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Seminars in Developmental Biology最新文献

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Neutrophins and neurite outgrowth in the peripheral nervous system 中性粒细胞和神经突生长在周围神经系统
Seminars in Developmental Biology Pub Date : 1994-12-01 DOI: 10.1006/sedb.1994.1050
Uwe Ernsberger, Hermann Rohrer
{"title":"Neutrophins and neurite outgrowth in the peripheral nervous system","authors":"Uwe Ernsberger,&nbsp;Hermann Rohrer","doi":"10.1006/sedb.1994.1050","DOIUrl":"10.1006/sedb.1994.1050","url":null,"abstract":"<div><p>In this review we summarize evidence for the involvement of neutrophins in the regulation of neurite outgrowth in the peripheral nervous system. Recent studies have shown that many neurons at early developmental stages respond to NT3 by increased survival and morphological differentiation in vitro. In addition, NT3 mRNA can be detected at this time in embryonic tissues trespassed by outgrowing neurites. Later during development, the NT3 response may be lost and replaced by a NGF response. The data show that an early NGF-independent, NT3-sensitive and a late NGF-responsive period can be distinguished for different developing peripheral neurons in vitro and raise the possibility that neurite outgrowth may be influenced by the different neutrophins, acting at distinct developmental periods in vivo.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 6","pages":"Pages 403-410"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83488214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Cell fate and axonal projections from the cerebral cortex 大脑皮层的细胞命运和轴突投射
Seminars in Developmental Biology Pub Date : 1994-12-01 DOI: 10.1006/sedb.1994.1046
Magdalena Götz, Jack Price
{"title":"Cell fate and axonal projections from the cerebral cortex","authors":"Magdalena Götz,&nbsp;Jack Price","doi":"10.1006/sedb.1994.1046","DOIUrl":"10.1006/sedb.1994.1046","url":null,"abstract":"<div><p>The formation of axonal connections in the nervous system involves cell-specific decisions of the growth cone. In this article we examine the contribution of early fate decisions to axonal pathfinding. Evidence is accumulating that different neuronal cell types in the cerebral cortex are specified during their final mitosis. It would seem that cortical projection neurons are pre-specified to choose particular pathways, since the newly generated neurons send out their axons in the correct direction from the onset of outgrowth. Pathfinding decisions that are made much later during development, such as the recognition of specific target-derived chemoattractants and the retraction of inappropriate axon collaterals, also seem to be at least partially pre-specified at much earlier developmental stages. Hence, the early determination of a neuron's phenotype includes the specification of axonal growth occuring over a protracted phase of development. Understanding more about the regulative events targeted to the growth cone should help us to unravel the decisions made by this specialized neuronal organelle.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 6","pages":"Pages 359-369"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74051903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Introduction: Mechanisms of axonal guidance in the CNS 导论:中枢神经系统轴突引导的机制
Seminars in Developmental Biology Pub Date : 1994-12-01 DOI: 10.1006/sedb.1994.1044
Roger Morris, Marie-Catherine Tiveron
{"title":"Introduction: Mechanisms of axonal guidance in the CNS","authors":"Roger Morris,&nbsp;Marie-Catherine Tiveron","doi":"10.1006/sedb.1994.1044","DOIUrl":"10.1006/sedb.1994.1044","url":null,"abstract":"","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 6","pages":"Page 347"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74586312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
How the growth cone recognizes and responds to its environment 生长锥如何识别和响应其环境
Seminars in Developmental Biology Pub Date : 1994-12-01 DOI: 10.1006/sedb.1994.1049
Roger J. Morris, Marie-Catherine Tiveron
{"title":"How the growth cone recognizes and responds to its environment","authors":"Roger J. Morris,&nbsp;Marie-Catherine Tiveron","doi":"10.1006/sedb.1994.1049","DOIUrl":"10.1006/sedb.1994.1049","url":null,"abstract":"<div><p>Four interactive processes—adhesion, guidance, migration and growth—combine to direct the axonal growth cone to its targets. It is becoming clear that the sensors of the external environment, the axonal receptors and adhesion molecules, activate second messenger systems in the growth cone. This allows a cytoplasmic integration of guidance signals acting upon the growth cone, that feeds back upon the adhesion molecules and the cytoskeleton to select the direction of growth. Movement is primarily generated by the actin microfilaments, growth is dependent upon the microtubules. This review examines the interdependence of these processes during the initial phase of axon elongation, using examples from insects to mammals.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 6","pages":"Pages 391-402"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84464257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Introduction: Genetic approaches to human developmental syndromes 引言:人类发育综合征的遗传方法
Seminars in Developmental Biology Pub Date : 1994-10-01 DOI: 10.1006/sedb.1994.1035
Veronica van Heyningen
{"title":"Introduction: Genetic approaches to human developmental syndromes","authors":"Veronica van Heyningen","doi":"10.1006/sedb.1994.1035","DOIUrl":"https://doi.org/10.1006/sedb.1994.1035","url":null,"abstract":"","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 5","pages":"Pages 273-274"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92071770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Imprinting mechanisms and genes involved in Prader-Willi and Angelman syndromes Prader-Willi综合征和Angelman综合征的印迹机制和基因
Seminars in Developmental Biology Pub Date : 1994-10-01 DOI: 10.1006/sedb.1994.1040
Robert D. Nicholls
