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The function of the ATG8 in the cilia and cortical microtubule maintenance of Euplotes amieti.
Wu, Junlin; Sheng, Yan; Mai, Shihuan; Zhong, Yanhao; Dai, Shengrong; Luo, Yupeng; Sheng, Xin.
Afiliação
  • Wu J; Department of Biochemistry, Zunyi Medical University, Zunyi, 563000, People's Republic of China.
  • Sheng Y; Laboratory of Basic Medical Morphology, Zunyi Medical University, Zunyi, 563000, People's Republic of China.
  • Mai S; School of Medical Imaging, Zunyi Medical University, Zunyi, 563000, People's Republic of China.
  • Zhong Y; School of Medical Imaging, Zunyi Medical University, Zunyi, 563000, People's Republic of China.
  • Dai S; School of Medical Imaging, Zunyi Medical University, Zunyi, 563000, People's Republic of China.
  • Luo Y; School of Medical Imaging, Zunyi Medical University, Zunyi, 563000, People's Republic of China.
  • Sheng X; Department of Biochemistry, Zunyi Medical University, Zunyi, 563000, People's Republic of China. xshengbio@163.com.
Protoplasma ; 2024 May 20.
Article em En | MEDLINE | ID: mdl-38769089
ABSTRACT
Autophagy regulates the formation of primary cilia, which in turn affects autophagy. The relationship between autophagy and cilia is known to be bidirectional although the specific mechanisms involved have yet to be elucidated. In this study, we found for the first time that ATG8 protein localizes in the basal body of the dorsal kineties and the base of the ventral cirri in Euplotes amieti. ATG8 protein maintains the structural integrity of cilia and plays a role in the construction of the cortical ciliature and microtubule cytoskeleton associated with cilia. ATG8 gene interference leads to the degradation of IFT88, the transport protein in cilia, thus inhibiting the generation of cilia, and affecting the swing of cilia. This influences the swimming speed and cilia pattern, leading to death in Euplotes amieti.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article