Journal of Developmental Biology最新文献_第10页

Sculpting an Embryo: The Interplay between Mechanical Force and Cell Division. 雕刻胚胎：机械力与细胞分裂的相互作用

IF 2.2

Journal of Developmental Biology Pub Date : 2022-09-01 DOI: 10.3390/jdb10030037

Nawseen Tarannum, Rohan Singh, Sarah Woolner

引用次数: 0

Drosophila melanogaster as a Tool for Amyotrophic Lateral Sclerosis Research. 作为肌萎缩侧索硬化研究工具的黑腹果蝇。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-08-30 DOI: 10.3390/jdb10030036

Krupa N Hegde, Ajay Srivastava

{"title":"Drosophila melanogaster as a Tool for Amyotrophic Lateral Sclerosis Research.","authors":"Krupa N Hegde, Ajay Srivastava","doi":"10.3390/jdb10030036","DOIUrl":"https://doi.org/10.3390/jdb10030036","url":null,"abstract":"Reliable animal model systems are an integral part of biological research. Ever since Thomas Hunt Morgan won a Nobel Prize for genetic work done using the fruit fly (Drosophila melanogaster) as a model organism, it has played a larger and more important role in genetic research. Drosophila models have long been used to study neurodegenerative diseases and have aided in identifying key disease progression biological pathways. Due to the availability of a vast array of genetic manipulation tools, its relatively short lifespan, and its ability to produce many progenies, D. melanogaster has provided the ability to conduct large-scale genetic screens to elucidate possible genetic and molecular interactions in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's Disease, and Amyotrophic Lateral Sclerosis (ALS). With regards to ALS, many of the gene mutations that have been discovered to be linked to the disease have been modeled in Drosophila to provide a look into a detailed model of pathogenesis. The aim of this review is to summarize key and newer developments in ALS research that have utilized Drosophila and to provide insight into the profound use of Drosophila as a tool for modeling this disease.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2022-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9505035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33469066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Feedback Regulation of Signaling Pathways for Precise Pre-Placodal Ectoderm Formation in Vertebrate Embryos. 反馈调节信号通路，促进脊椎动物胚胎前板外胚层的精确形成

IF 2.2

Journal of Developmental Biology Pub Date : 2022-08-26 DOI: 10.3390/jdb10030035

Tatsuo Michiue, Kohei Tsukano

引用次数: 0

Special Issue "Hox Genes in Development: New Paradigms". 特刊“发育中的Hox基因:新范式”。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-08-18 DOI: 10.3390/jdb10030034

Samir Merabet

引用次数: 0

Cleft Palate in Apert Syndrome. 先天性腭裂综合征。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-08-11 DOI: 10.3390/jdb10030033

Delayna Willie, Greg Holmes, Ethylin Wang Jabs, Meng Wu

{"title":"Cleft Palate in Apert Syndrome.","authors":"Delayna Willie, Greg Holmes, Ethylin Wang Jabs, Meng Wu","doi":"10.3390/jdb10030033","DOIUrl":"https://doi.org/10.3390/jdb10030033","url":null,"abstract":"Apert syndrome is a rare genetic disorder characterized by craniosynostosis, midface retrusion, and limb anomalies. Cleft palate occurs in a subset of Apert syndrome patients. Although the genetic causes underlying Apert syndrome have been identified, the downstream signaling pathways and cellular mechanisms responsible for cleft palate are still elusive. To find clues for the pathogenic mechanisms of palatal defects in Apert syndrome, we review the clinical characteristics of the palate in cases of Apert syndrome, the palatal phenotypes in mouse models, and the potential signaling mechanisms involved in palatal defects. In Apert syndrome patients, cleft of the soft palate is more frequent than of the hard palate. The length of the hard palate is decreased. Cleft palate is associated most commonly with the S252W variant of FGFR2. In addition to cleft palate, high-arched palate, lateral palatal swelling, or bifid uvula are common in Apert syndrome patients. Mouse models of Apert syndrome display palatal defects, providing valuable tools to understand the underlying mechanisms. The mutations in FGFR2 causing Apert syndrome may change a signaling network in epithelial-mesenchymal interactions during palatogenesis. Understanding the pathogenic mechanisms of palatal defects in Apert syndrome may shed light on potential novel therapeutic solutions.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2022-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40412852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

