Variation in seed production schedule among individual trees of a deciduous oak species <Emphasis Type="Italic">Quercus serrata</Emphasis>: its relation to seed characteristics

Intraspecific variation in seed production schedule and its effects on seed characteristics were examined in the deciduous oak species Quercus serrata in Iwate Prefecture, northern Japan. Seed production schedule differed markedly among 31 individual trees. The median dates of seed production differed by over 1 month between the earliest and latest individuals. Relationships between seed production schedule and seed characteristics were investigated at two different scales: the among-tree scale and the within-tree scale. At the within-tree scale, analyses revealed that the seeds dispersed by a tree later in the season tended to be larger in size and lower in tannin concentration. Similarly, at the among-tree scale, analysis revealed that trees with a later seed production schedule produced on average larger acorns. However, no clear tendency was observed between seed production schedule and mean tannin concentration. The observed variation in seed production schedule is likely to affect seed fate per se, and also via changes in seed characteristics.     

Genome-wide CRISPR Screens in T Helper Cells Reveal Pervasive Crosstalk between Activation and Differentiation

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Al(3+) interaction sites of calmodulin and the Al(3+) effect on target binding of calmodulin

The interaction between calmodulin (CaM) and Al(3+) was studied by spectroscopic methods. Heteronuclear two-dimensional NMR data indicated that peaks related to the both lobes and middle of the central helix of CaM are largely affected by Al(3+). But chemical shift perturbation suggested that overall conformation of Ca(2+)-loaded CaM is not changed by Al(3+) binding. It is thought that Al(3+) interaction to the middle of the central helix is a key for the property of CaM's target recognition. If the structure and/or flexibility of the central helix are/is changed by Al(3+), target affinity to CaM must be influenced by Al(3+). Thus, we performed surface plasmon resonance experiments to observe the effect of Al(3+) on the target recognition by CaM. The data clearly indicated that target affinity to CaM is reduced by addition of Al(3+). All the results presented here support a hypothesis that Al(3+) may affect on the Ca(2+) signaling pathway in cells.     

Microsomal glutathione S-transferase 1 in the retinal pigment epithelium: protection against oxidative stress and a potential role in aging

High oxygen tension, exposure to light, and the biochemical events of vision generate significant oxidative stress in the retina and the retinal pigment epithelium (RPE). Understanding the mechanisms and basis of susceptibility to progressive retinal diseases involving oxidative damage such as age-related macular degeneration (AMD) remains a major challenge. Here microsomal glutathione S-transferase (MGST1) is shown to be a dominant, highly expressed enzyme in bovine and mouse RPE microsomes that displays significant reduction activity toward synthetic peroxides, oxidized RPE lipids, and oxidized retinoids. This enzymatic reduction activity (GPx) can be partially neutralized with a monoclonal anti-MGST1 antibody developed in this study. MGST1-transfected HEK293 cells exhibited greater viability (70 +/- 4% survival) compared with untransfected control cells (46 +/- 4% survival) when challenged with 20 microM H(2)O(2), and greater viability of MGST1-transfected cells following challenge with oxidized docosahexaenoic acid was also observed. Cultured ARPE19 cells transfected with silencing MGST1 siRNAs exhibited lower expression of MGST1 (12% and 26% of the controls) and significantly lower GPx activity (44 +/- 13%) and, thus, were more susceptible to oxidative damage. Immunoblotting revealed that the in vivo expression of MGST1 in mouse RPE decreases 3-4-fold with age, to trace levels in 18-month-old mice. GPx activity in the RPE was also found to be reduced in 12-month-old mice to approximately 67%. These results support an important protective function for MGST1 against oxidative insult in the RPE that decreases with age and suggest that this enzyme may play a role in the development of age-related diseases such as AMD.     

