Relevant bibliographies by topics / Developing telencephalon

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Academic literature on the topic 'Developing telencephalon'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Developing telencephalon"

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Grove, E. A., S. Tole, J. Limon, L. Yip, and C. W. Ragsdale. "The hem of the embryonic cerebral cortex is defined by the expression of multiple Wnt genes and is compromised in Gli3-deficient mice." Development 125, no. 12 (June 15, 1998): 2315–25. http://dx.doi.org/10.1242/dev.125.12.2315.

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In the developing vertebrate CNS, members of the Wnt gene family are characteristically expressed at signaling centers that pattern adjacent parts of the neural tube. To identify candidate signaling centers in the telencephalon, we isolated Wnt gene fragments from cDNA derived from embryonic mouse telencephalon. In situ hybridization experiments demonstrate that one of the isolated Wnt genes, Wnt7a, is broadly expressed in the embryonic telencephalon. By contrast, three others, Wnt3a, 5a and a novel mouse Wnt gene, Wnt2b, are expressed only at the medial edge of the telencephalon, defining the hem of the cerebral cortex. The Wnt-rich cortical hem is a transient, neuron-containing, neuroepithelial structure that forms a boundary between the hippocampus and the telencephalic choroid plexus epithelium (CPe) throughout their embryonic development. Indicating a close developmental relationship between the cortical hem and the CPe, Wnt gene expression is upregulated in the cortical hem both before and just as the CPe begins to form, and persists until birth. In addition, although the cortical hem does not show features of differentiated CPe, such as expression of transthyretin mRNA, the CPe and cortical hem are linked by shared expression of members of the Bmp and Msx gene families. In the extra-toesJ (XtJ) mouse mutant, telencephalic CPe fails to develop. We show that Wnt gene expression is deficient at the cortical hem in XtJ/XtJ mice, but that the expression of other telencephalic developmental control genes, including Wnt7a, is maintained. The XtJ mutant carries a deletion in Gli3, a vertebrate homolog of the Drosophila gene cubitus interruptus (ci), which encodes a transcriptional regulator of the Drosophila Wnt gene, wingless. Our observations indicate that Gli3 participates in Wnt gene regulation in the vertebrate telencephalon, and suggest that the loss of telencephalic choroid plexus in XtJ mice is due to defects in the cortical hem that include Wnt gene misregulation.
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Striedter, Georg F., and Christine J. Charvet. "Telencephalon enlargement by the convergent evolution of expanded subventricular zones." Biology Letters 5, no. 1 (October 7, 2008): 134–37. http://dx.doi.org/10.1098/rsbl.2008.0439.

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Some mammals and birds independently evolved an enlarged telencephalon. They appear to have done so, at least in part, by developing a thick telencephalic subventricular zone (SVZ). We suggest that this correlation between telencephalic enlargement and SVZ expansion is due to a mechanical constraint acting on the proliferative ventricular zone (VZ). Essentially, we argue that rapid proliferation in the VZ after post-mitotic cells in the overlying mantle zone have begun to form limits the VZ's tangential expandability and forces some proliferating cells to emigrate from the VZ and expand the pool of proliferating cells that comprise the SVZ.
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Shinya, Minori, Sumito Koshida, Atsushi Sawada, Atsushi Kuroiwa, and Hiroyuki Takeda. "Fgf signalling through MAPK cascade is required for development of the subpallial telencephalon in zebrafish embryos." Development 128, no. 21 (November 1, 2001): 4153–64. http://dx.doi.org/10.1242/dev.128.21.4153.

