Mind bomb 1-expressing intermediate progenitors generate Notch signaling to maintain radial glial cells

被引：161

作者：

Yoon, Ki-Jun ^{[1
]}

Koo, Bon-Kyoung ^{[1
]}

Im, Sun-Kyoung ^{[1
]}

Jeong, Hyun-Woo ^{[1
]}

Ghirn, Jaewang ^{[1
]}

Kwon, Min-chul ^{[1
]}

Moon, Jin-Sook ^{[1
]}

Miyata, Takaki ^{[2
]}

Kong, Young-Yun ^{[1
]}

机构：

[1] Pohang Univ Sci & Technol, Div Mol & Life Sci, Pohang 790784, Kyungbuk, South Korea

[2] Nagoya Univ, Grad Sch Med, Dept Anat & Cell Biol, Showa Ku, Aichi 4668550, Japan

来源：

NEURON | 2008年 / 58卷 / 04期

关键词：

D O I：

10.1016/j.neuron.2008.03.018

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Notch signaling is critical for the sternness of radial glial cells (RGCs) during embryonic neurogenesis. Although Notch-signal-receiving events in RGCs have been well characterized; the signal-sending mechanism by the adjacent cells is poorly understood. Here, we report that conditional inactivation of mind bomb-1 (mib1), an essential component for Notch ligand endocytosis, in mice using the nestin and hGFAP promoters resulted in complete loss of Notch activation, which leads to depletion of RGCs, and premature differentiation into intermediate progenitors (IPs) and finally neurons, which were reverted by the introduction of active Notch1. Interestingly, Mib1 expression is restricted in the migrating IPs and newborn neurons, but not in RGCs. Moreover, sorted Mib1(+) IPs and neurons can send the Notch signal to neighboring cells. Our results reveal that not only newborn neurons but also IPs are essential Notch-ligand-presenting cells for maintaining RGC sternness during both symmetric and asymmetric divisions.

引用

页码：519 / 531

页数：13

共 49 条

[1] Loss of occludin and functional tight junctions, but not ZO-1, during neural tube closure - Remodeling of the neuroepithelium prior to neurogenesis [J].