A game theoretical model of deforestation in human-environment relationships

We studied a two-person game regarding deforestation in human-environment relationships. Each landowner manages a single land parcel where the state of land-use is forested, agricultural, or abandoned. The landowner has two strategies available: forest conservation and deforestation. The choice of deforestation provides a high return to the landowner, but it degrades the forest ecosystem services produced on a neighboring land parcel managed by a different landowner. Given spatial interactions between the two landowners, each landowner decides which strategy to choose by comparing the expected discounted utility of each strategy. Expected discounted utility is determined by taking into account the current and future utilities to be received, according to the state transition on the two land parcels. The state transition is described by a Markov chain that incorporates a landowner's choice about whether to deforest and the dynamics of agricultural abandonment and forest regeneration. By considering a stationary distribution of the Markov chain for land-use transitions, we derive explicit conditions for Nash equilibrium. We found that a slow regeneration of forests favors mutual cooperation (forest conservation). As the forest regenerates faster, mutual cooperation transforms to double Nash equilibria (mutual cooperation and mutual defection), and finally mutual defection (deforestation) leads to a unique Nash equilibrium. Two different types of social dilemma emerge in our deforestation game. The stag-hunt dilemma is most likely to occur under an unsustainable resource supply, where forest regenerates extremely slowly but agricultural abandonment happens quite rapidly. In contrast, the prisoner's dilemma is likely under a persistent or circulating supply of resources, where forest regenerates rapidly and agricultural abandonment occurs slowly or rapidly. These results show how humans and the environment mutually shape the dilemma structure in forest management, implying that solutions to dilemmas depend on environmental properties.     

Protective Role of Fas-FasL Signaling in Lethal Infection with Herpes Simplex Virus Type 2 in Mice

Herpes simplex virus type 2 (HSV-2) induces acute local infection followed by latent infection in the nervous system and often leads to the development of lethal encephalitis in immunocompromised hosts. The mechanisms of immune protection against lethal HSV-2 infection, however, have not been clarified. In this study, we examined the roles of Fas-Fas ligand (FasL) signaling in lethal infection with HSV-2 by using mice with mutated Fas (lpr) or FasL (gld) in C57BL/6 background. Both lpr and gld mice exhibited higher mortality than wild-type (WT) C57BL/6 mice after infection with virulent HSV-2 strain 186 and showed significantly increased viral titers in the spinal cord compared with WT mice 9 days after infection, just before the mice started to die. There were no differences in the numbers of CD4⁺ and CD8⁺ T cells infiltrated in the spinal cord or in the levels of HSV-2-specific gamma interferon produced by those cells in a comparison of lpr and WT mice 9 days after infection. Adoptive transfer studies demonstrated that CD4⁺ T cells from WT mice protected gld mice from lethal infection by HSV-2. Furthermore, CD4⁺ T cells infiltrated in the spinal cord of HSV-2-infected WT mice expressed functional FasL that induced apoptosis of Fas-expressing target cells in vitro. These results suggest that FasL-mediated cytotoxic activity of CD4⁺ T cells plays an important role in host defense against lethal infection with HSV-2.Fas-Fas ligand (FasL) signaling-induced apoptotic cell death has pleiotropic roles in T-cell-mediated host defense mechanisms. First, Fas and FasL are expressed on activated T cells and thereby limit their number by inducing suicide or fratricide. It is generally accepted that Fas-mediated activation-induced cell death plays a predominant role during chronic infection, whereas starvation-induced cell death mediated by the proapoptotic BH3-only subgroup of the Bcl-2 protein family is the main mechanism for T-cell death during termination of immune responses in acute infection (30). Fas-FasL signaling might also play a role in T-cell development, as suggested by an accumulation of T-cell receptor αβ-positive (TCR αβ⁺) CD4⁻ CD8⁻ T cells expressing B220 in lymphoid organs of mice with mutated Fas (lpr) or FasL (gld) although the origin and functions of such double-negative T cells are still a matter of debate (21). Lastly, Fas-FasL interaction can be directly involved in host defense by inducing apoptosis of infected cells to facilitate pathogen clearance (23). Therefore, the roles of Fas-FasL signaling in immune responses for host defense might vary depending on the pathogen.Herpes simplex virus type 2 (HSV-2) is an alphaherpesvirus that causes genital herpes, the most common viral sexually transmitted disease (29). After initial infection in the vaginal epithelium, HSV-2 invades local nerve termini, travels via retrograde axonal transport to neuronal cell bodies in sensory ganglia, and establishes latent infection (13). However, especially in neonates and immunocompromised hosts, HSV-2 can cause lethal central nervous system (CNS) infection, which indicates the importance of immune systems in limiting the pathogenicity of HSV-2. Immune responses against HSV-2 have been studied in various murine models using different strains of virus and routes of inoculation, with or without vaccination with an attenuated strain of HSV-2. In such vaccination models, CD4⁺ T cells producing gamma interferon (IFN-γ) predominantly conferred protection against challenge with a virulent strain of HSV-2 (11, 19), whereas various subsets of lymphocytes, including NK cells, NK T cells, and TCR γδ T cells as well as CD4⁺ T cells were reported to be involved in host defense against primary infection with virulent HSV-2 (3, 15, 24), in which IFN-γ also played an important role (9). Fas-FasL signaling was shown to be dispensable for the clearance of an attenuated strain of HSV-2, which lacks thymidine kinase and causes only transient mild vaginal pathologies but not neurologic diseases (6, 16). Similarly Fas-mediated apoptosis was not involved in the vaccination effect of the attenuated HSV-2 (11). However, the roles of Fas-FasL signaling in host defense against a virulent strain of HSV-2 have not been clarified.In this study, we examined the roles of Fas-FasL signaling in a murine model of HSV-2 infection by using a highly virulent HSV-2 strain 186 with lpr and gld mice. We found that FasL-Fas signaling plays an important role in host defense against lethal HSV-2 infection.     

