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The meiotic cycle reduces ploidy through two consecutive M phases, meiosis I and meiosis II, without an intervening S phase. To maintain ploidy through successive generations, meiosis must be followed by mitosis after the recovery of diploidy by fertilization. However, the coordination from meiotic to mitotic cycle is still unclear. Mos, the c-mos protooncogene product, is a key regulator of meiosis in vertebrates. In contrast to the previous observation that Mos functions only in vertebrate oocytes that arrest at meiotic metaphase II, here we isolate the first invertebrate mos from starfish and show that Mos functions also in starfish oocytes that arrest after the completion of meiosis II but not at metaphase II. In the absence of Mos, meiosis I is followed directly by repeated embryonic mitotic cycles, and its reinstatement restores meiosis II and subsequent cell cycle arrest. These observations imply that after meiosis I, oocytes have a competence to progress through the embryonic mitotic cycle, but that Mos diverts the cell cycle to execute meiosis II and remains to restrain the return to the mitotic cycle. We propose that a role of Mos that is conserved in invertebrate and vertebrate oocytes is not to support metaphase II arrest but to prevent the meiotic͞mitotic conversion after meiosis I until fertilization, directing meiosis II to ensure the reduction of ploidy.

SummaryIn mice arthritis model induced by anti-type II collagen (CII) antibodies and lipopolysaccharide (LPS), most of cells that infiltrated into the joint space were neutrophils. To investigate the role of neutrophils in the pathogenesis of arthritis, we depleted the neutrophils in vivo by injection of the antibody against Gr-1 expressed mainly on neutrophils. The neutrophil depletion completely inhibited the arthritis development. Furthermore, neutrophil depletion in mice that had already developed arthritis ameliorated the disease. These results showed that neutrophils are indispensable not only for the development, but also for the maintenance of arthritis. Next, we tried to develop arthritis in C5-deficient mice to investigate the involvement of C5a, one of chemotactic factors for neutrophils. C5-deficient mice showed significant reduction in arthritis development in comparison with wild type mice. Injection of pertussis toxin (Ptx) into the mice, which inhibits the signals from the inhibitory G-protein coupled-receptors including the C5a receptor, suppressed the development of arthritis. Furthermore, Ptx also ameliorated the arthritis when injected into mice that had already developed the disease. These results suggest the important role of chemotactic factors involving C5a and inhibitory G-protein (Gi)-coupled receptors not only in the development, but also in the maintenance of arthritis.

Anti-type II collagen (anti-CII) Ab is a well-known autoantibody observed in patients with rheumatoid arthritis. Injection of anti-CII Ab and LPS induces arthritis in mice in which anti-CII Ab as well as inflammatory cytokines, IL-1β and TNF-α, play critical roles. We investigated the involvement of IgG FcRs (FcγRs) in this arthritis model. BALB/c mice injected with the F(ab′)2 of anti-CII Ab showed no signs of arthritis. Arthritis development was not observed in FcRγ−/− mice and was partially suppressed in FcγRIII−/− mice despite the binding of anti-CII Ab and C3 to cartilage surface. Surprisingly, BALB/c mice lacking FcγRIIB, which is known as an inhibitory FcγR, developed arthritis with no exacerbation in arthritis score compared with wild-type (WT) mice, and only slight exacerbation was observed in the histopathological analysis. In contrast, aged FcγRIIB−/− BALB/c mice developed arthritis without LPS injection, suggesting an augmented susceptibility to arthritis in aged FcγRIIB−/− mice. No significant difference was observed among BALB/c-WT, -FcRγ−/−, and -FcγRIIB−/− mice on cytokine production induced by anti-CII Ab and LPS injection. Severe arthritis developed in BALB/c-WT and -FcγRIIB−/− mice, but not in BALB/c-FcRγ−/− mice, after the injection of anti-CII Ab and inflammatory cytokines. These results suggest that the reason behind the nondevelopment of arthritis in FcRγ−/− BALB/c mice is not due to a disorder in transient cytokine production, but to an irregularity downstream of cytokine production.

The thermal conductivity of polycrystalline samples of (Na,Ca)Co2O4 is found to be unusually low, 20 mW/cmK at 280 K. On the assumption of the Wiedemann-Franz law, the lattice thermal conductivity is estimated to be 18 mW/cmK at 280 K, and it does not change appreciably with the substitution of Ca for Na. A quantitative analysis has revealed that the phonon mean free path is comparable with the lattice parameters, where the point-defect scattering plays an important role. Electronically the same samples show a metallic conduction down to 4.2 K, which strongly suggests that NaCo2O4 exhibits a glass-like poor thermal conduction together with a metal-like good electrical conduction. The present study further suggests that a strongly correlated system with layered structure can act as a material of a phonon glass and an electron crystal.