Document Detail


Normal ciliogenesis requires synergy between the cystic kidney disease genes MKS-3 and NPHP-4.
MedLine Citation:
PMID:  20150540     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cilia dysfunction contributes to renal cyst formation in multiple human syndromes including nephronophthisis (NPHP), Meckel-Gruber syndrome (MKS), Joubert syndrome (JBTS), and Bardet-Beidl syndrome (BBS). Although genetically heterogeneous, these diseases share several loci that affect cilia and/or basal body proteins, but the functions and interactions of these gene products are incompletely understood. Here, we report that the ciliated sensory neurons (CSNs) of C. elegans express the putative transmembrane protein MKS-3, which localized to the distal end of their dendrites and to the cilium base but not to the cilium itself. Localization of MKS-3 and other known MKS and NPHP proteins partially overlapped. By analyzing mks-3 mutants, we found that ciliogenesis did not require MKS-3; instead, cilia elongated and cilia-mediated chemoreception was abnormal. Genetic analysis indicated that mks-3 functions in a pathway with other mks genes. Furthermore, mks-1 and mks-3 genetically interacted with a separate pathway (involving nphp-1 and nphp-4) to influence proper positioning, orientation, and formation of cilia. Combined disruption of nphp and mks pathways had cell nonautonomous effects on C. elegans sensilla. Taken together, these data demonstrate the importance of mutational load on the presentation and severity of ciliopathies and expand the understanding of the interactions between ciliopathy genes.
Authors:
Corey L Williams; Svetlana V Masyukova; Bradley K Yoder
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-02-11
Journal Detail:
Title:  Journal of the American Society of Nephrology : JASN     Volume:  21     ISSN:  1533-3450     ISO Abbreviation:  J. Am. Soc. Nephrol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-03     Completed Date:  2010-06-21     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  9013836     Medline TA:  J Am Soc Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  782-93     Citation Subset:  IM    
Affiliation:
Department of Cell Biology, University of Alabama at Birmingham Medical Center, Birmingham, Alabama, USA.
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MeSH Terms
Descriptor/Qualifier:
Alleles
Animals
Caenorhabditis elegans
Caenorhabditis elegans Proteins / chemistry,  genetics,  metabolism*
Chemotaxis
Cilia / metabolism
Gene Expression Regulation
Kidney Diseases, Cystic / genetics,  metabolism
Membrane Proteins / chemistry,  genetics,  metabolism*
Sensory Receptor Cells / metabolism
Transcription Factors / metabolism
Grant Support
ID/Acronym/Agency:
R01 DK065655/DK/NIDDK NIH HHS; R01 DK62758/DK/NIDDK NIH HHS; T32 DK007545-22/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Caenorhabditis elegans Proteins; 0/DAF-19 protein, C elegans; 0/MKS-3 protein, C elegans; 0/Membrane Proteins; 0/Transcription Factors; 0/nephrocystin 4, C elegans
Comments/Corrections
Comment In:
J Am Soc Nephrol. 2010 May;21(5):724-6   [PMID:  20395369 ]

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