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Gene Review

Invs  -  inversin

Mus musculus

Synonyms: AI428552, AW455512, Inv, Inversin, Inversion of embryo turning protein, ...
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Disease relevance of Invs

  • Cystic kidney disease has been linked to mutations in the Invs gene in mice with inversion of embryonic turning (inv/inv) and the INVS (NPHP2) gene in infants with nephronophthisis type 2 (NPHP2) [1].
  • In inv/inv mice, a known mouse model for human situs inversus, in which the directionality of heart looping is inverted, flectin expression pattern is mirror image of that of normal mouse embryos during looping stages [2].
  • Mice homozygous for a mutation in the Invs gene (inv mouse) die during the first week after birth as a result of renal and liver failure [3].
  • The Inv::GFP transgene rescued the laterality defects and polycystic kidney disease of Inv/Inv mice, indicating that the fusion protein is functional [4].
  • Mice that are homozygous for a mutation in the inv gene (inv/inv) develop renal cysts resembling autosomal-recessive polycystic kidney disease [5].

Psychiatry related information on Invs

  • We have mapped the human alpha 7-nicotinic receptor subunit gene to chromosome 15, band q14, a region frequently rearranged in patients carrying a bisatellite 15 chromosome, large inv dup (15), whose clinical features include mental retardation and seizures [6].

High impact information on Invs

  • Fluid flow increases inversin levels in ciliated tubular epithelial cells and seems to regulate this crucial switch between Wnt signaling pathways during renal development [7].
  • Mutations of the ciliary protein inversin cause nephronophthisis type II, an autosomal recessive cystic kidney disease characterized by extensive renal cysts, situs inversus and renal failure [7].
  • Characterization of complementing and non-complementing YAC transgenic families revealed that correction of the inv mutant phenotype was concordant with integration and intact expression of this novel gene, which we have named inversin (Invs) [8].
  • Visceral left-right asymmetry occurs in all vertebrates, but the inversion of embryo turning (inv) mouse, which resulted following a random transgene insertion, is the only model in which these asymmetries are consistently reversed [8].
  • Asymmetric expression patterns of the genes nodal and lefty are reversed in the inv mutant, indicating that inv may act early in left/right determination [9].

Biological context of Invs

  • We thus made Foxj1/inv double mutant mice and analyzed their phenotype [10].
  • The inv (inversion of embryonic turning) mutation in mice was created previously by random insertional mutagenesis; it produces both a constant reversal of left/right polarity (situs inversus) and cyst formation in the kidneys [9].
  • Analysis of the transgenic genome and the structure of the candidate gene indicate that the candidate gene is the only gene that is disrupted in inv mutants [9].
  • Our data support a role for inversin in primary cilia and involvement in the cell cycle [11].
  • We now provide evidence that inversin interacts with the anaphase promoting complex protein Apc2 [11].

Anatomical context of Invs

  • An inversin-specific antibody reveals a dynamic expression pattern throughout the cell cycle and strong expression in the primary cilia of renal epithelium [11].
  • Inversin forms a complex with catenins and N-cadherin in polarized epithelial cells [5].
  • Plasma membrane allocation of inversin is dependent upon cell-cell contacts and was redistributed when cell adhesion was disrupted after incubation of the cell monolayer with low-calcium/EGTA medium [5].
  • Injection of mouse inv mRNA into the right blastomere of Xenopus embryos at the two-cell stage randomized the left-right asymmetry of the embryo and altered the patterns of Xnr-1 and Pitx2 expression [12].
  • In addition, inv mutants presented decreased ability to colonize the Peyer's patches, the small intestinal wall, and the spleen when administered perorally, although when administered intraperitoneally, they showed no difference in their ability to colonize the spleen compared to the wild-type parent strain [13].

Associations of Invs with chemical compounds

  • A series of indanyl derivatives of diethylstilbestrol (DES) have recently been identified as inv vivo metabolites of DES [14].
  • To attempt to reduce binding to luminal mucus, Y. pseudotuberculosis yadA and inv yadA strains were analyzed [15].
  • Invariant NKT (inv. NKT) cells co-express an invariant alpha beta T cell receptor and the NK receptor NK1.1 and, upon CD1d-restricted recognition of the glycosphingolipid antigen alpha-galactosyl ceramide (alphaGalCer), secrete large amounts of regulatory cytokines [16].

Physical interactions of Invs


Other interactions of Invs

  • In the inversion of embryonic turning (inv) mouse mutant, which has aberrant L-R development, NKX3.2 was expressed predominantly on the left side [17].
  • Here mice homozygous for the dHAND and inv mutations are demonstrated to have only a right-sided ventricle which is morphologically a left (systemic) ventricle [18].
  • Interestingly, this asymmetric expression pattern is randomized in the iv mutant and reversed in the inv mutant, indicating that LPlunc1 is downstream of iv and inv [19].
  • Inversin (Inv), a protein that contains ankyrin repeats, plays a key role in left-right determination during mammalian embryonic development, but its precise function remains unknown [4].

Analytical, diagnostic and therapeutic context of Invs


  1. Renal cysts of inv/inv mice resemble early infantile nephronophthisis. Phillips, C.L., Miller, K.J., Filson, A.J., Nürnberger, J., Clendenon, J.L., Cook, G.W., Dunn, K.W., Overbeek, P.A., Gattone, V.H., Bacallao, R.L. J. Am. Soc. Nephrol. (2004) [Pubmed]
  2. Differential expression of flectin in the extracellular matrix and left-right asymmetry in mouse embryonic heart during looping stages. Tsuda, T., Majumder, K., Linask, K.K. Dev. Genet. (1998) [Pubmed]
  3. Differential tissue distribution of the Invs gene product inversin. Nürnberger, J., Kavapurackal, R., Zhang, S.J., Opazo Saez, A., Heusch, G., Philipp, T., Pietruck, F., Kribben, A. Cell Tissue Res. (2006) [Pubmed]
  4. The left-right determinant Inversin is a component of node monocilia and other 9+0 cilia. Watanabe, D., Saijoh, Y., Nonaka, S., Sasaki, G., Ikawa, Y., Yokoyama, T., Hamada, H. Development (2003) [Pubmed]
  5. Inversin forms a complex with catenins and N-cadherin in polarized epithelial cells. Nürnberger, J., Bacallao, R.L., Phillips, C.L. Mol. Biol. Cell (2002) [Pubmed]
  6. Molecular cloning and chromosomal localization of the human alpha 7-nicotinic receptor subunit gene (CHRNA7). Chini, B., Raimond, E., Elgoyhen, A.B., Moralli, D., Balzaretti, M., Heinemann, S. Genomics (1994) [Pubmed]
  7. Inversin, the gene product mutated in nephronophthisis type II, functions as a molecular switch between Wnt signaling pathways. Simons, M., Gloy, J., Ganner, A., Bullerkotte, A., Bashkurov, M., Krönig, C., Schermer, B., Benzing, T., Cabello, O.A., Jenny, A., Mlodzik, M., Polok, B., Driever, W., Obara, T., Walz, G. Nat. Genet. (2005) [Pubmed]
  8. Inversin, a novel gene in the vertebrate left-right axis pathway, is partially deleted in the inv mouse. Morgan, D., Turnpenny, L., Goodship, J., Dai, W., Majumder, K., Matthews, L., Gardner, A., Schuster, G., Vien, L., Harrison, W., Elder, F.F., Penman-Splitt, M., Overbeek, P., Strachan, T. Nat. Genet. (1998) [Pubmed]
  9. Cloning of inv, a gene that controls left/right asymmetry and kidney development. Mochizuki, T., Saijoh, Y., Tsuchiya, K., Shirayoshi, Y., Takai, S., Taya, C., Yonekawa, H., Yamada, K., Nihei, H., Nakatsuji, N., Overbeek, P.A., Hamada, H., Yokoyama, T. Nature (1998) [Pubmed]
  10. Roles of the Foxj1 and Inv genes in the left-right determination of internal organs in mice. Tamakoshi, T., Itakura, T., Chandra, A., Uezato, T., Yang, Z., Xue, X.D., Wang, B., Hackett, B.P., Yokoyama, T., Miura, N. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  11. Expression analyses and interaction with the anaphase promoting complex protein Apc2 suggest a role for inversin in primary cilia and involvement in the cell cycle. Morgan, D., Eley, L., Sayer, J., Strachan, T., Yates, L.M., Craighead, A.S., Goodship, J.A. Hum. Mol. Genet. (2002) [Pubmed]
  12. Calmodulin binds to inv protein: implication for the regulation of inv function. Yasuhiko, Y., Imai, F., Ookubo, K., Takakuwa, Y., Shiokawa, K., Yokoyama, T. Dev. Growth Differ. (2001) [Pubmed]
  13. Cloning and molecular characterization of genes whose products allow Salmonella typhimurium to penetrate tissue culture cells. Galán, J.E., Curtiss, R. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  14. Molecular structures of metabolites and analogues of diethylstilbestrol and their relationship to receptor binding and biological activity. Duax, W.L., Swenson, D.C., Strong, P.D., Korach, K.S., McLachlan, J., Metzler, M. Mol. Pharmacol. (1984) [Pubmed]
  15. Invasin-dependent and invasin-independent pathways for translocation of Yersinia pseudotuberculosis across the Peyer's patch intestinal epithelium. Marra, A., Isberg, R.R. Infect. Immun. (1997) [Pubmed]
  16. Activation of invariant NKT cells by alphaGalCer administration protects mice from MOG35-55-induced EAE: critical roles for administration route and IFN-gamma. Furlan, R., Bergami, A., Cantarella, D., Brambilla, E., Taniguchi, M., Dellabona, P., Casorati, G., Martino, G. Eur. J. Immunol. (2003) [Pubmed]
  17. The homeobox gene NKX3.2 is a target of left-right signalling and is expressed on opposite sides in chick and mouse embryos. Schneider, A., Mijalski, T., Schlange, T., Dai, W., Overbeek, P., Arnold, H.H., Brand, T. Curr. Biol. (1999) [Pubmed]
  18. The bHLH factors, dHAND and eHAND, specify pulmonary and systemic cardiac ventricles independent of left-right sidedness. Thomas, T., Yamagishi, H., Overbeek, P.A., Olson, E.N., Srivastava, D. Dev. Biol. (1998) [Pubmed]
  19. Identification of a novel left-right asymmetrically expressed gene in the mouse belonging to the BPI/PLUNC superfamily. Hou, J., Yashiro, K., Okazaki, Y., Saijoh, Y., Hayashizaki, Y., Hamada, H. Dev. Dyn. (2004) [Pubmed]
  20. Analysis of multiple Invs transcripts in mouse and MDCK cells. Ward, H.H., Wang, J., Phillips, C. Genomics (2004) [Pubmed]
  21. Molecular cloning of a gene for inversion of embryo turning (inv) with cystic kidney. Mochizuki, T., Tsuchiya, K., Yokoyama, T. Nephrol. Dial. Transplant. (2002) [Pubmed]
  22. Primary cilia of inv/inv mouse renal epithelial cells sense physiological fluid flow: bending of primary cilia and Ca2+ influx. Shiba, D., Takamatsu, T., Yokoyama, T. Cell Struct. Funct. (2005) [Pubmed]
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