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The telencephalon is formed in the most anterior part of the central nervous system (CNS) and is organised into ventral subpallial and dorsal pallial domains. In mice, it has been demonstrated that Fgf signalling has an important role in induction and patterning of the telencephalon. However, the precise role of Fgf signalling is still unclear, owing to overlapping functions of Fgf family genes. To address this, we have examined, in zebrafish embryos, the activation of Ras/mitogen-activated protein kinase (MAPK), one of the major downstream targets of Fgf signalling. Immunohistochemical analysis reveals that an extracellular signal-regulated kinase (ERK), a vertebrate MAPK is activated in the anterior neural boundary (ANB) of the developing CNS at early segmentation stages. Experiments with Fgf inhibitors reveal that ERK activation at this stage is totally dependent on Fgf signalling. Interestingly, a substantial amount of ERK activation is observed in ace mutants in which fgf8 gene is mutated. We then examine the function of Fgf signalling in telencephalic development by use of several inhibitors to Fgf signalling cascade, including dominant-negative forms of Ras (RasN17) and the Fgf receptor (Fgfr), and a chemical inhibitor of Fgfr, SU5402. In treated embryos, the induction of telencephalic territory normally proceeded but the development of the subpallial telencephalon was suppressed, indicating that Fgf signalling is required for the regionalisation within the telencephalon. Finally, antisense experiments with morpholino-modified oligonucleotides suggest that zebrafish fgf3, which is also expressed in the ANB, co-operates with fgf8 in subpallial development.
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Chapouton, P., A. Gartner, and M. Gotz. "The role of Pax6 in restricting cell migration between developing cortex and basal ganglia." Development 126, no. 24 (December 15, 1999): 5569–79. http://dx.doi.org/10.1242/dev.126.24.5569.

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It is not clear to what extent restricted cell migration contributes to patterning of the developing telencephalon, since both restricted and widespread cell migration have been observed. Here, we have analysed dorso-ventral cell migration in the telencephalon of Pax6 mutant mice (Small Eye). The transcription factor Pax6 is expressed in the dorsal telencephalon, the cerebral cortex. Focal injections of adenoviral vectors containing the green fluorescent protein were used to follow and quantify cell movements between two adjacent regions in the developing telencephalon, the cerebral cortex and the ganglionic eminence (the prospective basal ganglia). The analysis in wild-type mice confirmed that the cortico-striatal boundary acts as a semipermeable filter and allows a proportion of cells from the ganglionic eminence to invade the cortex, but not vice versa. Ventro-dorsal cell migration was strongly enhanced in the Pax6 mutant. An essential function of Pax6 in the regionalisation of the telencephalon is then to limit the invasion of the cortex by cells originating in the ganglionic eminence. Cortical cells, however, remain confined to the cortex in the Pax6 mutant. Thus, dorsal and ventral cells are restricted to their respective territories by distinct mechanisms.
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Smith, D. "Retinoic Acid Synthesis for the Developing Telencephalon." Cerebral Cortex 11, no. 10 (October 1, 2001): 894–905. http://dx.doi.org/10.1093/cercor/11.10.894.

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Girós, Amparo, Javier Morante, Cristina Gil-Sanz, Alfonso Fairén, and Mercedes Costell. "Perlecan controls neurogenesis in the developing telencephalon." BMC Developmental Biology 7, no. 1 (2007): 29. http://dx.doi.org/10.1186/1471-213x-7-29.

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Pineda, Daniel, Beatriz García, José Luis Olmos, José Carlos Dávila, María Ángeles Real, and Salvador Guirado. "Semaphorin5A expression in the developing chick telencephalon." Brain Research Bulletin 66, no. 4-6 (September 2005): 436–40. http://dx.doi.org/10.1016/j.brainresbull.2005.02.011.

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Tichy, Julia, Jenny Zinke, Benedikt Bunz, Richard Meyermann, Patrick N. Harter, and Michel Mittelbronn. "Expression Profile of Sonic Hedgehog Pathway Members in the Developing Human Fetal Brain." BioMed Research International 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/494269.

