Cells and Development最新文献

{"title":"“And it was the worst possible result, because it actually worked:” An interview with Richard Harland","authors":"","doi":"10.1016/j.cdev.2024.203910","DOIUrl":"10.1016/j.cdev.2024.203910","url":null,"abstract":"<div><p>One hundred years ago, Hilde Mangold and Hans Spemann published their seminal paper on what came to be known as The Organizer, but seven decades would pass before the molecular basis of this remarkable phenomenon was revealed. Richard Harland and his laboratory played a key role in that discovery, and in this interview he discusses not just the science and the people but also other important factors like mental health and luck.</p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"178 ","pages":"Article 203910"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667290124000111/pdfft?md5=1c24d95e395730785b1704875cdcecaa&pid=1-s2.0-S2667290124000111-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060740","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}

{"title":"Get to know the Editors of CELLS & DEVELOPMENT","authors":"","doi":"10.1016/j.cdev.2024.203939","DOIUrl":"10.1016/j.cdev.2024.203939","url":null,"abstract":"","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"178 ","pages":"Article 203939"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141890258","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}

{"title":"Reprint of: Celebrating Spemann-Mangold at 100: An interview with Eddy De Robertis","authors":"","doi":"10.1016/j.cdev.2024.203917","DOIUrl":"10.1016/j.cdev.2024.203917","url":null,"abstract":"","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"178 ","pages":"Article 203917"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667290124000184/pdfft?md5=9a31b07f5ff4d07a52c68210acd68152&pid=1-s2.0-S2667290124000184-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140307132","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}

{"title":"Induction of Embryonic Primordia by Implantation of Organizers from a Different Species","authors":"Hans Spemann,&nbsp;Hilde Mangold (née Pröscholdt)","doi":"10.1016/j.cdev.2024.203940","DOIUrl":"10.1016/j.cdev.2024.203940","url":null,"abstract":"","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"178 ","pages":"Article 203940"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141856671","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}

{"title":"Characterization of agouti-signaling protein (ASIP) in the bovine ovary and throughout early embryogenesis","authors":"","doi":"10.1016/j.cdev.2024.203930","DOIUrl":"10.1016/j.cdev.2024.203930","url":null,"abstract":"<div><p><span><span>The oocyte expresses certain genes during </span>folliculogenesis<span> to regulate the acquisition of oocyte competence<span>. Oocyte competence, or oocyte quality, is directly related to the ability of the oocyte to result in a successful pregnancy following fertilization. Presently, approximately 40 % of bovine<span> embryos will develop to the blastocyst<span><span> stage in vitro. Characterization of factors regulating these processes is crucial to improve the efficiency of bovine in vitro embryo production. We demonstrated that the secreted protein, agouti-signaling protein (ASIP) is highly abundant in the bovine oocyte and aimed to characterize its spatiotemporal expression profile in the ovary and throughout early </span>embryonic development. In addition to oocyte expression, </span></span></span></span></span><em>ASIP</em><span><span> was detected in granulosa, cumulus, and theca<span><span><span> cells isolated from antral follicles. Both gene expression data and immunofluorescent staining indicated ASIP declines with </span>oocyte maturation<span> which may indicate a potential role for ASIP in the attainment of oocyte competence. Microinjection of </span></span>zygotes using </span></span>small interfering RNA targeting </span><em>ASIP</em><span><span> led to a 16 % reduction in the rate of development to the blastocyst stage. Additionally, we examined potential ASIP signaling mechanisms through which ASIP may function to establish oocyte developmental competence. The expression of </span>melanocortin receptor </span><em>3</em> and <em>4</em><span> and the coreceptor attractin was detected in the oocyte and follicular cells<span>. The addition of cortisol during in vitro maturation was found to increase significantly oocyte </span></span><em>ASIP</em><span> levels. In conclusion, these results suggest a functional role for ASIP in promoting oocyte maturation and subsequent embryonic development, potentially through signaling mechanisms involving cortisol.</span></p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"179 ","pages":"Article 203930"},"PeriodicalIF":3.9,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141180979","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}

