myocardial regeneration. This review discusses recently acquired insights into the interplay between metabolism and myocardial proliferation, emphasizing postnatal metabolic transitions.
{"title":"Transition from fetal to postnatal state in the heart: Crosstalk between metabolism and regeneration","authors":"Tai Sada, Wataru Kimura","doi":"10.1111/dgd.12947","DOIUrl":"10.1111/dgd.12947","url":null,"abstract":"<p>Cardiovascular disease is the leading cause of mortality worldwide. Myocardial injury resulting from ischemia can be fatal because of the limited regenerative capacity of adult myocardium. Mammalian cardiomyocytes rapidly lose their proliferative capacities, with only a small fraction of adult myocardium remaining proliferative, which is insufficient to support post-injury recovery. Recent investigations have revealed that this decline in myocardial proliferative capacity is closely linked to perinatal metabolic shifts. Predominantly glycolytic fetal myocardial metabolism transitions towards mitochondrial fatty acid oxidation postnatally, which not only enables efficient production of ATP but also causes a dramatic reduction in cardiomyocyte proliferative capacity. Extensive research has elucidated the mechanisms behind this metabolic shift, as well as methods to modulate these metabolic pathways. Some of these methods have been successfully applied to enhance metabolic reprogramming and myocardial regeneration. This review discusses recently acquired insights into the interplay between metabolism and myocardial proliferation, emphasizing postnatal metabolic transitions.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"66 9","pages":"438-451"},"PeriodicalIF":1.7,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/dgd.12947","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142512319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Meri Walter-Manucharyan, Melanie Martin, Julia Pfützner, Franz Markert, Gerhard Rödel, Andreas Deussen, Andreas Hermann, Alexander Storch
Mitochondria are unique organelles that have their own genome (mtDNA) and perform various pivotal functions within a cell. Recently, evidence has highlighted the role of mitochondria in the process of stem cell differentiation, including differentiation of neural stem cells (NSCs). Here we studied the importance of mtDNA function in the early differentiation process of NSCs in two cell culture models: the CGR8-NS cell line that was derived from embryonic stem cells by a lineage selection technique, and primary NSCs that were isolated from embryonic day 14 mouse fetal forebrain. We detected a dramatic increase in mtDNA content upon NSC differentiation to adapt their mtDNA levels to their differentiated state, which was not accompanied by changes in mitochondrial transcription factor A expression. As chemical mtDNA depletion by ethidium bromide failed to generate living ρ° cell lines from both NSC types, we used inhibition of mtDNA polymerase-γ by 2′-3′-dideoxycytidine to reduce mtDNA replication and subsequently cellular mtDNA content. Inhibition of mtDNA replication upon NSC differentiation reduced neurogenesis but not gliogenesis. The mtDNA depletion did not change energy production/consumption or cellular reactive oxygen species (ROS) content in the NSC model used. In conclusion, mtDNA replication is essential for neurogenesis but not gliogenesis in fetal NSCs through as yet unknown mechanisms, which, however, are largely independent of energy/ROS metabolism.
{"title":"Mitochondrial DNA replication is essential for neurogenesis but not gliogenesis in fetal neural stem cells","authors":"Meri Walter-Manucharyan, Melanie Martin, Julia Pfützner, Franz Markert, Gerhard Rödel, Andreas Deussen, Andreas Hermann, Alexander Storch","doi":"10.1111/dgd.12946","DOIUrl":"10.1111/dgd.12946","url":null,"abstract":"<p>Mitochondria are unique organelles that have their own genome (mtDNA) and perform various pivotal functions within a cell. Recently, evidence has highlighted the role of mitochondria in the process of stem cell differentiation, including differentiation of neural stem cells (NSCs). Here we studied the importance of mtDNA function in the early differentiation process of NSCs in two cell culture models: the CGR8-NS cell line that was derived from embryonic stem cells by a lineage selection technique, and primary NSCs that were isolated from embryonic day 14 mouse fetal forebrain. We detected a dramatic increase in mtDNA content upon NSC differentiation to adapt their mtDNA levels to their differentiated state, which was not accompanied by changes in mitochondrial transcription factor A expression. As chemical mtDNA depletion by ethidium bromide failed to generate living ρ° cell lines from both NSC types, we used inhibition of mtDNA polymerase-γ by 2′-3′-dideoxycytidine to reduce mtDNA replication and subsequently cellular mtDNA content. Inhibition of mtDNA replication upon NSC differentiation reduced neurogenesis but not gliogenesis. The mtDNA depletion did not change energy production/consumption or cellular reactive oxygen species (ROS) content in the NSC model used. In conclusion, mtDNA replication is essential for neurogenesis but not gliogenesis in fetal NSCs through as yet unknown mechanisms, which, however, are largely independent of energy/ROS metabolism.</p>","PeriodicalId":50589,"journal":{"name":"Development Growth & Differentiation","volume":"66 8","pages":"398-413"},"PeriodicalIF":1.7,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/dgd.12946","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142512320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}