期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41467-017-00594-5
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资金
- Japan Society for the Promotion of Science (JSPS) (JSPS KAKENHI) [JP15J10835]
- Challenging Exploratory Research from JSPS (JSPS KAKENHI) [JP26640051, JP16K14590]
- Scientific Research on Innovative Areas 'Homeostatic Inflammation' (JSPS KAKENHI) from JSPS [JP24117705]
- Scientific Research on Innovative Areas 'CHROMOSOME ORCHESTRATION SYSTEM' (JSPS KAKENHI) from JSPS [JP15H05976]
- JSPS KAKENHI from JSPS [JP15H02369]
- Platform Project for Supporting in Drug Discovery and Life Science Research (Platform for Drug Discovery, Informatics, and Structural Life Science) from Japan Agency for Medical Research and Development (AMED)
- Grants-in-Aid for Scientific Research [15H02369, 16K14590] Funding Source: KAKEN
Unlike mammals, Xenopus laevis tadpoles possess high ability to regenerate their lost organs. In amphibians, the main source of regenerated tissues is lineage-restricted tissue stem cells, but the mechanisms underlying induction, maintenance and differentiation of these stem/progenitor cells in the regenerating organs are poorly understood. We previously reported that interleukin-11 (il-11) is highly expressed in the proliferating cells of regenerating Xenopus tadpole tails. Here, we show that il-11 knockdown (KD) shortens the regenerated tail length, and the phenotype is rescued by forced-il-11-expression in the KD tadpoles. Moreover, marker genes for undifferentiated notochord, muscle, and sensory neurons are downregulated in the KD tadpoles, and the forced-il-11-expression in intact tadpole tails induces expression of these marker genes. Our findings demonstrate that il-11 is necessary for organ regeneration, and suggest that IL-11 plays a key role in the induction and maintenance of undifferentiated progenitors across cell lineages during Xenopus tail regeneration.
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