Retinoic Acid from the Meninges Regulates Cortical Neuron Generation

Siegenthaler, Julie A.; Ashique, Amir M.; Zarbalis, Konstantinos; Patterson, Katelin P.; Hecht, Jonathan H.; Kane, Maureen A.; Folias, Alexandra E.; Choe, Youngshik; May, S. Randolph; Kume, Tsutomu; Napoli, Joseph L.; Peterson, Andrew S.; Pleasure, Samuel J.

doi:10.1016/j.cell.2009.10.004

Cited by 377 publications

(452 citation statements)

References 51 publications

Supporting

Mentioning

419

Contrasting

Order By: Relevance

“…To examine this more closely, we used an antibody against laminin, an ECM protein secreted by pial cells (22,23). Control embryos on ED7 show a continuous layer of laminin at the tectum's outer surface (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…At some point, radial glia begin to leave the cell cycle and become young neurons, which migrate away from the ventricular surface along the radial processes. The neurons are thought to stop their migration when they encounter a molecular signal, such as reelin or retinoic acid, secreted from specialized cells near the pial surface (22,23) (Fig. 7A).…”

Section: Resultsmentioning

confidence: 99%

“…Because the radial glia processes are attached to the pial surface (22,23,37,38), the differential tangential expansion creates laterally directed tension between the ventricular and pial surfaces. One way to relieve this tension is to let the tectum buckle into the ventricle, creating macroscopic folds (Fig.…”

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2

McGowan

Alaama

Freise

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Comparative research has shown that evolutionary increases in brain region volumes often involve delays in neurogenesis. However, little is known about the influence of such changes on subsequent development. To get at this question, we injected FGF2-which delays cell cycle exit in mammalian neocortex-into the cerebral ventricles of chicks at embryonic day (ED) 4. This manipulation alters the development of the optic tectum dramatically. By ED7, the tectum of FGF2-treated birds is abnormally thin and has a reduced postmitotic layer, consistent with a delay in neurogenesis. FGF2 treatment also increases tectal volume and ventricular surface area, disturbs tectal lamination, and creates small discontinuities in the pia mater overlying the tectum. On ED12, the tectum is still larger in FGF2-treated embryos than in controls. However, lateral portions of the FGF2-treated tectum now exhibit volcano-like laminar disturbances that coincide with holes in the pia, and the caudomedial tectum exhibits prominent folds. To explain these observations, we propose that the tangential expansion of the ventricular surface in FGF2-treated tecta outpaces the expansion of the pial surface, creating abnormal mechanical stresses. Two alternative means of alleviating these stresses are tectal foliation and the formation of pial holes. The latter probably alter signaling gradients required for normal cell migration and may generate abnormal patterns of cerebrospinal fluid flow; both abnormalities would generate disturbances in tectal lamination. Overall, our findings suggest that evolutionary expansion of sheet-like, laminated brain regions requires a concomitant expansion of the pia mater.brain evolution | evolutionary developmental biology | proliferation | meninges | cortical folding E volutionary increases in brain region volumes are common (1).For example, the neocortex is disproportionately enlarged in primates relative to other mammals, and the telencephalon is disproportionately enlarged in parrots and songbirds relative to other birds (1-4). Recent work in evolutionary developmental neurobiology has shown that these evolutionary increases in brain region volumes are often caused by delays in cell cycle exit of neuronal precursors (5, 6). Among birds, for example, parrots and songbirds exhibit delayed telencephalic neurogenesis relative to chicken-like birds (7-9). Among mammals, cell cycle exit in the neocortex is similarly delayed in primates, which have a disproportionately enlarged neocortex (5, 10-12).Unfortunately, the downstream effects of delayed cell cycle exit on subsequent developmental processes and adult morphology remain poorly understood. One way to fill this gap in our knowledge is to experimentally recreate the key species differences in the laboratory by means of carefully selected developmental manipulations. A good example of this phenocopy approach was the creation of transgenic mice with a constitutively active form of β-catenin that prolongs proliferation, increases neocortical volume, and generates cortica...

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2

McGowan

Alaama

Freise

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Furthermore, the basal process is reported to receive from the meninges a retinoic acid signal that controls the proliferation of the progenitor cells. 49 Even though it is obvious that there is a clear relationship between brain size and percentage of oRGs out of all proliferating progenitors, 50 more studies are required to understand the physiological significance of oRGs. Interestingly, cyclin D2-positive cells are observed in the OSVZ, and the dotted staining of cyclin D2 is frequently seen in the basal side but not in the apical side 19 making it likely that these cells are oRGs.…”

Section: Acknowledgmentsmentioning

confidence: 99%

How to keep proliferative neural stem/progenitor cells

Tsunekawa

Osumi

2012

Cell Cycle

View full text Add to dashboard Cite

I t has long been argued that cell cycle regulators such as cyclins, cyclindependent kinases and their inhibitors affect the fate of neuronal progenitor cells. Recently, we identified that cyclin D2, which localizes at the basal tip of the radial glial cell (i.e., the neural progenitor in the developing neocortex), functions to give differential cell fates to its daughter cells just after cell division. This basally biased localization is due to transportation of cyclin D2 mRNA via its unique cis-regulatory sequence and local translation into cyclin D2 protein at the basal endfoot. During division of the neural progenitor cells, cyclin D2 protein is inherited by the daughter cell that retain the basal process, resulting in asymmetric distribution of cyclin D2 protein between the two daughter cells. Cyclin D2 is similarly localized in the human fetal cortical primordium, suggesting a common mechanism for the maintenance of neural progenitors and a possible scenario in evolution of primate brains. Here we introduce our recent findings and discuss how cyclin D2 functions in mammalian brain development and evolution.

show abstract

“…The meninges control some aspects of cortical neurogenesis and neuronal migration (6,7). Meninges in the brain and spinal cord may also directly harbor stem cells under basal conditions (8) and in response to insults, such as stroke and spinal cord injury (9,10).…”

mentioning

confidence: 99%

Intermediate filament protein nestin is expressed in developing meninges

Yay¹,

Özdamar²,

Canöz³

et al. 2014

BLL

View full text Add to dashboard Cite

Abstract:Background: Nestin is a type VI intermediate fi lament protein known as a marker for progenitor cells that can be mostly found in tissues during the embryonic and fetal periods. In our study, we aimed to determine the expression of nestin in meninges covering the brain tissue at different developmental stages and in the new born. Methods: In this study 10 human fetuses in different development stages between developmental weeks 9-34 and a newborn brain tissue were used. Fetuses in paraffi n section were stained with H+E and nestin immunohistochemical staining protocol was performed. Results: In this study, in the human meninges intense nestin expression was detected as early as in the 9th week of development. Intensity of this expression gradually decreased in later stages of development and nestin expression still persisted in a small population of newborn meningeal cells. Conclusion:In the present study, nestin positive cells gradually diminished in the developing and maturing meninges during the fetal period. This probably depends on initiation of a decrease in nestin expression and replacement with other tissue-specifi c intermediate fi laments while the differentiation process continues. These differences can make signifi cant contributions to the investigation and diagnosis of various pathological disorders (Tab. 1, Fig. 3, Ref. 36). Text in PDF www.elis.sk.

show abstract

Retinoic Acid from the Meninges Regulates Cortical Neuron Generation

Cited by 377 publications

References 51 publications

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2

How to keep proliferative neural stem/progenitor cells

Intermediate filament protein nestin is expressed in developing meninges

Contact Info

Product

Resources

About