Cloning of inv, a gene that controls left/right asymmetry and kidney development

Toshio Mochizuki, Yukio Saijoh, Ken Tsuchiya, Yasuaki Shirayoshi, Setsuo Takai, Choji Taya, Hiromichi Yonekawa, Kiyomi Yamada, Hiroshi Nihei, Norio Nakatsuji, Paul A. Overbeek, Hiroshi Hamada and Takahiko Yokoyama ()
Additional contact information
Toshio Mochizuki: Kidney Center
Yukio Saijoh: Institute for Molecular and Cellular Biology, Osaka University
Ken Tsuchiya: Kidney Center
Yasuaki Shirayoshi: Mammalian Development Laboratory, National Institute of Genetics
Setsuo Takai: Research Institute, International Medical Center of Japan
Choji Taya: The Tokyo Metropolitan Institute of Medical Science
Hiromichi Yonekawa: The Tokyo Metropolitan Institute of Medical Science
Kiyomi Yamada: Research Institute, International Medical Center of Japan
Hiroshi Nihei: Kidney Center
Norio Nakatsuji: Mammalian Development Laboratory, National Institute of Genetics
Hiroshi Hamada: Institute for Molecular and Cellular Biology, Osaka University
Takahiko Yokoyama: Tokyo Women's Medical University, School of Medicine

Nature, 1998, vol. 395, issue 6698, 177-181

Abstract: Abstract Most vertebrate internal organs show a distinctive left/right asymmetry. The inv (inversion of embryonic turning) mutation in mice was created previously by random insertional mutagenesis1; it produces both a constant reversal of left/right polarity (situs inversus) and cyst formation in the kidneys2. Asymmetric expression patterns of the genes nodal and lefty are reversed in the inv mutant3,4,5,6, indicating that inv may act early in left/right determination. Here we identify a new gene located at the inv locus. The encoded protein contains 15 consecutive repeats of an Ank/Swi6 motif7,8 at its amino terminus. Expression of the gene is the highest in the kidneys and liver among adult tissues, and is seen in presomite-stage embryos. 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. Transgenic introduction of a minigene encoding the candidate protein restores normal left/right asymmetry and kidney development in the inv mutant, confirming the identity of the candidate gene.

Date: 1998
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DOI: 10.1038/26006

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