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 ...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.展开更多
基金the National Key Research and Development Program of China(2017YFA0103700)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDA16020903)the National Natural Science Foundation of China(91739301,91339205,and 31229002).
文摘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.
