Journal article
Expression and Localization of CaBP Ca2+ Binding Proteins in the Mouse Cochlea
PloS one, Vol.11(1), pp.e0147495-e0147495
2016
DOI: 10.1371/journal.pone.0147495
PMCID: PMC4725724
PMID: 26809054
Abstract
CaBPs are a family of EF-hand Ca2+ binding proteins that are structurally similar to calmodulin. CaBPs can interact with, and yet differentially modulate, effectors that are regulated by calmodulin, such as Cav1 voltage-gated Ca2+ channels. Immunolabeling studies suggest that multiple CaBP family members (CaBP1, 2, 4, and 5) are expressed in the cochlea. To gain insights into the respective auditory functions of these CaBPs, we characterized the expression and cellular localization of CaBPs in the mouse cochlea. By quantitative reverse transcription PCR, we show that CaBP1 and CaBP2 are the major CaBPs expressed in mouse cochlea both before and after hearing onset. Of the three alternatively spliced variants of CaBP1 (caldendrin, CaBP1-L, and CaBP1-S) and CaBP2 (CaBP2-alt, CaBP2-L, CaBP2-S), caldendrin and CaBP2-alt are the most abundant. By in situ hybridization, probes recognizing caldendrin strongly label the spiral ganglion, while probes designed to recognize all three isoforms of CaBP1 weakly label both the inner and outer hair cells as well as the spiral ganglion. Within the spiral ganglion, caldendrin/CaBP1 labeling is associated with cells resembling satellite glial cells. CaBP2-alt is strongly expressed in inner hair cells both before and after hearing onset. Probes designed to recognize all three variants of CaBP2 strongly label inner hair cells before hearing onset and outer hair cells after the onset of hearing. Thus, CaBP1 and CaBP2 may have overlapping roles in regulating Ca2+ signaling in the hair cells, and CaBP1 may have an additional function in the spiral ganglion. Our findings provide a framework for understanding the role of CaBP family members in the auditory periphery.
Details
- Title: Subtitle
- Expression and Localization of CaBP Ca2+ Binding Proteins in the Mouse Cochlea
- Creators
- Tian Yang - Department of Neurology, University of Iowa, Iowa City, Iowa, United States of AmericaElizabeth S Scholl - Department of Neurology, University of Iowa, Iowa City, Iowa, United States of AmericaNing Pan - Department of Biology, University of Iowa, Iowa City, Iowa, United States of AmericaBernd Fritzsch - Department of Biology, University of Iowa, Iowa City, Iowa, United States of AmericaFrançoise Haeseleer - Department of Physiology and Biophysics, University of Washington, Seattle, Washington, United States of AmericaAmy Lee - Department of Neurology, University of Iowa, Iowa City, Iowa, United States of America
- Resource Type
- Journal article
- Publication Details
- PloS one, Vol.11(1), pp.e0147495-e0147495
- DOI
- 10.1371/journal.pone.0147495
- PMID
- 26809054
- PMCID
- PMC4725724
- NLM abbreviation
- PLoS One
- ISSN
- 1932-6203
- eISSN
- 1932-6203
- Publisher
- Public Library of Science; United States
- Grant note
- DC009433 / NIDCD NIH HHS R55 DC009433 / NIDCD NIH HHS P30 DC010362 / NIDCD NIH HHS R01 EY020850 / NEI NIH HHS R01 DC009433 / NIDCD NIH HHS DC010362 / NIDCD NIH HHS EY020850 / NEI NIH HHS NS084190 / NINDS NIH HHS R01 NS084190 / NINDS NIH HHS
- Language
- English
- Date published
- 2016
- Academic Unit
- Molecular Physiology and Biophysics; Iowa Neuroscience Institute; Biology; Craniofacial Anomalies Research Center
- Record Identifier
- 9984070602702771
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