Impaired adult neurogenesis in mice lacking the transcription factor E2F1
Impaired adult neurogenesis in mice lacking the transcription factor E2F1
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DOI：
10.1006/mcne.2002.1176
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发表时间：
2002-10-01
影响因子：
3.5
通讯作者：
Kuhn, HG
中科院分区：
文献类型：
--
作者：
Cooper-Kuhn, CM;Vroemen, M;Kuhn, HG
在神经系统发育过程中，神经干细胞的命运--增殖、分化或凋亡--受到各种信号的控制，如生长因子。在这里，我们证明了转录因子E2 F1，这是由几个信号级联被激活的生长因子为目标，参与在成人大脑中的神经发生。当分析E2 F1缺陷小鼠的大脑时，我们发现侧脑室壁和海马的增殖区的干细胞和祖细胞分裂显著减少。结果，成年嗅球和齿状回新生神经元的产生减少。成人小脑的神经元细胞计数显示，一个温和的，但显着的小脑萎缩，而新皮质神经元不受影响，这表明E2 F1缺乏症产生的主要是出生后的表型。结果表明E2 F1参与控制出生后和成年大脑中的增殖和神经元细胞数量。
During nervous system development the fate of neural stem cells-whether to undergo proliferation, differentiation, or apoptosis-is controlled by various signals, such as growth factors. Here, we demonstrate that the transcription factor E2F1, which is targeted by several signaling cascades that are activated by growth factors, is involved in neurogenesis in the adult brain. When analyzing the brains of E2F1-deficient mice, we found significantly decreased stem cell and progenitor division in the proliferative zones of the lateral ventricle wall and the hippocampus. As a consequence, the production of newborn neurons in the adult olfactory bulb and dentate gyrus was decreased. Neuronal cell counts of the adult cerebellum revealed a mild but significant cerebellar atrophy, whereas neocortical neurons were unaffected, suggesting that E2F1 deficiency produces a predominantly postnatal phenotype. The results indicate an involvement of E2F1 in controlling proliferation and neuronal cell numbers in the postnatal and adult brain.