PUBLICATION

Genetic interaction between Bardet-Biedl syndrome genes and implications for limb patterning

Authors
Tayeh, M.K., Yen, H.J., Beck, J.S., Searby, C.C., Westfall, T.A., Griesbach, H., Sheffield, V.C., and Slusarski, D.C.
ID
ZDB-PUB-080408-14
Date
2008
Source
Human molecular genetics   17(13): 1956-1967 (Journal)
Registered Authors
Slusarski, Diane C.
Keywords
none
MeSH Terms
  • Animals
  • Bardet-Biedl Syndrome/genetics*
  • Bardet-Biedl Syndrome/physiopathology*
  • Body Patterning*
  • Cartilage/pathology
  • Disease Models, Animal*
  • Embryo, Nonmammalian/metabolism
  • Embryo, Nonmammalian/physiology
  • Extremities/embryology*
  • Extremities/physiopathology
  • Gene Expression Regulation
  • Gene Silencing
  • Hedgehog Proteins/metabolism
  • Humans
  • Phenotype
  • Polydactyly/genetics
  • Polydactyly/physiopathology
  • Species Specificity
  • Zebrafish
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed
18381349 Full text @ Hum. Mol. Genet.
Abstract
BBS is a pleiotropic genetically heterogeneous disorder characterized by obesity, retinopathy, polydactyly, cognitive impairment, renal and cardiac anomalies, as well as hypertension and diabetes. Multiple genes are known to independently cause BBS. These genes do not appear to code for the same functional category of proteins; yet mutation of each results in a similar phenotype. Gene knockdown of different bbs genes in zebrafish show strikingly overlapping phenotypes including defective melanosome transport and disruption of the ciliated Kupffer's vesicle. Here, we demonstrate that individual knockdown of bbs1 and bbs3 results in the same prototypical phenotypes as previously reported for other BBS genes. We utilize the zebrafish system to comprehensively determine whether simultaneous pair-wise knockdown of BBS genes reveals genetic interactions between BBS genes. Using this approach, we demonstrate eight genetic interactions between a subset of BBS genes. The synergistic relationships between distinct combinations are not due to functional redundancy but indicate specific interactions within a multi-subunit BBS complex. In addition, we utilize the zebrafish model system to investigate limb development. Human polydactyly is a cardinal feature of BBS not reproduced in Bbs-mouse models. We evaluated zebrafish fin bud patterning and observed altered Sonic hedgehog (SHH) expression and subsequent changes to fin skeletal elements. The SHH fin bud phenotype was also used to confirm specific genetic interactions between BBS genes. This study reveals an in vivo requirement for BBS function in limb bud patterning. Our results provide important new insights into the mechanism and biological significance of BBS.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping