Mun Hyowon, Lee Eun Ji, Park Minah, Oh Goo Taeg, Park Jong Hoon
Department of Biological Science, Sookmyung Women's University, Seoul, South Korea.
Department of Biology, Ewha Women's University, Seoul, South Korea.
Front Cell Dev Biol. 2020 Jun 10;8:465. doi: 10.3389/fcell.2020.00465. eCollection 2020.
Autophagy is a catabolic process required for maintaining intracellular energy homeostasis. It eliminates harmful proteins and recycles functional macromolecules back into the cell via cargo breakdown. Autophagy is generally suppressed under fed conditions and induced by serum starvation; therefore, it is considered to be a nutrient-sensing mechanism. Cilia, finger-like organelles harboring multiple receptors along their surface, are energy-sensing structures that are also triggered by serum deprivation. Herein, we verified the effect of autophagy alterations on cilia assembly and the specific underlying mechanisms. Autophagy flux altered either by drugs or autophagy-targeting siRNAs strongly inhibited ciliogenesis, and this inhibition was affected by p62, an autophagy regulator, via Pten/Dvl2/AurKA signaling.
自噬是维持细胞内能量稳态所需的分解代谢过程。它清除有害蛋白质，并通过货物分解将功能性大分子再循环回细胞内。自噬通常在进食条件下受到抑制，并由血清饥饿诱导；因此，它被认为是一种营养感应机制。纤毛是沿其表面带有多种受体的指状细胞器，是能量感应结构，也由血清剥夺触发。在此，我们验证了自噬改变对纤毛组装的影响及其具体潜在机制。药物或靶向自噬的小干扰RNA改变自噬通量会强烈抑制纤毛发生，并且这种抑制受到自噬调节因子p62通过Pten/Dvl2/AurKA信号传导的影响。
