Next Article in Journal
Metagenomic Insights into the Bacterial Functions of a Diesel-Degrading Consortium for the Rhizoremediation of Diesel-Polluted Soil
Next Article in Special Issue
Loss of a Fragile Chromosome Region leads to the Screwy Phenotype in Paramecium tetraurelia
Previous Article in Journal
A SIX6 Nonsense Variant in Golden Retrievers with Congenital Eye Malformations
Previous Article in Special Issue
Functional Proteomics of Nuclear Proteins in Tetrahymena thermophila: A Review
Open AccessArticle

A Novel Role for Polycystin-2 (Pkd2) in P. tetraurelia as a Probable Mg2+ Channel Necessary for Mg2+-Induced Behavior

1
State University of New York at Plattsburgh, 101 Broad Street, Plattsburgh, NY 12901, USA
2
Department of Biology, University of Vermont, 120 Marsh Life Science, 109 Carrigan Drive, Burlington, VT 05405, USA
*
Author to whom correspondence should be addressed.
Genes 2019, 10(6), 455; https://doi.org/10.3390/genes10060455
Received: 11 April 2019 / Revised: 5 June 2019 / Accepted: 11 June 2019 / Published: 14 June 2019
(This article belongs to the Special Issue Ciliate Genetics and Epigenetics)
A human ciliopathy gene codes for Polycystin-2 (Pkd2), a non-selective cation channel. Here, the Pkd2 channel was explored in the ciliate Paramecium tetraurelia using combinations of RNA interference, over-expression, and epitope-tagging, in a search for function and novel interacting partners. Upon depletion of Pkd2, cells exhibited a phenotype similar to eccentric (XntA1), a Paramecium mutant lacking the inward Ca2+-dependent Mg2+ conductance. Further investigation showed both Pkd2 and XntA localize to the cilia and cell membrane, but do not require one another for trafficking. The XntA-myc protein co-immunoprecipitates Pkd2-FLAG, but not vice versa, suggesting two populations of Pkd2-FLAG, one of which interacts with XntA. Electrophysiology data showed that depletion and over-expression of Pkd2 led to smaller and larger depolarizations in Mg2+ solutions, respectively. Over-expression of Pkd2-FLAG in the XntA1 mutant caused slower swimming, supporting an increase in Mg2+ permeability, in agreement with the electrophysiology data. We propose that Pkd2 in P. tetraurelia collaborates with XntA for Mg2+-induced behavior. Our data suggest Pkd2 is sufficient and necessary for Mg2+ conductance and membrane permeability to Mg2+, and that Pkd2 is potentially a Mg2+-permeable channel. View Full-Text
Keywords: Polycystin-2; channelopathy; cilia; cell body membrane; magnesium channel; electrophysiology; behavior; over-expression; trafficking Polycystin-2; channelopathy; cilia; cell body membrane; magnesium channel; electrophysiology; behavior; over-expression; trafficking
Show Figures

Figure 1

MDPI and ACS Style

Valentine, M.S.; Yano, J.; Van Houten, J. A Novel Role for Polycystin-2 (Pkd2) in P. tetraurelia as a Probable Mg2+ Channel Necessary for Mg2+-Induced Behavior. Genes 2019, 10, 455. https://doi.org/10.3390/genes10060455

AMA Style

Valentine MS, Yano J, Van Houten J. A Novel Role for Polycystin-2 (Pkd2) in P. tetraurelia as a Probable Mg2+ Channel Necessary for Mg2+-Induced Behavior. Genes. 2019; 10(6):455. https://doi.org/10.3390/genes10060455

Chicago/Turabian Style

Valentine, Megan S.; Yano, Junji; Van Houten, Judith. 2019. "A Novel Role for Polycystin-2 (Pkd2) in P. tetraurelia as a Probable Mg2+ Channel Necessary for Mg2+-Induced Behavior" Genes 10, no. 6: 455. https://doi.org/10.3390/genes10060455

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop