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Development, Vol 127, Issue 11 2347-2355, Copyright © 2000 by Company of Biologists

JOURNAL ARTICLES

The Oak Ridge Polycystic Kidney (orpk) disease gene is required for left-right axis determination

NS Murcia, WG Richards, BK Yoder, ML Mucenski, JR Dunlap and RP Woychik
Department of Pediatrics, Rainbow Babies and Children's Hospital, Case Western Reserve University, Cleveland, OH 44106, USA.

Analysis of several mutations in the mouse is providing useful insights into the nature of the genes required for the establishment of the left-right axis during early development. Here we describe a new targeted allele of the mouse Tg737 gene, Tg737(Delta)2-3(beta)Gal), which causes defects in left-right asymmetry and other abnormalities during embryogenesis. The Tg737 gene was originally identified based on its association with the mouse Oak Ridge Polycystic Kidney (orpk) insertional mutation, which causes polycystic kidney disease and other defects. Complementation tests between the original orpk mutation and the new targeted knock-out mutation demonstrate that Tg737(Delta)2-3(beta)Gal) behaves as an allele of Tg737. The differences in the phenotype between the two mutations suggest that the orpk mutation is a hypomorphic allele of the Tg737 gene. Unlike the orpk allele, where all homozygotes survive to birth, embryos homozygous for the Tg737(Delta)2-3(beta)Gal) mutation arrest in development at mid-gestation and exhibit neural tube defects, enlargement of the pericardial sac and, most notably, left-right asymmetry defects. At mid-gestation the direction of heart looping is randomized, and at earlier stages in development lefty-2 and nodal, which are normally expressed asymmetrically, exhibit symmetrical expression in the mutant embryos. Additionally, we determined that the ventral node cells in mutant embryos fail to express the central cilium, which is a characteristic and potentially functional feature of these cells. The expression of both Shh and Hnf3(beta) is downregulated in the midline at E8.0, indicating that there are significant alterations in midline development in the Tg737(Delta)2-3(beta)Gal) homozygous embryos. We propose that the failure of ventral node cells to fully mature alters their ability to undergo differentiation as they migrate out of the node to contribute to the developing midline structures. Analysis of this new knockout allele allows us to define a critical role for the Tg737 gene during early embryogenesis. We have named the product of the Tg737 gene Polaris, which is based on the various polarity related defects associated with the different alleles of the Tg737 gene.
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C. SOMMARDAHL, M. COTTRELL, J. E. WILKINSON, R. P. WOYCHIK, and D. K. JOHNSON
Phenotypic variations of orpk mutation and chromosomal localization of modifiers influencing kidney phenotype
Physiol Genomics, December 21, 2001; 7(2): 127 - 134.
[Abstract] [Full Text] [PDF]

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 Proc. Natl. Acad. Sci. USAHome page
L. S. B. Goldstein
Kinesin molecular motors: Transport pathways, receptors, and human disease
PNAS, June 19, 2001; 98(13): 6999 - 7003.
[Abstract] [Full Text] [PDF]

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 Mol. Biol. CellHome page
P. D. Taulman, C. J. Haycraft, D. F. Balkovetz, and B. K. Yoder
Polaris, a Protein Involved in Left-Right Axis Patterning, Localizes to Basal Bodies and Cilia
Mol. Biol. Cell, March 1, 2001; 12(3): 589 - 599.
[Abstract] [Full Text]

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 DevelopmentHome page
C. Haycraft, P Swoboda, P. Taulman, J. Thomas, and B. Yoder
The C. elegans homolog of the murine cystic kidney disease gene Tg737 functions in a ciliogenic pathway and is disrupted in osm-5 mutant worms
Development, January 5, 2001; 128(9): 1493 - 1505.
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 JCBHome page
G. J. Pazour, B. L. Dickert, Y. Vucica, E. S. Seeley, J. L. Rosenbaum, G. B. Witman, and D. G. Cole
Chlamydomonas IFT88 and Its Mouse Homologue, Polycystic Kidney Disease Gene Tg737, Are Required for Assembly of Cilia and Flagella
J. Cell Biol., October 30, 2000; 151(3): 709 - 718.
[Abstract] [Full Text] [PDF]

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 J. Biol. Chem.Home page
L. Song and W. L. Dentler
Flagellar Protein Dynamics in Chlamydomonas
J. Biol. Chem., August 3, 2001; 276(32): 29754 - 29763.
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 JCBHome page
G. J. Pazour, S. A. Baker, J. A. Deane, D. G. Cole, B. L. Dickert, J. L. Rosenbaum, G. B. Witman, and J. C. Besharse
The intraflagellar transport protein, IFT88, is essential for vertebrate photoreceptor assembly and maintenance
J. Cell Biol., April 1, 2002; 157(1): 103 - 114.
[Abstract] [Full Text] [PDF]


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