PUBLICATION

Depletion of zebrafish Tcap leads to muscular dystrophy via disrupting sarcomere-membrane interaction, not sarcomere assembly

Authors
Zhang, R., Yang, J., Zhu, J., and Xu, X.
ID
ZDB-PUB-090819-2
Date
2009
Source
Human molecular genetics   18(21): 4130-4140 (Journal)
Registered Authors
Xu, Xiaolei, Yang, Jingchun, Zhang, Ruilin
Keywords
none
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • Animals, Genetically Modified
  • Connectin
  • Embryo, Nonmammalian/embryology
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/ultrastructure
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Green Fluorescent Proteins/genetics
  • Green Fluorescent Proteins/metabolism
  • Humans
  • In Situ Hybridization
  • Microscopy, Electron, Transmission
  • Molecular Sequence Data
  • Muscle Proteins/classification
  • Muscle Proteins/genetics
  • Muscle Proteins/metabolism*
  • Muscular Dystrophies, Limb-Girdle/genetics
  • Muscular Dystrophies, Limb-Girdle/metabolism
  • Muscular Dystrophy, Animal/genetics
  • Muscular Dystrophy, Animal/metabolism*
  • Mutation
  • Phylogeny
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sarcomeres/metabolism*
  • Sequence Homology, Amino Acid
  • Swimming
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
19679566 Full text @ Hum. Mol. Genet.
Abstract
Tcap/telethonin encodes a Z-disc protein that plays important roles in sarcomere assembly, sarcomere-membrane interaction and stretch sensing. It remains unclear why mutations in Tcap lead to limb-girdle muscular dystrophy 2G (LGMD2G) in human patients. Here, we cloned tcap in zebrafish and conducted genetic studies. We show that tcap is functionally conserved, as the Tcap protein appears in the sarcomeric Z-disc and reduction of Tcap resulted in muscular dystrophy-like phenotypes including deformed muscle structure and impaired swimming ability. However, the observations that Tcap integrates into the sarcomere at a stage after the Z-disc becomes periodic, and that the sarcomere remains intact in tcap morphants, suggest that defective sarcomere assembly does not contribute to this particular type of muscular dystrophy. Instead, a defective interaction between the sarcomere and plasma membrane was detected, which was further underscored by the disrupted development of the T-tubule system. Pertinent to a potential function in stretch sensor signaling, zebrafish tcap exhibits a variable expression pattern during somitogenesis. The variable expression is inducible by stretch force, and the expression level of Tcap is negatively regulated by integrin-link kinase (ILK), a protein kinase that is involved in stretch sensing signaling. Together, our genetic studies of tcap in zebrafish suggested that pathogenesis in LGMD2G is due to a disruption of sarcomere-T-tubular interaction, but not of sarcomere assembly per se. In addition, our data prompted a novel hypothesis that predicts that the transcription level of Tcap can be regulated by the stretch force to ensure proper sarcomere-membrane interaction in striated muscles.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping