Description: The repeated transgression and regression of coastlines mediated by the late Quaternary glacial–interglacial cycles make the northwest Pacific a hot spot to study marine speciation and population diversity. The red alga Agarophyton vermiculophyllum is an ecologically important species native to the northwest Pacific, capturing considerable research interest due to its wide-range invasiveness in Europe and North America. However, the knowledge of phylogeographic structure and intraspecific genetic diversity across the entire native range was still scarce. Here, we used 1,214-bp of mitochondrial cytochrome c oxidase subunit 1 (cox1) to explore phylogeographic patterns, lineage structure, and population genetic differentiation of 48 A. vermiculophyllum populations in the northwest Pacific. Our DNA data revealed overall high haplotype diversity and low nucleotide diversity and five phylogeographically structured genetic lineages that diverged significantly from each other. S-DIVA analysis showed the ancestors of A. vermiculophyllum originating from multiple areas encompassing the Japan–Pacific coast, East and South China Seas. This combined evidence indicates that A. vermiculophyllum might have survived in multiple scattered glacial refugia during the late Quaternary climate oscillations in the northwest Pacific. Such knowledge may help to better understand how palaeoclimate interacted with contemporary environments to contribute to intraspecific genetic variation and provide a new perspective for conserving natural resource of A. vermiculophyllum in the northwest Pacific.

Description: Ocean warming is one of the most important factors in shaping the spatial distribution and genetic biodiversity of marine organisms worldwide. The northwest Pacific has been broadly illustrated as an essential seaweed diversity hotspot. However, few studies have yet investigated in this region on whether and how past and ongoing climate warming impacted the distribution and genetic pools of coastal seaweeds. Here, we chose the invasive species Gracilaria vermiculophylla as a model, and identified multiple genetic lineages in the native range through genome-scale microsatellite genotyping. Subsequently, by reconstructing decadal trends of sea surface temperature (SST) change between 1978 and 2018, we found that SST in northern Japan and the East China Sea indeed increased broadly by 0.25-0.4°C/decade. The projections of species distribution models (SDMs) under different future climate change scenarios (RCP 2.6, RCP 4.5, RCP 6.0 and RCP 8.5) indicated that a unique genetic pool of G. vermiculophylla at its current southern range limit (i.e. the South China Sea) is at high risk of disappearance, and that the populations at its current northern range limit (i.e. in Hokkaido region) will undergo poleward expansions, particularly by the year 2100. Such responses, along with this species’ limited dispersal potential, may considerably alter the contemporary distribution and genetic composition of G. vermiculophylla in the northwest Pacific, and ultimately threaten ecological services provided by this habitat-forming species and other associated functional roles.

Description: Momentum transfer across the wind-driven breaking air-water interface under strong wind conditions was experimentally investigated using a high-speed wind-wave tank together with field measurements at normal wind speeds. An eddy correlation method was utilized to measure roughness length and drag coefficient from wind velocity components measured by laser Doppler and phase Doppler anemometers. As a result, a new model for the roughness length and drag coefficient was proposed for predicting momentum transfer across the sea surface under both normal and strong wind conditions using the universal relationship between energy and significant frequency of wind waves normalized by the roughness length. The model shows that the roughness length and drag coefficient are uniquely determined at all wind speeds by energy and significant frequency of wind waves, and they can be given against U10 only from the measurements of the wave parameters and one-point mean air velocity in the logarithmic law region.

Description: Background: The laboratory mouse model is commonly employed to study the pathogenesis of encephalitic flaviviruses such as Japanese encephalitis virus (JEV). However, it is known that some strains of these viruses do not elicit a typical mortality dose response curve from this organism after peripheral infection and the reason for it has not yet been fully understood. It is suggested that induction of more vigorous Type-I IFN (IFN-I) response might control early virus dissemination following increasing infectious challenge doses of the virus. Thus, the objective of this study was to examine this suggested role of IFN-I in the mortality of mice infected with various doses of JEV. Methods: Inbred 129 mice and their IFNAR KO (A129) mice were subcutaneously inoculated with 100, 102, 104 or 106 pfu of JaOArS982 strain of JEV. Mice were weighed daily and observed for clinical signs. Virus titers in the brains and spleens of JEV-infected mice were determined by plaque forming assays. The upregulated mRNA levels of genes related to IFN-I response of mice were examined by real-time PCR. Results: The mortality rates of 129 mice infected with JaOArS982 did not significantly increase despite the increase in inoculation dose and no significant difference of viral loads was observed between their brains. However, there was clear elevation of the mRNA levels of interferon regulatory factor (IRF)3, IRF7, IRF9, MDA5 and RIG-I at 24 hours post-infection depending on the inoculation dose. In A129 mice, length of survival days and the viral loads of spleen and brain were observed to be inoculation dose-dependent. Conclusions: From these results, it is suggested that early IFN-I response elicited by high inoculation doses of JEV provides an anti-viral effect during the early phase of infection. Accordingly, virus replication is counteracted by IFN-I response at each increasing inoculation dose resulting in the interference of impending severe disease course or fatal outcome; hence, this might explain the inoculation dose-independent mortality in mice caused by Japanese encephalitis virus.