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The Sonic Hedgehog (SHH) pathway plays a central role in the developing mammalian CNS. In our study, we aimed to investigate the spatiotemporalSHHpathway expression pattern in human fetal brains. We analyzed 22 normal fetal brains for Shh, Patched, Smoothened, and Gli1-3 expression by immunohistochemistry. In the telencephalon, strongest expression of Shh, Smoothened, and Gli2 was found in the cortical plate (CP) and ventricular zone. Patched was strongly upregulated in the ventricular zone and Gli1 in the CP. In the cerebellum,SHHpathway members were strongly expressed in the external granular layer (EGL).SHHpathway members significantly decreased over time in the ventricular and subventricular zone and in the cerebellar EGL, while increasing levels were found in more superficial telencephalic layers. Our findings show thatSHHpathway members are strongly expressed in areas important for proliferation and differentiation and indicate a temporal expression gradient in telencephalic and cerebellar layers probably due to decreased proliferation of progenitor cells and increased differentiation. Our data about the spatiotemporal expression ofSHHpathway members in the developing human brain serves as a base for the understanding of both normal and pathological CNS development.
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Zappone, M. V., R. Galli, R. Catena, N. Meani, S. De Biasi, E. Mattei, C. Tiveron, et al. "Sox2 regulatory sequences direct expression of a (beta)-geo transgene to telencephalic neural stem cells and precursors of the mouse embryo, revealing regionalization of gene expression in CNS stem cells." Development 127, no. 11 (June 1, 2000): 2367–82. http://dx.doi.org/10.1242/dev.127.11.2367.

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Sox2 is one of the earliest known transcription factors expressed in the developing neural tube. Although it is expressed throughout the early neuroepithelium, we show that its later expression must depend on the activity of more than one regionally restricted enhancer element. Thus, by using transgenic assays and by homologous recombination-mediated deletion, we identify a region upstream of Sox2 (−5.7 to −3.3 kb) which can not only drive expression of a (beta)-geo transgene to the developing dorsal telencephalon, but which is required to do so in the context of the endogenous gene. The critical enhancer can be further delimited to an 800 bp fragment of DNA surrounding a nuclease hypersensitive site within this region, as this is sufficient to confer telencephalic expression to a 3.3 kb fragment including the Sox2 promoter, which is otherwise inactive in the CNS. Expression of the 5.7 kb Sox2(beta)-geo transgene localizes to the neural plate and later to the telencephalic ventricular zone. We show, by in vitro clonogenic assays, that transgene-expressing (and thus G418-resistant) ventricular zone cells include cells displaying functional properties of stem cells, i.e. self-renewal and multipotentiality. We further show that the majority of telencephalic stem cells express the transgene, and this expression is largely maintained over two months in culture (more than 40 cell divisions) in the absence of G418 selective pressure. In contrast, stem cells grown in parallel from the spinal cord never express the transgene, and die in G418. Expression of endogenous telencephalic genes was similarly observed in long-term cultures derived from the dorsal telencephalon, but not in spinal cord-derived cultures. Thus, neural stem cells of the midgestation embryo are endowed with region-specific gene expression (at least with respect to some networks of transcription factors, such as that driving telencephalic expression of the Sox2 transgene), which can be inherited through multiple divisions outside the embryonic environment.
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Rakic, Sonja, and Nada Zecevic. "Programmed cell death in the developing human telencephalon." European Journal of Neuroscience 12, no. 8 (August 2000): 2721–34. http://dx.doi.org/10.1046/j.1460-9568.2000.00153.x.

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Dissertations / Theses on the topic "Developing telencephalon"

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Chapouton, Prisca. "Regionalization of the developing mouse telencephalon." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-11597.

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Sarma, Subrot. "Gene expression analysis in the developing human telencephalon." Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443196.

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Qin, Shenyue. "Regional Contributions to Neuronal Diversity in the Developing Mouse Telencephalon." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1505125562574288.

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Frowein, Julia von. "The Role of Emx1 and Emx2 in the developing chick telencephalon." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-37285.

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Mi, Da. "Investigation of gene networks by which Pax6 regulates progenitor cell proliferation in the developing telencephalon." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/17923.

