Neoblast-enriched zinc finger protein FIR1 triggers local proliferation during planarian regeneration.
10.1007/s13238-018-0512-0
- Author:
Xiao-Shuai HAN
1
;
Chen WANG
1
;
Fang-Hao GUO
1
;
Shuang HUANG
2
;
Yong-Wen QIN
2
;
Xian-Xian ZHAO
2
;
Qing JING
3
Author Information
1. Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, China.
2. Department of Cardiology, Changhai Hospital, Shanghai, 200433, China.
3. Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, China. qjing@sibs.ac.cn.
- Publication Type:Journal Article
- Keywords:
Dis3l2;
Schmidtea mediterranea;
adult stem cells;
local proliferation;
planarians;
wound recognition
- From:
Protein & Cell
2019;10(1):43-59
- CountryChina
- Language:English
-
Abstract:
Regeneration, relying mainly on resident adult stem cells, is widespread. However, the mechanism by which stem cells initiate proliferation during this process in vivo is unclear. Using planarian as a model, we screened 46 transcripts showing potential function in the regulation of local stem cell proliferation following 48 h regeneration. By analyzing the regeneration defects and the mitotic activity of animals under administration of RNA interference (RNAi), we identified factor for initiating regeneration 1 (Fir1) required for local proliferation. Our findings reveal that Fir1, enriched in neoblasts, promotes planarian regeneration in any tissue-missing context. Further, we demonstrate that DIS3 like 3'-5' exoribonuclease 2 (Dis3l2) is required for Fir1 phenotype. Besides, RNAi knockdown of Fir1 causes a decrease of neoblast wound response genes following amputation. These findings suggest that Fir1 recognizes regenerative signals and promotes DIS3L2 proteins to trigger neoblast proliferation following amputation and provide a mechanism critical for stem cell response to injury.
