title: C. elegans maximum velocity correlates with healthspan and is maintained in worms with an insulin receptor mutation.
abstract: Ageing is marked by physical decline. Caenorhabditis elegans is a valuable model for identifying genetic regulatory mechanisms of ageing and longevity. Here we report a simple method to assess C. elegans' maximum physical ability based on the worms' maximum movement velocity. We show maximum velocity declines with age, correlates well with longevity, accurately reports movement ability and, if measured in mid-adulthood, is predictive of maximal lifespan. Contrary to recent findings, we observe that maximum velocity of worm with mutations in daf-2(e1370) insulin/IGF-1 signalling scales with lifespan. Because of increased odorant receptor expression, daf-2(e1370) mutants prefer food over exploration, causing previous on-food motility assays to underestimate movement ability and, thus, worm health. Finally, a disease-burden analysis of published data reveals that the daf-2(e1370) mutation improves quality of life, and therefore combines lifespan extension with various signs of an increased healthspan.
authors.affiliation: Center for Plant Aging Research, Institute for Basic Science, Daegu 42988, Republic of Korea.
authors.forename: Jeong-Hoon
authors.initials: JH
authors.lastname: Hahm
authors.affiliation: Center for Plant Aging Research, Institute for Basic Science, Daegu 42988, Republic of Korea.
authors.forename: Sunhee
authors.initials: S
authors.lastname: Kim
authors.affiliation: Department of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, 148 Carl Icahn Laboratory, Washington Road, Princeton, New Jersey 08544, USA.
authors.forename: Race
authors.initials: R
authors.lastname: DiLoreto
authors.affiliation: Department of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, 148 Carl Icahn Laboratory, Washington Road, Princeton, New Jersey 08544, USA.
authors.forename: Cheng
authors.identifier: http://orcid.org/0000-0003-0365-8273
authors.initials: C
authors.lastname: Shi
authors.affiliation: Department of Life Sciences and School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang, Gyeongbuk 790-784, Republic of Korea.
authors.forename: Seung-Jae V
authors.initials: SJ
authors.lastname: Lee
authors.affiliation: Department of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, 148 Carl Icahn Laboratory, Washington Road, Princeton, New Jersey 08544, USA.
authors.forename: Coleen T
authors.initials: CT
authors.lastname: Murphy
authors.affiliation: Center for Plant Aging Research, Institute for Basic Science, Daegu 42988, Republic of Korea.|Department of New Biology, DGIST, Daegu 42988, Republic of Korea.
authors.forename: Hong Gil
authors.initials: HG
authors.lastname: Nam
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D029742:Caenorhabditis elegans Proteins / Q000235:genetics* / Q000378:metabolism; D005260:Female; D007328:Insulin / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D008136:Longevity; D008297:Male; D009154:Mutation; D011972:Receptor, Insulin / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D029742:Caenorhabditis elegans Proteins; D007328:Insulin; D007334:Insulin-Like Growth Factor I; C107483:DAF-2 protein, C elegans; D011972:Receptor, Insulin