PUBLICATION
Muscle defects due to perturbed somite segmentation contribute to late adult scoliosis
- Authors
- Lleras-Forero, L., Newham, E., Teufel, S., Kawakami, K., Hartmann, C., Hammond, C.L., Knight, R.D., Schulte-Merker, S.
- ID
- ZDB-PUB-201002-172
- Date
- 2020
- Source
- Aging 12(18): 18603-18621 (Journal)
- Registered Authors
- Hammond, Chrissy, Kawakami, Koichi, Knight, Robert, Schulte-Merker, Stefan
- Keywords
- adult degenerative scoliosis, aging, muscle, vertebral defects, zebrafish
- MeSH Terms
- none
- PubMed
- 32979261 Full text @ Aging (Albany NY)
Citation
Lleras-Forero, L., Newham, E., Teufel, S., Kawakami, K., Hartmann, C., Hammond, C.L., Knight, R.D., Schulte-Merker, S. (2020) Muscle defects due to perturbed somite segmentation contribute to late adult scoliosis. Aging. 12(18):18603-18621.
Abstract
Scoliosis is an abnormal bending of the body axis. Truncated vertebrae or a debilitated ability to control the musculature in the back can cause this condition, but in most cases the causative reason for scoliosis is unknown (idiopathic). Using mutants for somite clock genes with mild defects in the vertebral column, we here show that early defects in somitogenesis are not overcome during development and have long lasting and profound consequences for muscle fiber organization, structure and whole muscle volume. These mutants present only mild alterations in the vertebral column, and muscle shortcomings are uncoupled from skeletal defects. None of the mutants presents an overt musculoskeletal phenotype at larval or early adult stages, presumably due to compensatory growth mechanisms. Scoliosis becomes only apparent during aging. We conclude that adult degenerative scoliosis is due to disturbed crosstalk between vertebrae and muscles during early development, resulting in subsequent adult muscle weakness and bending of the body axis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping