Description: Marine teleosts can absorb imbibed seawater (SW) to maintain water balance, with esophageal desalination playing an essential role. NaCl absorption from luminal SW was enhanced 10-fold in the esophagus of SW-acclimated eels, and removal of Na + or Cl – from luminal SW abolished the facilitated absorption, indicating coupled transport. Mucosal/serosal application of various blockers for Na + /Cl – transporters profoundly decreased the absorption. Among the transporter genes expressed in eel esophagus detected by RNA-seq, dimethyl amiloride-sensitive Na + /H + exchanger (NHE3) and 4,4'-diisothiocyano-2,2'-disulfonic acid-sensitive Cl – / HCO3– exchanger (AE) coupled by the scaffolding protein on the apical membrane of epithelial cells, and ouabain-sensitive Na + -K + -ATPases (NKA1α1c and NKA3α) and diphenylamine-2-carboxylic acid-sensitive Cl – channel (CLCN2) on the basolateral membrane, may be responsible for enhanced transcellular NaCl transport because of their profound upregulation after SW acclimation. Upregulated carbonic anhydrase 2a (CA2a) supplies H + and HCO3– for activation of the coupled NHE and AE. Apical hydrochlorothiazide-sensitive Na + -Cl – cotransporters and basolateral Na + - HCO3– cotransporter (NBCe1) and AE1 are other possible candidates. Concerning the low water permeability that is typically seen in marine teleost esophagus, downregulated aquaporin genes ( aqp1a and aqp3 ) and upregulated claudin gene ( cldn15a ) are candidates for transcellular/paracellular route. In situ hybridization showed that these upregulated transporters and tight-junction protein genes were expressed in the absorptive columnar epithelial cells of eel esophagus. These results allow us to provide a full picture of the molecular mechanism of active desalination and low water permeability that are characteristic to marine teleost esophagus and gain deeper insights into the role of gastrointestinal tracts in SW acclimation.

Description: During the structure formation, charged and neutral chemical species may have separated from each other at the gravitational contraction in primordial magnetic field (PMF). A gradient in the PMF in a direction perpendicular to the field direction leads to the Lorentz force on the charged species. Resultantly, an ambipolar diffusion occurs, and charged species can move differently from neutral species, which collapses gravitationally during the structure formation. We assume a gravitational contraction of neutral matter in a spherically symmetric structure, and calculate fluid motions of charged and neutral species. It is shown that the charged fluid, i.e. proton, electron, and 7 Li + , can significantly decouple from the neutral fluid depending on the field amplitude. The charged species can, therefore, escape from the gravitational collapse. We take the structure mass, the epoch of the gravitational collapse, and the comoving Lorenz force as parameters. We then identify a parameter region for an effective chemical separation. This type of chemical separation can reduce the abundance ratio of Li/H in early structures because of inefficient contraction of 7 Li + ion. Therefore, it may explain Li abundances of Galactic metal-poor stars which are smaller than the prediction in standard big bang nucleosynthesis model. Amplitudes of the PMFs are controlled by a magnetohydrodynamic turbulence. The upper limit on the field amplitude derived from the turbulence effect is close to the value required for the chemical separation.

Description: Versican (Vcan)/proteoglycan (PG)-M is a large chondroitin sulfate proteoglycan which forms a proteoglycan/hyaluronan (HA) aggregate in the extracellular matrix (ECM). We tried to generate the Vcan knockout mice by a conventional method, which resulted in mutant mice Vcan 3/3 whose Vcan lacks the A subdomain of the G1 domain. The Vcan knockout embryos died during the early development stage due to heart defects, but some Vcan 3/3 embryos survived through to the neonatal period. The hearts in Vcan 3/3 newborn mice showed normal cardiac looping, but had ventricular septal defects. Their atrioventricular canal (AVC) cushion was much smaller than those of wild-type (WT) embryos, and the extracellular space for cardiac jelly was narrow. The Vcan deposition in the Vcan 3/3 AVC cushion had decreased, whereas the HA deposition was maintained and condensed. In the tip of ventricular septa, both Vcan and HA had decreased. The cell proliferation based on the number of Ki67-positive cells had remarkably increased in both the AVC cushion and ventricular septa, compared with that of WT embryos. Vcan 3/3 seemed to have endocardial and mesenchymal mixed characteristics. When the ex vivo explant culture of these regions was performed on the collagen gel, hardly any migration to make sufficient space for the ECM construction was apparent. Our results suggest that the proteoglycan aggregates are necessary in both the AVC cushion and ventricular septa to fuse interventricular septa, and the Vcan A subdomain plays an essential role for the interventricular septal formation by constituting the proteoglycan aggregates.