Variations in the C3, C3a receptor, and C5 genes affect susceptibility to bronchial asthma

Bronchial asthma (BA) is a common chronic inflammatory disease characterized by hyperresponsive airways, excess mucus production, eosinophil activation, and the production of IgE. The complement system plays an immunoregulatory role at the interface of innate and acquired immunities. Recent studies have provided evidence that C3, C3a receptor, and C5 are linked to airway hyperresponsiveness. To determine whether genetic variations in the genes of the complement system affect susceptibility to BA, we screened single nucleotide polymorphisms (SNPs) in C3, C5, the C3a receptor gene (C3AR1), and the C5a receptor gene (C5R1) and performed association studies in the Japanese population. The results of this SNP case-control study suggested an association between 4896C/T in the C3 gene and atopic childhood BA (P=0.0078) as well as adult BA (P=0.010). When patient data were stratified according to elevated total IgE levels, 4896C/T was more closely associated with adult BA (P=0.0016). A patient-only association study suggested that severity of childhood BA was associated with 1526G/A of the C3AR1 gene (P=0.0057). We identified a high-risk haplotype of the C3 gene for childhood (P=0.0021) and adult BA (P=0.0058) and a low-risk haplotype for adult BA (P=0.00011). We also identified a haplotype of the C5 gene that was protective against childhood BA (P=1.4×10^–6) and adult BA (P=0.00063). These results suggest that the C3 and C5 pathways of the complement system play important roles in the pathogenesis of BA and that polymorphisms of these genes affect susceptibility to BA.     

Protective effects of quercetin and its metabolites on H2O2-induced chromosomal damage to WIL2-NS cells

We investigated chromosomal damage caused by a typical flavonoid, quercetin, and its two conjugates, quercetin-3-O-sulfate and isorhamnetin, and their protective effects against chromosomal damage induced by H2O2. The chromosomal damage was detected by the cytokinesis-block micronucleus (CBMN) assay using a lymphoblastoid cell line, WIL2-NS. We found that quercetin itself induced chromosomal damage at 10 microM, but quercetin-3-O-sulfate and isorhamnetin did not induce damage up to 30 microM. In the medium used for the CBMN assay, quercetin (at 100 microM) generated a high concentration of H2O2, but the two conjugates did not at the same concentration. On the other hand, pretreatment with quercetin (at 1 microM), quercetin-3-O-sulfate (at 10 microM), and isorhamnetin (at 5 microM) prevented H2O2-induced chromosomal damage to WIL2-NS cells. These findings suggest that the induction and prevention of H2O2-induced chromosomal damage are different between quercetin and its metabolites.