PUBLICATION

GLUT3 gene expression is critical for embryonic growth, brain development and survival

Authors
Carayannopoulos, M.O., Xiong, F., Jensen, P., Rios-Galdamez, Y., Huang, H., Lin, S., Devaskar, S.U.
ID
ZDB-PUB-200513-11
Date
2014
Source
Molecular genetics and metabolism   111: 477-83 (Journal)
Registered Authors
Huang, Haigen, Lin, Shuo
Keywords
Apoptosis, Embryonic growth restriction, Microcephaly
MeSH Terms
  • Animals
  • Apoptosis/genetics
  • Brain/embryology*
  • Brain/metabolism*
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/metabolism
  • Embryonic Development/genetics*
  • Gene Expression Regulation, Developmental*
  • Gene Knockdown Techniques
  • Glucose Transporter Type 3/genetics*
  • Glucose Transporter Type 3/metabolism
  • Humans
  • In Situ Hybridization
  • Phenotype
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Survival Analysis
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed
24529979 Full text @ Mol. Genet. Metab.
Abstract
Glucose is the primary energy source for eukaryotic cells and the predominant substrate for the brain. GLUT3 is essential for trans-placental glucose transport and highly expressed in the mammalian brain. To further elucidate the role of GLUT3 in embryonic development, we utilized the vertebrate whole animal model system of Danio rerio as a tractable system for defining the cellular and molecular mechanisms altered by impaired glucose transport and metabolism related to perturbed expression of GLUT3. The comparable orthologue of human GLUT3 was identified and the expression of this gene abrogated during early embryonic development. In a dose-dependent manner embryonic brain development was disrupted resulting in a phenotype of aberrant brain organogenesis, associated with embryonic growth restriction and increased cellular apoptosis. Rescue of the morphant phenotype was achieved by providing exogenous GLUT3 mRNA. We conclude that GLUT3 is critically important for brain organogenesis and embryonic growth. Disruption of GLUT3 is responsible for the phenotypic spectrum of embryonic growth restriction to demise and neural apoptosis with microcephaly.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes