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Published March 15, 2002 | public
Journal Article

Identification and Characterization of a Calcium Channel γ Subunit Expressed in Differentiating Neurons and Myoblasts

Abstract

Transient elevations of intracellular calcium (calcium transients) play critical roles in many developmental processes, including differentiation. Although the factors that regulate calcium transients are not clearly defined, calcium influx may be controlled by molecules interacting with calcium channels, including channel regulatory subunits. Here, we describe the chick γ4 regulatory subunit (CACNG4), the first such subunit to be characterized in early development. CACNG4 is expressed early in the cranial neural plate, and later in the cranial and dorsal root ganglia; importantly, the timing of this later expression correlates precisely with the onset of neuronal differentiation. CACNG4 expression is also observed in nonneuronal tissues undergoing differentiation, specifically the myotome and a subpopulation of differentiating myoblasts in the limb bud. Finally, within the distal cranial ganglia, we show that CACNG4 is expressed in placode-derived cells (prospective neurons), but also, surprisingly, in neural crest-derived cells, previously shown to form only glia in this location; contrary to these previous results, we find that neural crest cells can form neurons in the distal ganglia. Given the proposed role of CACNG4 in modulating calcium channels and its expression in differentiating cells, we suggest that CACNG4 may promote differentiation via regulation of intracellular calcium levels.

Additional Information

© 2002 Elsevier Science (USA). Received for publication September 14, 2001. Revised December 4, 2001. Accepted December 4, 2001. Published online February 11, 2002. We thank Yun Kee for the chick embryo library, Jack Sechrist for assistance with anatomical identification, and Helen McBride and Tanya Moreno for critical reading of the manuscript. This work was supported by grants from the NIH (DE13223 and NS41070) to M.B.F.; B.M.K. was supported by an undergraduate research fellowship from the Arnold and Mabel Beckman Foundation; C.V.H.B. was supported by American Heart Association Fellowships 1171-F11 and 0020097Y; and A.K.K. was supported by postdoctoral fellowships from the Cancer Research Fund of the Damon Runyon-Walter Winchell Foundation, and from the NIH (DE14134).

Additional details

Created:
August 21, 2023
Modified:
October 17, 2023