纤毛形成
纤毛
生物
细胞生物学
胶质2
自噬
RNA干扰
细胞周期
转录因子
基因敲除
刺猬信号通路
细胞
信号转导
细胞培养
核糖核酸
遗传学
基因
细胞凋亡
作者
Ching-Ju Hsiao,Chia Hsiang Chang,Ridwan Babatunde Ibrahim,I-Hsuan Lin,Chun‐Hung Wang,Won Jing Wang,Jin-Wu Tsai
摘要
The primary cilium is a tiny cell protrusion known to transduce key extracellular signals, including those of the sonic hedgehog pathway, which activates Gli transcription factors for various cellular functions. To understand the significance of the Gli2 transcription factor in fibroblasts, we establish a Gli2-knockout NIH3T3 cell line by CRISPR/Cas9 technology. Surprisingly, NIH3T3 fibroblasts lacking Gli2 expression through gene knockout or RNA interference possess longer primary cilia after stimulation of ciliogenesis by serum starvation. This lengthening of primary cilia is associated with enhanced autophagy-mediated Ofd1 degradation, and can be reversed by pharmacological and genetic inhibition of autophagy. Meanwhile, flow cytometry reveals that Gli2-/- NIH3T3 fibroblasts exhibit a delay in cell cycle re-entry after serum re-stimulation. Ablation of their primary cilia through Kif3a knockdown rescues the delay in cell cycle re-entry. These results suggest that Gli2 plays an unexpected role in cell cycle re-entry through an autophagy-mediated regulation on ciliary length in fibroblasts.
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