New Mutations in the 5' Region of the Notch Gene Affect Drosophila melanogaster Oogenesis. Notch基因5'区新突变影响黑腹果蝇的卵发生。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-08-09 DOI: 10.3390/jdb10030032

Elena I Volkova, Natalya V Dorogova, Oleg V Andreyenkov, Saveliy A Tikhomirov, Sergey A Demakov

{"title":"New Mutations in the 5' Region of the Notch Gene Affect Drosophila melanogaster Oogenesis.","authors":"Elena I Volkova, Natalya V Dorogova, Oleg V Andreyenkov, Saveliy A Tikhomirov, Sergey A Demakov","doi":"10.3390/jdb10030032","DOIUrl":"https://doi.org/10.3390/jdb10030032","url":null,"abstract":"The Notch pathway is an important and evolutionarily conserved signaling system involved in the development of multicellular organisms. Notch signaling plays an important role in the regulation of proliferation and differentiation of many cell types. In this study, we report new aspects of Notch gene participation in oogenesis using our previously generated mutations. The mutations consist of an insertion of an auxiliary element of a transgene construct into the first intron of the gene and a series of directed deletions within the 5' regulatory region of Notch. We showed that some of these mutations affect Drosophila oogenesis. This insertion, either alone or in combination with the deletion of an insulator sequence, led to lower expression of Notch in the ovaries. As a result, the formation of egg chambers was disturbed in middle oogenesis. These abnormalities have not been described previously and imply one more function of Notch in oogenesis. It can be assumed that Notch is associated with not only follicular epithelium morphogenesis but also cellular mechanisms of oocyte growth.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2022-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40412849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Role of Protein Kinase CK2 in Development and Disease Progression: A Critical Review. 蛋白激酶CK2在发育和疾病进展中的作用:综述

IF 2.7

Journal of Developmental Biology Pub Date : 2022-07-27 DOI: 10.3390/jdb10030031

Daniel Halloran, Venu Pandit, Anja Nohe

{"title":"The Role of Protein Kinase CK2 in Development and Disease Progression: A Critical Review.","authors":"Daniel Halloran, Venu Pandit, Anja Nohe","doi":"10.3390/jdb10030031","DOIUrl":"https://doi.org/10.3390/jdb10030031","url":null,"abstract":"Protein kinase CK2 (CK2) is a ubiquitous holoenzyme involved in a wide array of developmental processes. The involvement of CK2 in events such as neurogenesis, cardiogenesis, skeletogenesis, and spermatogenesis is essential for the viability of almost all organisms, and its role has been conserved throughout evolution. Further into adulthood, CK2 continues to function as a key regulator of pathways affecting crucial processes such as osteogenesis, adipogenesis, chondrogenesis, neuron differentiation, and the immune response. Due to its vast role in a multitude of pathways, aberrant functioning of this kinase leads to embryonic lethality and numerous diseases and disorders, including cancer and neurological disorders. As a result, CK2 is a popular target for interventions aiming to treat the aforementioned diseases. Specifically, two CK2 inhibitors, namely CX-4945 and CIBG-300, are in the early stages of clinical testing and exhibit promise for treating cancer and other disorders. Further, other researchers around the world are focusing on CK2 to treat bone disorders. This review summarizes the current understanding of CK2 in development, the structure of CK2, the targets and signaling pathways of CK2, the implication of CK2 in disease progression, and the recent therapeutics developed to inhibit the dysregulation of CK2 function in various diseases.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2022-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40412850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Acetaminophen Disrupts the Development of Pharyngeal Arch-Derived Cartilage and Muscle in Zebrafish. 对乙酰氨基酚破坏斑马鱼咽弓源性软骨和肌肉的发育。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-07-14 DOI: 10.3390/jdb10030030

