千葉県君津市川谷地域に露出する中部更新統柿ノ木台層から産出する冷湧水化石群集: その時空分布と共産する自生炭酸塩

金沢大学国際基幹教育院 GS教育系冷湧水性群集が房総半島の中部更新統柿ノ木台層の陸棚相から産出する．群集は，化学合成二枚貝類から排他的になり，著しく13Cに枯渇した自生炭酸塩と共産することから，AOM（嫌気的メタン酸化）に依存していたと考えられる．自生炭酸塩は巣穴壁面と巣穴周囲の堆積物中に沈殿し，巣穴からスナモグリ類の爪化石と糞化石が産出することから，これらはスナモグリ類の巣穴であると考えられる．スナモグリ類はメタン生成帯まで巣穴を堀り，海水を巣穴深部へ供給し，AOMを活性化させることによって巣穴中の硫化水素イオン濃度を上昇させた．溶存酸素濃度が高い巣穴浅部では，硫黄酸化菌が繁茂し，スナモグリ類の食糧となった．巣穴深部では，浮遊する生物源炭酸塩などを核とした針状アラゴナイトが重力方向に沈下して炭酸塩ジオペタル状構造を形成し，巣穴周囲の堆積物中では，リン酸イオン濃度の上昇により高Mgカルサイトが，また硫酸イオンの枯渇によりドロマイトが沈殿した．Cold-seep-dependent molluscan assemblages occur in the outer-shelf facies of the middle Pleistocene Kakinokidai Formation of the Kazusa Group, a forearc basin-fill sequence on the Pacific side of central Japan, in strata corresponding to the interval 707.6-667.0 ka. The assemblages consist exclusively of chemosymbiotic bivalves (lucinids, thyasirids, and solemyids) and are associated with 13C-depleted authigenic carbonates (δ13C = −61.60‰ to −10.96‰ VPDB), which suggest that their main carbon source was anaerobic oxidation of methane (AOM). Authigenic carbonate precipitates are common on burrow walls (mainly acicular aragonite) and the surrounding sediments (mainly micritic high-Mg calcite and dolomite). The burrows are cylindrical, 1.5-3.0 cm in diameter, and >1 m long. Callianassid claws and the trace fossil Palaxius (probable callianassid fecal pellets) in the burrow carbonates suggest that the burrows were produced by sediment-dwelling callianassid decapods.\nWe propose the following formation mechanism of burrows and their related authigenic carbonates. Firstly, callianassids produced deep burrows, penetrating the AOM zone and reaching the methanogenic zone. Methane then seeped into the burrows and AOM occurred in its deeper parts, promoted by a supply of seawater via callianassid activity, resulting in an increase in the concentration of hydrogen sulfide ions. Thiobacteria flourished in the shallower parts of the burrows, which were enriched in dissolved oxygen, and provided a source of food for the callianassids. In the deeper parts of the burrows, acicular aragonite precipitated around suspended carbonate nuclei and sank to the bottoms of the burrows, forming geopetal-like carbonate structures. In the surrounding sediment, high-Mg calcite precipitated in response to an increase in the concentration of phosphate ions (due to the decomposition of organic matter), and dolomite precipitated in response to decreasing concentrations of sulfate ions (caused by active AOM)

Roles of GP33, a guinea pig cytomegalovirus-encoded G protein-coupled receptor homolog, in cellular signaling, viral growth and inflammation in vitro and in vivo.

Cytomegaloviruses (CMVs) encode cellular homologs to evade host immune functions. In this study, we analyzed the roles of GP33, a guinea pig CMV (GPCMV)-encoded G protein-coupled receptor (GPCR) homolog, in cellular signaling, viral growth and pathogenesis. The cDNA structure of GP33 was determined by RACE. The effects of GP33 on some signaling pathways were analyzed in transient transfection assays. The redET two-step recombination system for a BAC containing the GPCMV genome was used to construct a mutant GPCMV containing an early stop codon in the GP33 gene (Δ33) and a rescued GPCMV (r33). We found the following: 1) GP33 activated the CRE- and NFAT-, but not the NFκB-mediated signaling pathway. 2) GP33 was dispensable for infection in tissue cultures and in normal animals. 3) In pregnant animals, viral loads of r33 in the livers, lungs, spleens, and placentas at 6 days post-infection were higher than those of Δ33, although the viruses were cleared by 3 weeks post-infection. 4) The presence of GP33 was associated with frequent lesions, including alveolar hemorrhage in the lungs, and inflammation in the lungs, livers, and spleens of the dams. Our findings suggest that GP33 has critical roles in the pathogenesis of GPCMV during pregnancy. We hypothesize that GP33-mediated signaling activates cytokine secretion from the infected cells, which results in inflammation in some of the maternal organs and the placentas. Alternatively, GP33 may facilitate transient inflammation that is induced by the chemokine network specific to the pregnancy