Structural disorganization of pronephric glomerulus in Zebrafish mpp5a/nagie oko mutant

Authors

  • Koichiro Ichimura,

    1. Department of Cell Biology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma
    2. Department of Anatomy and Life Structure, Juntendo University School of Medicine, Tokyo, Japan
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  • Yayoi Fukuyo,

    1. Department of Cell Biology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma
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  • Tomomi Nakamura,

    1. Department of Cell Biology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma
    2. Department of Biological Science and Technology, Graduate school of Industrial Science and Technology, Tokyo University of Science, Noda, Chiba, Japan
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  • Rebecca Powell,

    1. Department of Cell Biology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma
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  • Tatsuo Sakai,

    1. Department of Anatomy and Life Structure, Juntendo University School of Medicine, Tokyo, Japan
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  • Tomoko Obara

    Corresponding author
    1. Department of Cell Biology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma
    • Department of Cell Biology, University of Oklahoma Health Science Center, 975 NE 10th St., BRC256, Oklahoma City, OK 73104, USA
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Abstract

Background: The podocyte slit diaphragm (SD) is an essential component of the selective filtration barrier in the glomerulus. Several structural proteins required for formation and maintenance of SD have been identified; however, molecular mechanisms regulating these proteins are still limited. Results: Here, we demonstrate that MAGUK p55 subfamily member 5a (Mpp5a)/Nagie oko, a component of the Crb multi-protein complex, was colocalized with an SD-associated protein ZO-1 in the zebrafish pronephric glomerulus. To characterize the function of Mpp5a, zebrafish mpp5am520 mutant embryos, which are known to have defects in cardiac and neuronal morphogenesis, were analyzed. These mutants failed to merge the bilateral glomerular primordia and to form the glomerular capillary and mesangium, but the foot processes and SD showed normal appearance. The structural disorganization in the mpp5am520 mutant glomerulus was quite similar to that of a cardiac troponin T2a/tnnt2a/silent heart knockdown zebrafish, which exhibited circulatory failure due to lack of heart beating. Conclusions: Mpp5a is not prerequisite to form podocyte slit diaphragm in the pronephric glomerular development in zebrafish. The structural disorganization of the pronephric glomerulus in the mpp5am520 mutant is likely to result from circulatory failure, rather than the anomaly of Mpp5a protein in the glomerulus. Developmental Dynamics, 2012. © 2012 Wiley Periodicals, Inc.

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