{"title":"Imprinting mechanisms and genes involved in Prader-Willi and Angelman syndromes","authors":"Robert D. Nicholls","doi":"10.1006/sedb.1994.1040","DOIUrl":"10.1006/sedb.1994.1040","url":null,"abstract":"<div><p>Prader-Willi (PWS) and Angelman (AS) syndromes illustrate a disease paradigm of genomic imprinting, an epigenetic modification of DNA that results in parent-of-origin specific expression during embryogenesis and in the adult. From genetic data, at least two imprinted genes may be required for the classical PWS phenotype, whereas AS probably involves a single imprinted gene, and rare familial forms of both disorders involve imprinting mutations. In addition, the nonimprinted P gene is associated with pigmentation disorders in PWS, AS and oculocutaneous albinism. Identification of new genes, delineation of small deletions in unique patients, and direct screening for imprinted sequences, should soon identify candidate genes for PWS and AS. The mechanism of imprinting involves DNA methylation and replication timing, and appears to include multiple imprinted genes within a large imprinted domain. Imprinting of these genes may be regulated in cis, by an imprinting control element (ICE). Future studies can be expected to unravel the gene identities and imprinting mechanisms involved in these fascinating disorders; ultimately it may be possible to reactivate imprinted gene expression as a therapeutic approach.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 5","pages":"Pages 311-322"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88440925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
DiGeorge syndrome and related birth defects 乔治综合症和相关的先天缺陷
Seminars in Developmental Biology Pub Date : 1994-10-01 DOI: 10.1006/sedb.1994.1039
Peter James Scambler
{"title":"DiGeorge syndrome and related birth defects","authors":"Peter James Scambler","doi":"10.1006/sedb.1994.1039","DOIUrl":"10.1006/sedb.1994.1039","url":null,"abstract":"<div><p>Classically, DiGeorge syndrome patients have congenital heart defects, particularly involving the outflow tract, hypocalcaemia, cell-mediated immune deficiency, learning or behavioural problems, craniofacial dysmorphism and hemizygosity for a region of human chromosome 22q11. This chromosomal abnormality is now known to cause other syndromal defects and apparently isolated congenital heart disease. Although most patients have a large deletion, at least 2 Mb, a critical region of 300 kbp has been defined. Within this region a putative transcriptional regulator called TUPLE-1 has been identified. TUPLE-1 is proposed as a candidate gene for the 22q11 haploinsufficiency syndromes.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 5","pages":"Pages 303-310"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83626204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Denys-Drash syndrome: a role for the WT1 tumour suppressor gene in urogenital development Denys-Drash综合征:WT1肿瘤抑制基因在泌尿生殖发育中的作用
Seminars in Developmental Biology Pub Date : 1994-10-01 DOI: 10.1006/sedb.1994.1042
Wendy Bruening, Jerry Pelletier
{"title":"Denys-Drash syndrome: a role for the WT1 tumour suppressor gene in urogenital development","authors":"Wendy Bruening,&nbsp;Jerry Pelletier","doi":"10.1006/sedb.1994.1042","DOIUrl":"10.1006/sedb.1994.1042","url":null,"abstract":"Abstract The study of inherited disease provides unique insight into basic developmental and biochemical processes. By linking the pathogenesis of complex malformations to mutations of specific genes, the function of those genes in normal developmental biology can be inferred. One such disorder is the Denys-Drash syndrome, where identification of genetic lesions within the WT1 tumour suppressor gene has provided astonishing insight into events regulating development of the urogenital system.","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 5","pages":"Pages 333-343"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82587159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
Holoprosencephaly as a genetic model for normal craniofacial development 全前脑畸形是正常颅面发育的遗传模型
Seminars in Developmental Biology Pub Date : 1994-10-01 DOI: 10.1006/sedb.1994.1038
Maximilian Muenke
{"title":"Holoprosencephaly as a genetic model for normal craniofacial development","authors":"Maximilian Muenke","doi":"10.1006/sedb.1994.1038","DOIUrl":"10.1006/sedb.1994.1038","url":null,"abstract":"<div><p>Holoprosencephaly is a common developmental defect of the forebrain and midface in humans. Clinical expression is variable, extending in unbroken sequence from a small brain with a single cerebral ventricle and cyclopia to clinically unaffected carriers in familial holoprosencephaly. Significant aetiological heterogeneity in holoprosencephaly has been demonstrated including both genetic and environmental causes. Genetic approaches, such us positional cloning of genes involved in holoprosencephaly will result in a better understanding of normal development of the brain and face and, ultimately, elucidate the basic genetic defects which programme the abnormal formation seen in holoprosencephaly.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 5","pages":"Pages 293-301"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81072668","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: 68
PAX genes in human developmental anomalies 人类发育异常中的PAX基因
Seminars in Developmental Biology Pub Date : 1994-10-01 DOI: 10.1006/sedb.1994.1041
Andrew P. Read, Veronica van Heyningen
{"title":"PAX genes in human developmental anomalies","authors":"Andrew P. Read,&nbsp;Veronica van Heyningen","doi":"10.1006/sedb.1994.1041","DOIUrl":"10.1006/sedb.1994.1041","url":null,"abstract":"<div><p>Pax genes encode the highly conserved 128 amino acid paired domain, first seen in the Drosophila paired gene. Humans and mice each have nine Pax genes, scattered across the genome. They are mostly expressed in the developing nervous system, with some specific expression in adults, and they control important aspects of cell growth and differentiation. Development is sensitive to Pax gene dosage. Loss of function mutations in PAX3 and PAX6 cause Waardenburg syndrome and aniridia, respectively, while a gain of function mutation in which PAX3 forms a chimaeric gene by fusion to the FKHR transcription factor causes the paediatric tumour alveolar rhabdomyosarcoma. Pax gene mutations are likely to underlie other developmental syndromes and cancers.</p></div>","PeriodicalId":101155,"journal":{"name":"Seminars in Developmental Biology","volume":"5 5","pages":"Pages 323-332"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/sedb.1994.1041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82048663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 9
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