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The Pax6 encodes a highly conserved transcriptional regulator that contains two DNA binding domains, the paired domain (PD) and homeodomain (HD). In mammals, Pax6 is widely expressed in a complex spatiotemporal pattern during the development of the eye, olfactory bulbs and central nervous system and plays important roles in pattern formation, cell fate determination and cell cycle progression in these regions. Normal development requires Pax6 to be present in certain cells with correct levels, which implies that Pax6 expression is tightly controlled and that different levels need to be maintained across different regions as they develop. To gain better insight into the regulatory mechanisms of Pax6 expression, a series of tauGFP-Pax6 transgenic reporter mouse lines was previously generated in which the expression of tauGFP is under the control of putative Pax6 regulatory elements. Here, I have characterized the functional importance these regulatory elements by comparing the pattern of tauGFP expression with endogenous Pax6 expression in transgenic mice containing either complete or truncated versions of the reporter. I showed that the expression of tauGFP reporter exhibits the known Pax6 expression pattern in forebrain and eye, except for some minor discrepancy within the telecephalon. The loss of tauGFP expression within the eye and thalamus was observed in transgenic lines carrying truncated reporter sequences lacking the downstream regulatory region (DDR) of Pax6. Analysis of the pattern of GFP reporter expression in transgenic lines that vary in the extent of their putative Pax6 regulatory elements revealed the functional significance of these elements and also implied the existence of unknown distal regulatory elements, outside of the reporter sequences, which control Pax6 expression in the telecephalon. I went on to study a Pax6-dependent signaling pathway through which Pax6 controls progenitor cell proliferation in the developing telencephalon. Comparison of cell cycle parameters between Pax6+/+ and Pax6sey/sey progenitors suggested that correct levels of Pax6 are crucial in regulating progenitor cell proliferation. To address the possible molecular basis of the cell cycle defect observed in Pax6sey/sey embryos, the expression of a number of cell cycle genes was analyzed by qRT-PCR in the lateral cortex of Pax6+/+ and Pax6sey/sey embryos, which confirmed the significantly altered expression levels of these genes. Of them, Cdk6 was further identified as a direct target of Pax6 and the interaction of putative binding sites with Pax6 protein was confirmed by EMSA in vitro and by qChIP in vivo. In addition, the functional role of these Pax6 binding sites, through which Pax6 represses the transcription of Cdk6, was further evaluated by luciferase assays. Activation of Cdk6 is required for pRb phosphorylation as well as induction of the pRB/E2F pathway, and in turn promotes the G1-S cell-cycle transition. An increase in pRb phosphorylation accompanied by changes in pRb subcellular distribution and up-regulation of E2F downstream targets were observed in the cortex of Pax6sey/sey embryos. In contrast, a reduction of Cdk6 expression and pRb phosphorylation was found in HEK293 cells overexpressing Pax6. Collectively, these findings provided new insight into the molecular mechanism of Pax6-dependent regulation of progenitor cell proliferation in the developing telecephalon.
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Wilkie, Alison Louise. "A study of the developing melanoblast and telencephalon lineages in the mouse embryo by in vitro manipulation and retrospective clonal analysis." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23260.

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A primary neural tube culture assay was used to study the early stages of melanoblast specification, proliferation, and migration. This assay was used to study the roles of different cell signalling pathways known to affect melanoblast development in vivo. KITL significantly affected both the proportion of crest cells that were melanoblasts and the distance they migrated, while EDN3 only affected melanoblast numbers. HGF increased the migration distance of melanoblasts in culture, while MSH affected neither melanoblast migration nor numbers. Studies of adult chimaeras derived from embryos carrying different coat colour markers have suggested that total melanoblast population is derived from a small number of progenitors, each generating a discrete unilateral transverse band of colour with minimal mixing between clones. In this study, two complementary approaches were used to assess the behaviour of labelled clones during development. Firstly, aggregation chimaeras were made between Dct-LacZ and non-transgenic embryos. The Dct promoter drives expression from E10 in melanoblasts and in cells of the telencephalon. Resultant patterns of labelled melanoblasts were studied during mid-gestation. Secondly, transgenic mice were generated that carry a modified LaacZ reporter construct containing a 300bp duplication (LaacZ) under the control of the Dct promoter. The LaacZ transgene is normally inactive, but it reverts to wild type LacZ at low frequency, labelling a cell and all its progeny apparently at random. Together, chimaeric and mosaic embryos suggested the melanoblast population is derived from a large number of progenitors, a pool of melanoblasts may reside in the cervical region, and melanoblasts within a clone show considerable longitudinal migration, suggesting there is significant axial mixing between clones. Interestingly, radially arrayed labelled clones were also generated in the telencephalon in Dct-LaacZ embryos.
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Chapouton, Prisca [Verfasser]. "Regionalization of the developing mouse telencephalon : cellular and molecular mechanisms / Prisca Chapouton." 2002. http://d-nb.info/968814964/34.

