The Distinct Temporal Origins of Olfactory Bulb Interneuron Subtypes

Batista-Brito, Renata; Close, Jennie; Machold, Robert; Fishell, Gord

doi:10.1523/jneurosci.5625-07.2008

Cited by 255 publications

(367 citation statements)

References 64 publications

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“…This enhancer is particularly important because it controls Dlx expression in subpopulation(s) of interneurons that migrate to the dorsal cortex and OB. Furthermore, the enhancer activity is known to be high specifically in the ventral telencephalic regions severely affected by the absence of Rb (Ferguson et al, 2002;Ghanem et al, 2007;Batista-Brito et al, 2008). To test this possibility in vivo, we first generated Rb conditional mutants carrying LacZ reporter genes under the control of the human ␤-globin minimal promoter and the Dlx1/2-I12b enhancer (I12b-LacZ).…”

Section: Rb Is Required For the Proper Maturation And Migration Of Obmentioning

confidence: 99%

The Rb/E2F Pathway Modulates Neurogenesis through Direct Regulation of the Dlx1/Dlx2 Bigene Cluster

Ghanem¹,

Andrusiak²,

Svoboda³

et al. 2012

Journal of Neuroscience

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During brain morphogenesis, the mechanisms through which the cell cycle machinery integrates with differentiation signals remain elusive. Here we show that the Rb/E2F pathway regulates key aspects of differentiation and migration through direct control of the Dlx1 and Dlx2 homeodomain proteins, required for interneuron specification. Rb deficiency results in a dramatic reduction of Dlx1 and Dlx2 gene expression manifested by loss of interneuron subtypes and severe migration defects in the mouse brain. The Rb/E2F pathway modulates Dlx1/Dlx2 regulation through direct interaction with a Dlx forebrain-specific enhancer, I12b, and the Dlx1/Dlx2 proximal promoter regions, through repressor E2F sites both in vitro and in vivo. In the absence of Rb, we demonstrate that repressor E2Fs inhibit Dlx transcription at the Dlx1/Dlx2 promoters and Dlx1/2-I12b enhancer to suppress differentiation. Our findings support a model whereby the cell cycle machinery not only controls cell division but also modulates neuronal differentiation and migration through direct regulation of the Dlx1/Dlx2 bigene cluster during embryonic development.

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Section: Rb Is Required For the Proper Maturation And Migration Of Obmentioning

confidence: 99%

The Rb/E2F Pathway Modulates Neurogenesis through Direct Regulation of the Dlx1/Dlx2 Bigene Cluster

Ghanem¹,

Andrusiak²,

Svoboda³

et al. 2012

Journal of Neuroscience

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“…8 I-L; 69 cells counted). In the adult OB, among all newly generated neurons, the majority are granular cells; a small number of them are periglomerular cells and a very small number are external plexiform interneurons (Altman, 1969;Bayer, 1983;Lois and Alvarez-Buylla, 1994;Winner et al, 2002;Hack et al, 2005;Batista-Brito et al, 2008;Yang, 2008). Notably, many of the newly born granular cells, the majority of the newly born periglomerular cells and all of the newly born external plexiform interneurons express CR (Winner et al, 2002;Batista-Brito et al, 2008;Yang, 2008).…”

Section: The Vast Majority Of Newborn Neurons In the Damaged Striatummentioning

confidence: 99%

Brain Injury Does Not Alter the Intrinsic Differentiation Potential of Adult Neuroblasts

Liu¹,

You²,

Li³

et al. 2009

J. Neurosci.

103

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Neuroblasts produced by the neural stem cells of the adult subventricular zone (SVZ) migrate into damaged brain areas after stroke or other brain injuries, and previous data have suggested that they generate regionally appropriate new neurons. To classify the types of neurons produced subsequent to ischemic injury, we combined BrdU or virus labeling with multiple neuronal markers to characterize new cells at different times after the induction of stroke. We show that SVZ neuroblasts give rise almost exclusively to calretininexpressing cells in the damaged striatum, resulting in the accumulation of these cells during long term recovery after stroke. The vast majority of SVZ neuroblasts as well as newly born young and mature neurons in the damaged striatum constitutively express the transcription factor Sp8, but do not express transcription factors characteristic of medium-sized spiny neurons, the primary striatal projection neurons lost after stroke. Our results suggest that adult neuroblasts do not alter their intrinsic differentiation potential after brain injury.

