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Boo, M. V., Chew, S. F., & Ip, Y. K. (2021). Basolateral Na⁺/Ca²⁺ exchanger 1 and Na⁺/K⁺-ATPase, which display light-enhanced gene and protein expression levels, could be involved in the absorption of exogenous Ca²⁺ through the ctenidium of the giant clam, Tridacna squamosa. Comparative Biochemistry and Physiology, Part A, 259, Article 110997. https://doi.org/10.1016/j.cbpa.2021.110997
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology
Giant clams perform light-enhanced shell formation (calcification) and therefore need to increase the uptake of exogenous Ca2+ during illumination. The ctenidium of the fluted giant clam, Tridacna squamosa, is involved in light-enhanced Ca2+ uptake. It expresses the pore-forming voltage-gated calcium channel (VGCC) subunit alpha 1 (CACNA1) in the apical membrane of the epithelial cells, and the protein expression level of CACNA1 is upregulated in the ctenidium during illumination. This study aimed to elucidate the mechanism involved in the transport of the absorbed Ca2+across the basolateral membrane of the ctenidial epithelial cells into the hemolymph. We obtained a homolog of Na+/Ca2+ exchanger 1 (NCX1-like) from the ctenidium of T. squamosa, which comprised 2418 bp, encoding a protein of 806 amino acids (88.9 kDa). NCX1-like had a basolateral localization in the epithelial cells of the ctenidial filaments and tertiary water channels. Illumination resulted in significant increases in the transcript and protein levels of NCX1-like/NCX1-like in the ctenidium. Hence, NCX1-like could operate in conjunction with VGCC to increase the transport of Ca2+ from the ambient seawater into the hemolymph during illumination. Illumination also resulted in the upregulation of the gene and protein expression levels of Na+/K+-ATPase (NKA) α-subunit (NKAα/NKAα) in the ctenidium of T. squamosa. As light-enhanced extrusion of Ca2+ into the hemolymph through NCX1-like would lead to a greater influx of extracellular Na+, the increased expression of the basolateral NKA was required to augment the capacity of intracellular Na+ homeostasis.
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