期刊
ISCIENCE
卷 23, 期 12, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2020.101738
关键词
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资金
- Japan Society for the Promotion of Science [JP16H06385, 15J12331, 18H06064, 19K16136]
- Japan Agency for Medical Research and Development through AMED-CREST [JP17gm0610004]
- AMED-Aging [JP20gm5010001]
- Graduate Program for Leaders in Life Innovation Leading Graduate School from the Ministry of Education, Culture, Sports, Science and Technology (MEXT)
- Japan Science Society
- Grants-in-Aid for Scientific Research [15J12331, 19K16136, 18H06064] Funding Source: KAKEN
Tissue interactions are critical for maintaining homeostasis; however, little is known about how remote tissue regulates regeneration. Previously, we established a genetic dual system that induces cell ablation in Drosophila larval imaginal discs and simultaneously manipulates genes in non-damaged tissues. Using humoral metabolome analysis and a genetic damage system, we found that the Tryptophan (Trp)-Kynurenine (Kyn) pathway in the fat body is required for disc repair. Genetic manipulation of Trp-Kyn metabolism in the fat body impaired disc regeneration without affecting wing development. In particular, the fat body-derived humoral kynurenic acid (KynA) was required for disc repair. The impairment of S-adenosylmethionine (SAM) synthesis from methionine (Met) in the fat body hampers the maintenance of KynA levels in hemolymph at the early stage of disc repair, suggesting a connection between Met-SAM and Trp-Kyn metabolisms. Our data indicate KynA from the fat body acts as a permissive metabolite for tissue repair and regeneration.
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