{"title":"FasL impacts Tgfb signaling in osteoblastic cells","authors":"","doi":"10.1016/j.cdev.2024.203929","DOIUrl":"10.1016/j.cdev.2024.203929","url":null,"abstract":"<div><p><span><span>Fas ligand (FasL, CD178) belongs to classical apoptotic molecules, however, recent evidence expands the spectrum of FasL functions into non-apoptotic processes which also applies for the bone. </span>Tgfb<span><span><span> subfamily members (Tgfb1, Tgfb2, Tgfb3) represent major components in osteogenic pathways and extracellular matrix. Their possible association with FasL has not yet been investigated but can be postulated. To test such a hypothesis, FasL deficient (gld) calvaria-derived cells were examined with a focus on the expression of </span>Tgfb receptor ligands. The </span>qPCR analysis revealed significantly increased expression of </span></span><em>Tgfb1</em>, <em>Tgfb2</em> and <em>Tgfb3</em><span> in gld cells. To check the </span><em>vice versa</em> effect, the gld cells were stimulated by soluble FasL. As a consequence, a dramatic decrease in expression levels of all three ligands was observed. This phenomenon was also confirmed in IDG-SW3 (osteoblastic cells of endochondral origin).</p><p>TFLink gateway identified Fosl2 as an exclusive candidate of FasL capable to impact expression of all three <span><em>Tgfb</em></span> ligands. However, <em>Fosl2</em><span> siRNA did not cause any significant changes in expression of </span><em>Tgfb</em><span> ligands. Therefore, the upregulation of the three ligands is likely to occur separately. In this respect, we tested the only exclusive candidate transcription factor for Tgfb3, Prrx1. Additionally, an overlapping candidate for Tgfb1 and Tgfb2, Mef2c capable to modulate expression of sclerostin, was examined. </span><em>Prrx1</em> as well as <em>Mef2c</em> were found upregulated in gld samples and their expression decreased after addition of FasL. The same effect of FasL treatment was observed in the IDG-SW3 model.</p><p>Taken together, FasL deficiency causes an increase in the expression of <em>Tgfb</em> ligands and stimulation by FasL reduces <em>Tgfb</em> expression in osteoblastic cells. The candidates mediating the effect comprise Prrx1 for Tgfb3 and Mef2c for Tgfb1/2. These results indicate FasL as a novel cytokine interfering with Tgfb signaling and thus the complex osteogenic network. The emerging non-apoptotic functions of FasL in bone development and maintenance should also be considered in treatment strategies such as the anti-osteoporotic factor.</p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"179 ","pages":"Article 203929"},"PeriodicalIF":3.9,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141176649","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}

{"title":"AZIN2 is associated with apoptosis of germ cells in undescended testis","authors":"","doi":"10.1016/j.cdev.2024.203925","DOIUrl":"10.1016/j.cdev.2024.203925","url":null,"abstract":"<div><p>Undescended testis (UDT), known as cryptorchidism (CRY), is a common congenital disorder in which one or both testicles do not descend normally into the scrotum. A unilateral UDT model was established by inducing UDT in mice through surgery. The results showed that the testis in the UDT model group was abnormal; the lumen of the seminiferous tubule was atrophic; apoptosis, necrosis and shedding were observed in many of the germ cells; the level of sex hormones was abnormal; and mature sperm was reduced. Subsequently, transcriptome sequencing was conducted on the testicular tissue of UDT model mice. Through analysis and verification of differential genes, AZIN2 was identified as playing a key role in the decline in male fertility caused by cryptorchidism. AZIN2 expression and spermine content was down-regulated in the testis of the UDT group. We then used a combination of hypoxanthine and xanthine to create a GC-1 cell damage model. In this model, AZIN2 expression and spermine content was down-regulated. When si-<em>Azin2</em> transfected GC-1 cells, cell viability and proliferation were decreased. However, in the GC-1 cell damage model transfected with <em>Azin2</em> over-expressed plasmid, AZIN2 expression and spermine content was up-regulated, reversing the cell damage caused by hypoxanthine and xanthine, and restoring the proliferation ability of GC-1 cells. These results indicate that in UDT, down-regulated AZIN2 expression is a factor in testicular damage. This discussion of the connection between AZIN2 and germ cells has important clinical significance as it provides an important reference for the diagnosis and treatment of cryptorchidism.</p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"179 ","pages":"Article 203925"},"PeriodicalIF":3.9,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141133702","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}

{"title":"Epigenetic inheritance of acquired traits via stem cells dedifferentiation/differentiation or transdifferentiation cycles","authors":"","doi":"10.1016/j.cdev.2024.203928","DOIUrl":"10.1016/j.cdev.2024.203928","url":null,"abstract":"<div><p><span><span><span>Inheritance of acquired characteristics is the once widely accepted idea that multiple modifications acquired by an organism during its life, can be inherited by the offspring. This belief is at least as old as Hippocrates and became popular in early 19th century, leading Lamarck to suggest his theory of evolution. Charles Darwin, along with other thinkers of the time attempted to explain the mechanism of acquired traits' inheritance by proposing the theory of </span>pangenesis<span>. While later this and similar theories were rejected because of the lack of hard evidence, the studies aimed at revealing the mechanism by which somatic information can be passed to germ cells have continued up to the present. In this paper, we present a new theory and provide supporting literature to explain this phenomenon. We hypothesize existence of pluripotent adult stem cells<span> that can serve as collectors and carriers of new epigenetic traits by entering different developmentally active organ/tissue compartments through blood circulation and acquiring new epigenetic marks though cycles of differentiation/dedifferentiation or transdifferentiation. During </span></span></span>gametogenesis, these epigenetically modified cells are attracted by gonads, transdifferentiate into germ cells, and pass the acquired </span>epigenetic modifications<span> collected from the entire body's somatic cells to the offspring.</span></p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"179 ","pages":"Article 203928"},"PeriodicalIF":3.9,"publicationDate":"2024-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141071285","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}

