Why the embryo still matters: CSF and the neuroepithelium as interdependent regulators of embryonic brain growth, morphogenesis and histiogenesis

Gato, Á.; Desmond, Mary E.

doi:10.1016/j.ydbio.2008.12.029

Cited by 87 publications

(96 citation statements)

References 69 publications

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“…Many such signals have been found in fetal CSF (fCSF), indicating that fCSF is part of the neurogenic niche (Owen-Lynch et al, 2003;Gato et al, 2005;Miyan et al, 2006;Johanson et al, 2008Johanson et al, , 2011Gato and Desmond, 2009). Two proteomic analyses of fetal CSF of rats and humans have revealed numerous compounds that likely are cues for diff erent phases of neurogenesis (Parada et al, 2005;Zappaterra et al, 2007).…”

Section: Alterations Of the Microenvironment Of The Neu-rogenic Nichementioning

confidence: 99%

A cell junction pathology of neural stem cells leads to abnormal neurogenesis and hydrocephalus

et al. 2012

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Most cells of the developing mammalian brain derive from the ventricular (VZ) and the subventricular (SVZ) zones. The VZ is formed by the multipotent radial glia/neural stem cells (NSCs) while the SVZ harbors the rapidly proliferative neural precursor cells (NPCs). Evidence from human and animal models indicates that the common history of hydrocephalus and brain maldevelopment starts early in embryonic life with disruption of the VZ and SVZ. We propose that a "cell junction pathology" involving adherent and gap junctions is a fi nal common outcome of a wide range of gene mutations resulting in proteins abnormally expressed by the VZ cells undergoing disruption. Disruption of the VZ during fetal development implies the loss of NSCs whereas VZ disruption during the perinatal period implies the loss of ependyma. The process of disruption occurs in specifi c regions of the ventricular system and at specifi c stages of brain development. This explains why only certain brain structures have an abnormal development, which in turn results in a specifi c neurological impairment of the newborn. Disruption of the VZ of the Sylvian aqueduct (SA) leads to aqueductal stenosis and hydrocephalus, while disruption of the VZ of telencephalon impairs neurogenesis. We are currently investigating whether grafting of NSCs/neurospheres from normal rats into the CSF of hydrocephalic mutants helps to diminish/repair the outcomes of VZ disruption.

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Section: Alterations Of the Microenvironment Of The Neu-rogenic Nichementioning

confidence: 99%

A cell junction pathology of neural stem cells leads to abnormal neurogenesis and hydrocephalus

et al. 2012

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“…For example, it has been suggested that FGF2 may act on neurogenesis by driving cells to terminal mitoses (Martin et al, 2006), and that the action of lipoproteins in this cellular process is the supply to the neuroepithelial cells of the necessary building materials (Parada et al, 2008b). Moreover, the presence of other neurogenic factors in the E-CSF has been suggested to account for overall neurogenesis (Martin et al, 2006;Parada at al., 2008a;Gato and Desmond, 2009). Our results show that mesencephalic neurogenesis in chick embryos is also driven by RA activity, which comes from the IsO, which in turn is regulated by E-CSF via the RBP and the all-trans retinol it contains.…”

Section: Ra Is Involved In Neurogenesis Induced By E-csfmentioning

confidence: 99%

“…Recently, it has been shown that E-CSF plays an important role in brain development at both embryonic and foetal stages and performs several crucial functions (reviewed by Gato and Desmond, 2009). …”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal fluid control of neurogenesis induced by retinoic acid during early brain development

Alonso

Martín

Carnicero

et al. 2011

Developmental Dynamics

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Embryonic‐cerebrospinal fluid (E‐CSF) plays crucial roles in early brain development including the control of neurogenesis. Although FGF2 and lipoproteins present in the E‐CSF have previously been shown to be involved in neurogenesis, the main factor triggering this process remains unknown. E‐CSF contains all‐trans‐retinol and retinol‐binding protein involved in the synthesis of retinoic acid (RA), a neurogenesis inducer. In early chick embryo brain, only the mesencephalic‐rombencephalic isthmus (IsO) is able to synthesize RA. Here we show that in chick embryo brain development: (1) E‐CSF helps to control RA synthesis in the IsO by means of the RBP and all‐trans‐retinol it contains; (2) E‐CSF has retinoic acid activity, which suggests it may act as a diffusion pathway for RA; and (3) the influence of E‐CSF on embryonic brain neurogenesis is to a large extent due to its involvement in RA synthesis. These data help to understand neurogenesis from neural progenitor cells. Developmental Dynamics 240:1650–1659, 2011. © 2011 Wiley‐Liss, Inc.

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“…As cerebrospinal fluid (CSF) contains a variety of signaling factors (Parada et al, 2008, Gato andDesmond, 2009;Huang et al, 2010;Johansson et al, 2010;Lehtinen et al, 2011) its composition might contribute to the unique niche environment of the neural stem cells lining the ventricle .…”

Section: Introductionmentioning

confidence: 99%

The transcription factor Otx2 regulates choroid plexus development and function

et al. 2013

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SUMMARYThe choroid plexuses (ChPs) are the main regulators of cerebrospinal fluid (CSF) composition and thereby also control the composition of a principal source of signaling molecules that is in direct contact with neural stem cells in the developing brain. The regulators of ChP development mediating the acquisition of a fate that differs from the neighboring neuroepithelial cells are poorly understood. Here, we demonstrate in mice a crucial role for the transcription factor Otx2 in the development and maintenance of ChP cells. Deletion of Otx2 by the Otx2-CreERT2 driver line at E9 resulted in a lack of all ChPs, whereas deletion by the Gdf7-Cre driver line affected predominately the hindbrain ChP, which was reduced in size, primarily owing to an increase in apoptosis upon Otx2 deletion. Strikingly, Otx2 was still required for the maintenance of hindbrain ChP cells at later stages when Otx2 deletion was induced at E15, demonstrating a central role of Otx2 in ChP development and maintenance. Moreover, the predominant defects in the hindbrain ChP mediated by Gdf7-Cre deletion of Otx2 revealed its key role in regulating early CSF composition, which was altered in protein content, including the levels of Wnt4 and the Wnt modulator Tgm2. Accordingly, proliferation and Wnt signaling levels were increased in the distant cerebral cortex, suggesting a role of the hindbrain ChP in regulating CSF composition, including key signaling molecules. Thus, Otx2 acts as a master regulator of ChP development, thereby influencing one of the principal sources of signaling in the developing brain, the CSF.

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Why the embryo still matters: CSF and the neuroepithelium as interdependent regulators of embryonic brain growth, morphogenesis and histiogenesis

Cited by 87 publications

References 69 publications

A cell junction pathology of neural stem cells leads to abnormal neurogenesis and hydrocephalus

A cell junction pathology of neural stem cells leads to abnormal neurogenesis and hydrocephalus

Cerebrospinal fluid control of neurogenesis induced by retinoic acid during early brain development

The transcription factor Otx2 regulates choroid plexus development and function

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