Molecular Cloning and Functional Analysis of Autophagy-related Gene Atg5 in Planarian Dugesia japonica
10.13865/j.cnki.cjbmb.2021.05.1138
- Author:
Ke-Xue MA
1
;
Fang-Ying GUO
1
;
Rui LI
1
;
Ge-Ge SONG
1
;
Meng WU
1
;
Guang-Wen CHEN
1
;
De-Zeng LIU
1
Author Information
1. Department of Cell Biology, College of Life Sciences, Henan Normal University
- Publication Type:Journal Article
- Keywords:
autophagy;
autophagy-related gene 5 (Atg5);
brain regeneration;
planarian;
RNA interfering (RNAi)
- From:
Chinese Journal of Biochemistry and Molecular Biology
2021;37(9):1233-1240
- CountryChina
- Language:Chinese
-
Abstract:
Autophagy-related gene 5 (Atg5) plays an essential role in autophagy, the loss of its function impairs neurogenesis and axon regeneration. However, the biological function of Atg5 has not been characterized in planarian. Planarian is an ideal model for the study of brain regeneration. It can regenerate a new brain de novo in 1 week following amputation. To explore the role of Atg5 in planarian brain regeneration, we dissected the molecular characteristics of Atg5 in planarian Dugesia japonica (DjAtg5) and examined its function by RNAi. The full-length cDNA of DjAtg5 is 1 014 bp encoding 284 amino acids. The deduced amino sequence of DjAtg5 contains the functional Pfam domain of ATG5 and highly conserved residues for ATG5-ATG12 interaction. After amputation, the transcrips of DjAtg5 are increased and mainly distributed in the newly regenerated brain on day 3-5 of regeneration. However, knockdown of DjAtg5 by RNAi does not impair the regeneration ability and brain structure reformation, nor affects the neoblasts proliferation. Our results suggest that DjAtg5 participates in re-formation of planarian brain structure following amputation, but it is not an important regulator for planarian regeneration. However, autophagy inhibitor 3-MA can block planarian regeneration, which suggests that autophagy is necessary for planarian regeneration.
