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  Stem cells and fluid flow drive cyst formation in an invertebrate excretory organ.

Vu, H. T. K., Rink, J. C., McKinney, S. A., McClain, M., Lakshmanaperumal, N., Alexander, R., et al. (2015). Stem cells and fluid flow drive cyst formation in an invertebrate excretory organ. eLife, 4: e07405. doi:10.7554/eLife.07405.

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Vu, H. T. K.1, Author              
Rink, J. C.1, Author              
McKinney, S. A., Author
McClain, M., Author
Lakshmanaperumal, N., Author
Alexander, R., Author
Alvarado, A. S., Author
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1Department of Tissue Dynamics and Regeneration, MPI for Biophysical Chemistry, Max Planck Society, ou_3181978              

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 Abstract: Cystic kidney diseases (CKDs) affect millions of people worldwide. The defining pathological features are fluid-filled cysts developing from nephric tubules due to defective flow sensing, cell proliferation and differentiation. The underlying molecular mechanisms, however, remain poorly understood, and the derived excretory systems of established invertebrate models (Caenorhabditis elegans and Drosophila melanogaster) are unsuitable to model CKDs. Systematic structure/function comparisons revealed that the combination of ultrafiltration and flow-associated filtrate modification that is central to CKD etiology is remarkably conserved between the planarian excretory system and the vertebrate nephron. Consistently, both RNA-mediated genetic interference (RNAi) of planarian orthologues of human CKD genes and inhibition of tubule flow led to tubular cystogenesis that share many features with vertebrate CKDs, suggesting deep mechanistic conservation. Our results demonstrate a common evolutionary origin of animal excretory systems and establish planarians as a novel and experimentally accessible invertebrate model for the study of human kidney pathologies.

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Language(s): eng - English
 Dates: 2015-06-09
 Publication Status: Published online
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 Rev. Type: Peer
 Identifiers: DOI: 10.7554/eLife.07405
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Title: eLife
Source Genre: Journal
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Pages: 28 Volume / Issue: 4 Sequence Number: e07405 Start / End Page: - Identifier: -