{"title":"Ex vivo organotypic bone slice culture reveals preferential chondrogenesis after sustained growth plate injury","authors":"","doi":"10.1016/j.cdev.2024.203927","DOIUrl":"10.1016/j.cdev.2024.203927","url":null,"abstract":"<div><p>Postnatal bone growth primarily relies on chondrocyte proliferation and osteogenic differentiation within the growth plate (GP) via endochondral ossification. Despite its importance, the GP is vulnerable to injuries, affecting 15–30 % of bone fractures. These injuries may lead to growth discrepancies, influence bone length and shape, and negatively affecting the patient's quality of life. This study aimed to investigate the molecular and cellular physiological and pathophysiological regeneration following sustained growth plate injury (GPI) in an ex vivo rat femur organotypic culture (OTC) model. Specifically, focusing on postnatal endochondral ossification process. 300 μm thick ex vivo bone cultures with a 2 mm long horizontal GPI was utilized. After 15 days of cultivation, gene expression analysis, histological and immunohistochemistry staining's were conducted to analyze key markers of endochondral ossification. In our OTCs we observed a significant increase in Sox9 expression due to GPI at day 15. The Ihh-PTHrP feedback loop was affected, favoring chondrocyte proliferation and maturation. Ihh levels increased significantly on day 7 and day 15, while PTHrP was downregulated on day 7. GPI had no impact on osteoclast number and activity, but gene expression analysis indicated OTCs' efforts to inhibit osteoclast differentiation and activation, thereby reducing bone resorption.</p><p>In conclusion, our study provides novel insights into the molecular and cellular mechanisms underlying postnatal bone growth and regeneration following growth plate injury (GPI). We demonstrate that chondrocyte proliferation and differentiation play pivotal roles in the regeneration process, with the Ihh-PTHrP feedback loop modulating these processes. Importantly, our ex vivo rat femur organotypic culture model allows for the detailed investigation of these processes, providing a valuable tool for future research in the field of skeletal biology and regenerative medicine.</p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"179 ","pages":"Article 203927"},"PeriodicalIF":3.9,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667290124000287/pdfft?md5=1728c6b31c7e35e3fef8b778d8a9485e&pid=1-s2.0-S2667290124000287-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140917263","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}

{"title":"Evaluating neural crest cell migration in a Col4a1 mutant mouse model of ocular anterior segment dysgenesis","authors":"","doi":"10.1016/j.cdev.2024.203926","DOIUrl":"10.1016/j.cdev.2024.203926","url":null,"abstract":"<div><p>The periocular mesenchyme (POM) is a transient migratory embryonic tissue derived from neural crest cells (NCCs) and paraxial mesoderm that gives rise to most of the structures in front of the eye. Morphogenetic defects of these structures can impair aqueous humor outflow, leading to elevated intraocular pressure and glaucoma. Mutations in collagen type IV alpha 1 (<em>COL4A1</em>) and alpha 2 (<em>COL4A2</em>) cause Gould syndrome – a multisystem disorder often characterized by variable cerebrovascular, ocular, renal, and neuromuscular manifestations. Approximately one-third of individuals with <em>COL4A1</em> and <em>COL4A2</em> mutations have ocular anterior segment dysgenesis (ASD), including congenital glaucoma resulting from abnormalities of POM-derived structures. POM differentiation has been a major focus of ASD research, but the underlying cellular mechanisms are still unclear. Moreover, earlier events including NCC migration and survival defects have been implicated in ASD; however, their roles are not as well understood. Vascular defects are among the most common consequences of <em>COL4A1</em> and <em>COL4A2</em> mutations and can influence NCC survival and migration. We therefore hypothesized that NCC migration might be impaired by <em>COL4A1</em> and <em>COL4A2</em> mutations. In this study, we used 3D confocal microscopy, gross morphology, and quantitative analyses to test NCC migration in <em>Col4a1</em> mutant mice. We show that homozygous <em>Col4a1</em> mutant embryos have severe embryonic growth retardation and lethality, and we identified a potential maternal effect on embryo development. Cerebrovascular defects in heterozygous <em>Col4a1</em> mutant embryos were present as early as E9.0, showing abnormal cerebral vasculature plexus remodeling compared to controls. We detected abnormal NCC migration within the diencephalic stream and the POM in heterozygous <em>Col4a1</em> mutants whereby mutant NCCs formed smaller diencephalic migratory streams and POMs. In these settings, migratory NCCs within the diencephalic stream and POM localize farther away from the developing vasculature. Our results show for the first time that <em>Col4a1</em> mutations lead to cranial NCCs migratory defects in the context of early onset defective angiogenesis without affecting cell numbers, possibly impacting the relation between NCCs and the blood vessels during ASD development.</p></div>","PeriodicalId":36123,"journal":{"name":"Cells and Development","volume":"179 ","pages":"Article 203926"},"PeriodicalIF":3.9,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667290124000275/pdfft?md5=5951e9f0aa655516a0c752134d2b1079&pid=1-s2.0-S2667290124000275-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140904807","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}