Zhang Haijun, Zhang Longbin, Sun Tao
Department of Cell and Developmental Biology, Weill Cornell Medical College, Cornell University, New York, NY, United States.
Department of Genetic Medicine, Weill Cornell Medical College, Cornell University, New York, NY, United States.
Front Mol Neurosci. 2018 Feb 19;11:44. doi: 10.3389/fnmol.2018.00044. eCollection 2018.
Proper proliferation and differentiation of neural progenitors (NPs) in the developing cerebral cortex are critical for normal brain formation and function. Emerging evidence has shown the importance of microRNAs (miRNAs) in regulating cortical development and the etiology of neurological disorders. Here we show that miR-26 is co-expressed with its host gene in the mouse embryonic cortex. We demonstrate that similar to its host gene Ctdsp2, miR-26 positively regulates proliferation of NPs through controlling the cell-cycle progression, by using miR-26 overexpression and sponge approaches. On the contrary, miR-26 target gene Emx2 limits expansion of cortical NPs, and promotes transcription of miR-26 host gene . Our study suggests that miR-26, its target Emx2 and its host gene cohesively regulate proliferation of NPs during the mouse cortical development.
神经祖细胞(NPs)在发育中的大脑皮层中进行适当的增殖和分化对于正常的脑形成和功能至关重要。新出现的证据表明,微小RNA(miRNAs)在调节皮层发育和神经疾病病因方面具有重要作用。在这里,我们表明miR-26在小鼠胚胎皮层中与其宿主基因共表达。我们通过使用miR-26过表达和海绵方法证明,与它的宿主基因Ctdsp2类似,miR-26通过控制细胞周期进程来正向调节NPs的增殖。相反,miR-26的靶基因Emx2限制皮层NPs的扩增,并促进miR-26宿主基因的转录。我们的研究表明,miR-26、其靶标Emx2及其宿主基因在小鼠皮层发育过程中协同调节NPs的增殖。