Derrick M Glasco, Zhidong Wang, Seonwoo Kang, Avery T Funkhouser

{"title":"Acetaminophen Disrupts the Development of Pharyngeal Arch-Derived Cartilage and Muscle in Zebrafish.","authors":"Derrick M Glasco, Zhidong Wang, Seonwoo Kang, Avery T Funkhouser","doi":"10.3390/jdb10030030","DOIUrl":"https://doi.org/10.3390/jdb10030030","url":null,"abstract":"Acetaminophen is a common analgesic, but its potential effects on early embryonic development are not well understood. Previous studies using zebrafish (Danio rerio) have described the effects of acetaminophen on liver development and physiology, and a few have described gross physiological and morphological defects. Using a high but non-embryonic lethal dose of acetaminophen, we probed for defects in zebrafish craniofacial cartilage development. Strikingly, acetaminophen treatment caused severe craniofacial cartilage defects, primarily affecting both the presence and morphology of pharyngeal arch-derived cartilages of the viscerocranium. Delaying acetaminophen treatment restored developing cartilages in an order correlated with their corresponding pharyngeal arches, suggesting that acetaminophen may target pharyngeal arch development. Craniofacial cartilages are derived from cranial neural crest cells; however, many neural crest cells were still seen along their expected migration paths, and most remaining cartilage precursors expressed the neural crest markers sox9a and sox10, then eventually col2a1 (type II collagen). Therefore, the defects are not primarily due to an early breakdown of neural crest or cartilage differentiation. Instead, apoptosis is increased around the developing pharyngeal arches prior to chondrogenesis, further suggesting that acetaminophen may target pharyngeal arch development. Many craniofacial muscles, which develop in close proximity to the affected cartilages, were also absent in treated larvae. Taken together, these results suggest that high amounts of acetaminophen can disrupt multiple aspects of craniofacial development in zebrafish.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2022-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40564716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

The Core Splicing Factors EFTUD2, SNRPB and TXNL4A Are Essential for Neural Crest and Craniofacial Development. 核心剪接因子EFTUD2、SNRPB和TXNL4A对神经嵴和颅面发育至关重要。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-07-08 DOI: 10.3390/jdb10030029

Byung-Yong Park, Melanie Tachi-Duprat, Chibuike Ihewulezi, Arun Devotta, Jean-Pierre Saint-Jeannet

{"title":"The Core Splicing Factors EFTUD2, SNRPB and TXNL4A Are Essential for Neural Crest and Craniofacial Development.","authors":"Byung-Yong Park, Melanie Tachi-Duprat, Chibuike Ihewulezi, Arun Devotta, Jean-Pierre Saint-Jeannet","doi":"10.3390/jdb10030029","DOIUrl":"https://doi.org/10.3390/jdb10030029","url":null,"abstract":"Mandibulofacial dysostosis (MFD) is a human congenital disorder characterized by hypoplastic neural-crest-derived craniofacial bones often associated with outer and middle ear defects. There is growing evidence that mutations in components of the spliceosome are a major cause for MFD. Genetic variants affecting the function of several core splicing factors, namely SF3B4, SF3B2, EFTUD2, SNRPB and TXNL4A, are responsible for MFD in five related but distinct syndromes known as Nager and Rodriguez syndromes (NRS), craniofacial microsomia (CFM), mandibulofacial dysostosis with microcephaly (MFDM), cerebro-costo-mandibular syndrome (CCMS) and Burn-McKeown syndrome (BMKS), respectively. Animal models of NRS and MFDM indicate that MFD results from an early depletion of neural crest progenitors through a mechanism that involves apoptosis. Here we characterize the knockdown phenotype of Eftud2, Snrpb and Txnl4a in Xenopus embryos at different stages of neural crest and craniofacial development. Our results point to defects in cranial neural crest cell formation as the likely culprit for MFD associated with EFTUD2, SNRPB and TXNL4A haploinsufficiency, and suggest a commonality in the etiology of these craniofacial spliceosomopathies.","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2022-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40564715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Advances in Understanding the Pathogenesis of Craniofacial Birth Defects. 颅面出生缺陷发病机制的研究进展。

IF 2.7

Journal of Developmental Biology Pub Date : 2022-07-01 DOI: 10.3390/jdb10030027

Andre L P Tavares, Sally A Moody

引用次数: 0