These movies represents locomotion of aged C. elegans at day1, 3, 5, 7, and 9 adult on OP50 bacteria after tap stimuli in wild type N2, mig-17 (k174) mutamts, mig-22 (k185) mutants, sqv-5 (k175) mutants, mig-17 (k174) mig-22 (k185) double mutants, and sqv-5 (k175) mig-22 (k185) double mutants. The anomunt of chondroitin in mig-22 (k185) mutants is two times conmpare to wild type. On the other hand, that in sqv-5 (k175) mutants is one tenth conmpare to wild type. Day 1 adult that did not have egg was collected. Then, animals are transfered to new plate at each two days until their behavior recoreded. In case of sqv-5 mutants, since some of them are sterile, we collected L4 larve at first. Then, we used these animals as day 1 adult at the next day.
See details in Shibata, et. al. (2024) Sci Rep.
Yukimasa Shibata, Yuri Tanaka, Hiroyuki Sasakura, Yuki Morioka, Toshihiro Sassa, Shion Fujii, Kaito Mitsuzumi, Masashi Ikeno, Yukihiko Kubota, Kenji Kimura, Hidenao Toyoda, Kosei Takeuchi, Kiyoji Nishiwaki (2024) Endogenous chondroitin extends the lifespan and healthspan in C. elegans., Scientific reports, Volume 14, Number 1, pp. 4813
Published in 2024 Feb 27 (Electronic publication in Feb. 27, 2024, midnight )
(Abstract) Chondroitin, a class of glycosaminoglycan polysaccharides, is found as proteoglycans in the extracellular matrix, plays a crucial role in tissue morphogenesis during development and axonal regeneration. Ingestion of chondroitin prolongs the lifespan of C. elegans. However, the roles of endogenous chondroitin in regulating lifespan and healthspan mostly remain to be investigated. Here, we demonstrate that a gain-of-function mutation in MIG-22, the chondroitin polymerizing factor (ChPF), results in elevated chondroitin levels and a significant extension of both the lifespan and healthspan in C. elegans. Importantly, the remarkable longevity observed in mig-22(gf) mutants is dependent on SQV-5/chondroitin synthase (ChSy), highlighting the pivotal role of chondroitin in controlling both lifespan and healthspan. Additionally, the mig-22(gf) mutation effectively suppresses the reduced healthspan associated with the loss of MIG-17/ADAMTS metalloprotease, a crucial for factor in basement membrane (BM) remodeling. Our findings suggest that chondroitin functions in the control of healthspan downstream of MIG-17, while regulating lifespan through a pathway independent of MIG-17.