Abstract
The olfactory epithelium (OE) of the mouse is an excellent model system for studying principles of neural stem cell biology because of its well-defined neuronal lineage and its ability to regenerate throughout life. To approach the molecular mechanisms of stem cell regulation in the OE, we have focused on Foxg1, also known as brain factor 1, which is a member of the Forkhead transcription factor family. Foxg1(-/-) mice show major defects in the OE at birth, suggesting that Foxg1 plays an important role in OE development. We find that Foxg1 is expressed in cells within the basal compartment of the OE, the location where OE stem and progenitor cells are known to reside. Since FoxG1 is known to regulate proliferation of neuronal progenitor cells during telencephalon development, we performed bromodeoxyuridine pulse-chase labeling of Sox2-expressing neural stem cells during primary OE neurogenesis. We found the percentage of Sox2-expressing cells that retained bromodeoxyuridine was twice as high in Foxg1(-/-) OE cells as in the wild type, suggesting that these cells are delayed and/or halted in their development in the absence of Foxg1. Our findings suggest that the proliferation and/or subsequent differentiation of Sox2-expressing neural stem cells in the OE is regulated by Foxg1.
Highlights
In the past decade, increasing attention has been paid to address the question of how cellautonomous and non-autonomous molecular mechanisms interact to control neurogenesis 1-5
In order to understand the basic principles that govern the generation and regeneration of neurons in the mammals, we have studied the molecular regulation of neurogenesis in a well-characterized neurogenic epithelium, the olfactory epithelium (OE) of the mouse 1, 3
Studies suggest that stem and TA progenitors are components of the so-called “globose” basal cell (GBC) population, and reside in the basal compartment of the OE atop the “horizontal” basal cells which are adjacent to the basal lamina 1, 5, 18, 24
Summary
In the past decade, increasing attention has been paid to address the question of how cellautonomous and non-autonomous molecular mechanisms interact to control neurogenesis 1-5 Such information is of particular importance for understanding the behavior of stem cells in the context of their use as a potential source of treatment for injured or diseased nervous system tissue. This process begins with OE neural stem cells, which retain a self-renewing ability. After surgical or chemical ablation the OE undergoes massive cell division and restores almost complete OE formation within two weeks 6, 11, 27 These characteristics strongly suggest that the OE maintains its neural stem cells during embryonic development, and throughout adult life. Sox[2] is expressed in the OE as well, and importantly it is detected in the basal layer where stem cells are known to be resided 1, 3
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