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Frowein, Julia von [Verfasser]. "The role of Emx1 and Emx2 in the developing chick telencephalon / Julia von Frowein." 2004. http://d-nb.info/975433466/34.

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Abbas, Eman Ahmed Ahmed Mohamed. "Role of chromatin remodelling BAF complex in fate regulation of ventral neural stem cells in the developing telencephalon." Doctoral thesis, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-1547-4.

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Books on the topic "Developing telencephalon"

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Kostovic, Ivica. Guidance Cues in the Developing Brain (Progress in Molecular and Subcellular Biology). Springer, 2003.

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Book chapters on the topic "Developing telencephalon"

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Judaš, M., N. J. Milošević, M. R. Rašin, M. Heffer-Lauc, and I. Kostović. "Complex Patterns and Simple Architects: Molecular Guidance Cues for Developing Axonal Pathways in the Telencephalon." In Guidance Cues in the Developing Brain, 1–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55557-2_1.

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Tole, Shubha, and Jean Hébert. "Telencephalon patterning." In Patterning and Cell Type Specification in the Developing CNS and PNS, 23–48. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-814405-3.00002-3.

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Tole, S., and J. Hébert. "Telencephalon Patterning." In Patterning and Cell Type Specification in the Developing CNS and PNS, 3–24. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-397265-1.00018-6.

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Encha-Razavi, Féréchté, Rebecca Folkerth, Brian N. Harding, Harry V. Vinters, and Jeffrey A. Golden. "Congenital Malformations and Perinatal Diseases." In Escourolle and Poirier's Manual of Basic Neuropathology, 257–77. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199929054.003.0011.

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This chapter describes and illustrates the changes of the CNS in congenital malformations and perinatal diseases; it also provides insights into the genetic abnormalities associated with these conditions. Congenital malformations include neurulation failure resulting in neural tube closure defects, disorders of development of the prosencephalon, malformations of the cortical plate (neuronal heterotopia, polymicrogyria, lissencephaly, and focal cortical dysplasia, a frequent cause of epilepsy in children), and disorders of hindbrain development, particularly malformations of the cerebellum. Destructive lesions of developing brain are described in association with a variety of situations generally resulting in “hypoxia-ischemia.” They may affect the neocortex, causing porencephaly or hydranencephaly, the basal ganglia (status marmoratus), or the white matter (perinatal telencephalic leukoencephalopathy and periventricular leukomalacia).
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Adle-Biassette, Homa, Brian Harding, and Jeffrey A. Golden. "Congenital Malformations and Perinatal Diseases." In Escourolle and Poirier's Manual of Basic Neuropathology, 275–98. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190675011.003.0011.

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This chapter describes and illustrates the changes of the central nervous system in congenital malformations and perinatal diseases; it also provides insights in the genetic abnormalities associated with these conditions. Congenital malformations include neurulation failure resulting in neural tube closure defects; disorders of development of the prosencephalon; malformations of the cortical plate (neuronal heterotopia, polymicrogyria, lissencephaly, and focal cortical dysplasia [a frequent cause of epilepsy in children]); and disorders of hindbrain development, particularly malformations of the cerebellum. Destructive lesions of developing brain are described in association with a variety of situations generally resulting in “hypoxia-ischemia.” They may affect the neocortex, causing porencephaly or hydranencephaly; the basal ganglia (status marmoratus); or the white matter (perinatal telencephalic leukoencephalopathy and periventricular leukomalacia).
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