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“…The spatial pattern and fate restriction is claimed to be established during embryonic development [79]. In addition, the type of interneurons generated is dependent on the temporal origin of the NSC, suggesting that either NSCs or the niche could be constantly changing [80,81]. Elucidating the molecular factors that underlie the patterning of NSCs might have important implication for clinical applications that aim to generate specific types of neurons and might lead to deviations from the original description of a stem cell that can generate any cell in the adult brain.…”

Section: The Neurogenic Niche and Its Factorsmentioning

confidence: 99%

Stem cells of the adult mammalian brain and their niche

Basak

Taylor

2008

Cell. Mol. Life Sci.

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Abstract. The mammalian brain is a paradox of evolution. Although the advance in complexity of the human brain has exceeded the development of other organs, it has practically lost the ability to regenerate, and damage is repaired mainly by functional plasticity. This disparity is, however, not due to the lack of progenitor cells in the adult mammalian brain, but to their diminished or repressed capacity to replace neurons in most brain regions. Here, we discuss the current literature describing the processes of neurogenesis in the adult mammalian brain, and the recent advances in adult neural stem cells (aNSCs) with a focus on their identity, cell cycle and niche signals. Understanding these processes may hopefully lead to therapies in the future to reinstate self-repair of the brain from endogenous progenitors.Keywords. Neural stem cells, neurogenesis, stem cell niche, adult brain, subventricular zone. The discovery of neurogenesis in the adult brainNSCs are the foundations of the brain during development, and despite poor regenerative capacity, they persist in the mammalian brain throughout postnatal development and into adulthood and continue to generate neurons. aNSCs self-renew and retain multipotency in almost all mammalian species analyzed, including humans. NSCs reside in specialized germinal layers where multiple cell-types interact with them and contribute to generate niches that control their fate choices and permit neurogenesis. Genetic and functional analyses have revealed roles for several genes and signaling pathways in controlling adult neurogenesis. However, the identities of the stem cells in the brain remain elusive, which presents an elementary problem for the interpretation of these results. In attempts to identify aNSCs, several groups have defined populations that contain cells with stem cell features, although unambiguous markers are still missing. Given their potential as putative tools for cell-based therapies, elucidating the molecular pathways that identify aNSCs and govern their cell fate is essential. Neurons in most regions of the adult mammalian brain are generated from NSCs and restricted progenitors during embryonic development before a switch to gliogenesis in peri-and postnatal development [1]. As early as the 1960s and 70s, newly generated neurons were identified by nucleotide analogue incorporation assays in adult rodents [2, 3]. These results, however, met with skepticism due to the poor regenerative capacity of the mammalian brain. Detailed studies went on to show extensive neurogenesis in the vocal control center in the brains of adult canaries, which correlates with seasonal song learning [4,5]. After a brief re-visitation to the topic in the mid-1980s, it was the use of retroviral lineage tracing assays that identified newborn neurons in the adult mammalian brain. These findings were quickly followed by the identification of zones with neurogenic capacity in

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The Distinct Temporal Origins of Olfactory Bulb Interneuron Subtypes

Cited by 255 publications

References 64 publications

The Rb/E2F Pathway Modulates Neurogenesis through Direct Regulation of the Dlx1/Dlx2 Bigene Cluster

The Rb/E2F Pathway Modulates Neurogenesis through Direct Regulation of the Dlx1/Dlx2 Bigene Cluster

Brain Injury Does Not Alter the Intrinsic Differentiation Potential of Adult Neuroblasts

Stem cells of the adult mammalian brain and their niche

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