PUBLICATION

Disruption of LRRK2 in Zebrafish leads to hyperactivity and weakened antibacterial response

Authors
Sheng, D., See, K., Hu, X., Yu, D., Wang, Y., Liu, Q., Li, F., Lu, M., Zhao, J., Liu, J.
ID
ZDB-PUB-180303-10
Date
2018
Source
Biochemical and Biophysical Research Communications   497(4): 1104-1109 (Journal)
Registered Authors
Kelvin, See Zhenwei
Keywords
LRRK2, Parkinson's disease, Zebrafish
MeSH Terms
  • Animals
  • Bacterial Infections/genetics
  • Bacterial Infections/immunology
  • Behavior, Animal
  • Hyperkinesis/etiology*
  • Immunity/genetics*
  • Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics*
  • Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/immunology
  • Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/physiology
  • Motor Activity/genetics
  • Mutagenesis, Site-Directed
  • Sequence Analysis, RNA
  • Zebrafish
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/immunology
  • Zebrafish Proteins/physiology
PubMed
29499195 Full text @ Biochem. Biophys. Res. Commun.
Abstract
As a protein with complex domain structure and roles in kinase, GTPase and scaffolding, LRRK2 is believed to be an important orchestration node leading to several cascades of signal transduction rather than one specific pathway. LRRK2 variants were found to be associated with Parkinson's disease, Crohn's disease and leprosy. Here we disrupt LRRK2 in zebrafish and found hyperactivity rather than hypoactivity in adult zebrafish mutants. By RNA-seq we found genes involved in infectious disease and immunological disease were notably affected. Functional studies also revealed a weakened antibacterial response in LRRK2 mutant. This mutant can be further explored for revealing molecular mechanisms and modeling of LRRK2 related diseases.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping