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Sex differences in and hormonal regulation of Kv1 potassium channel gene expression in the electric organ: Molecular control of a social signal
Author(s) -
Few W. Preston,
Zakon Harold H.
Publication year - 2007
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.20305
Subject(s) - biology , subfamily , sexual dimorphism , electric fish , gene , gene expression , potassium channel , microbiology and biotechnology , genetics , biophysics , endocrinology , fish <actinopterygii> , fishery
Electric fish communicate with electric organ (EO) discharges (EODs) that are sexually dimorphic, hormone‐sensitive, and often individually distinct. The cells of the EO (electrocytes) of the weakly electric fish Sternopygus possess delayed rectifying K + currents that systematically vary in their activation and deactivation kinetics, and this precise variation in K + current kinetics helps shape sex and individual differences in the EOD. Because members of the Kv1 subfamily produce delayed rectifier currents, we cloned a number of genes in the Kv1 subfamily from the EO of Sternopygus . Using our sequences and those from genome databases, we found that in teleost fish Kv1.1 and Kv1.2 exist as duplicate pairs (Kv1.1a&b, Kv1.2a&b) whereas Kv1.3 does not. Using real‐time quantitative RT‐PCR, we found that Kv1.1a and Kv1.2a, but not Kv1.2b, expression in the EO is higher in high EOD frequency females (which have fast EO K + currents) than in low EOD frequency males (which have slow EO K + currents). Systemic treatment with dihydrotestosterone decreased Kv1.1a and Kv1.2a, but not Kv1.2b, expression in the EO, whereas treatment with human chorionic gonadotropin (hCG) increased Kv1.2a but not Kv1.1a or Kv1.2b expression in the EO. Thus, systematic variation in the ratios of Kv1 channels expressed in the EO is correlated with individual differences in and sexual dimorphism of a communication signal. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007