Glucose, a carbohydrate metabolite, plays a major role in the energy supply for fish iono- and osmoregulation, and the way that glucose is transported in ionocytes is a critical process related to the functional operations of ionocytes. Eighteen members of glucose transporters (GLUTs, SLC2A) were cloned and identified from zebrafish. Previously, Na+,K+ -ATPase-rich (NaR), Na+-Cl- cotransporter-expressing (NCC), H+-ATPase-rich (HR), and glycogen-rich (GR) cells have been identified to be responsible for Ca2+ uptake, Cl- uptake, Na+ uptake, and the energy deposition, respectively, in zebrafish skin/gills. The purpose of the present study was to test the hypothesis of whether GLUT isoforms are specifically expressed and function in ionocytes to supply energy for ion regulatory mechanisms. On the basis of translational knockdown of foxi3a/3b (2 transcriptional factors related to the ionocytes’ differentiation) and triple in situ hybridization/immunocytochemistry, 3 GLUT isoforms, zglut1a, -6, and -13.1, were specifically localized in NaR/NCC cells, GR cells, and HR cells, respectively. mRNA expression of zglut1a in embryos and adult gills were stimulated by the low Ca2+ or low Cl- freshwater, which has been previously reported to upregulate the functions (monitored by epithelial Ca2+   channel, NCC mRNA) of NaR/NCC cells, respectively while that of zglut13.1 was stimulated only by low Na+, a situation to upregulate the function (monitored by carbonic anhydrase 15a mRNA) of HR cells. On the other hand, ambient ion compositions did not affect the zglut6 mRNA expression. Taken together, zGLUT1a, -6, and 13.1, the specific transporters in NaR/NCC cells, GR cells, and HR cells, may absorb glucose into the respective cells to fulfill different physiological demands.

Betanodaviruses are one of the serious pathogens in nervous necrosis viral (NNV) disease that brings about mortality in the larval stage of grouper. In this study, the efficacy of pretreatment, co-treatment, and posttreatment with the antimicrobial epinecidin-1 and hepcidin 1-5 peptides against a betanodavirus was evaluated by an intraperitoneal inoculation in grouper (Epinephelus coioides). The results showed that co-treatment of epinecidin-1 or hepcidin 1-5 with the virus was effective in promoting a significant decrease in grouper mortality. Re-challenge with virus again after 30 days in co-treated grouper groups showed a high survival suggesting that epinecidin-1 and hepcidin 1-5 enhance the fish survival. However, grouper inoculated with NNV and then inoculated with epinecidin-1 8 h later showed a significantly different survival from the group inoculated with virus alone, suggesting that epinecidin-1 can be used as a drug to rescue infected grouper. Infection after pretreatment, co-treatment, and posttreatment with epinecidin-1 or hepcidin 1-5 was verified by RT-PCR that shown downregulation of Mx2 and Mx3 gene expressions. All these data strongly suggest that epinecidin-1 and hepcidin 1-5 are effective peptides for protecting grouper larvae by reducing NNV infection.

The current gene regulatory network (GRN) of the sea urchin Strongylocentrotus purpuratus embryo describes the specification of the endomesodermal territories. However, the specification of the adjacent ectodermal territories of the embryo has been far less explored. Several recent studies on the cis-regulatory analysis of nodal and the early oral ectoderm determinants have provided clues on how the specification of this territory is initiated. Recently, a large-scale of gene regulatory network analysis was carried out in an effort to build the ectoderm specification GRN. The deduced ectodermal GRN model provides the first peek at the overall picture of ectoderm specification in the sea urchin embryo. This review integrates the current knowledge on the specification of the ectoderm by linking recent discoveries to the GRN model to understand the process of ectoderm specification in sea urchin embryos.
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