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Takenaka, N.

Publications and source records attributed to Takenaka, N..

3 recordsLinked to original sources

Adaptation to nighttime light via gene expression regulation in Drosophila suzukii

Urbanization causes environmental changes like habitat loss, fragmentation, and pollution, which reduce biodiversity. Urban organisms face stressors, such as heat islands, air and water pollution, and anthropogenic noise, all of which can disrupt their development, behavior, and physiology. While some species adapt to urban environments, their responses and the role of evolution in urbanization are limited, as most studies focus on phenotypic traits. Artificial light at night (ALAN), a common urban stressor, disrupts behaviors and physiological processes, including circadian rhythms, sleep, and reproduction. The present study examined ALANs effects on body size, survival, activity rhythms, and gene expression in Drosophila suzukii, a species found in urban and rural habitats. ALAN reduced wing and thorax sizes regardless of sex and origin, decreased survival in rural populations, and increased it in urban populations. ALAN elevated overall activity, especially in the early night, while urban females displayed reduced sensitivity regarding activity and sleep. The circadian rhythm length was disrupted in rural populations but not in urban populations. Transcriptomic analysis revealed ALAN-induced gene expression changes, particularly in urban females, with photoreceptor- and circadian rhythm-related genes responding differently between urban and rural populations. These results indicate that urban populations have evolved adaptive mechanisms to counter ALANs effects, likely mediated through gene regulation. This study highlights ALANs impact on diverse traits and its potential for adaptive evolution in urban environments. Evolutionary adaptations in traits related to urban stress responses may enhance the ecological success of D. suzukii in urban habitats.

evolutionary biology↗

Environmental Impacts of Serum-free Food-grade and Complex Culture Medium Production for Cultivated Meat

Culture medium accounts for most of the environmental impact of cultivated meat production. This study quantitatively evaluated and analyzed the environmental impact of producing a culture medium consisting of serum-free, food and complex ingredients for cultivated meat by performing a life cycle assessment (LCA) based on activity data at the laboratory scale. In addition, specific measures were proposed to reduce the environmental impact further. LCAs were performed at current and future production scales. This study also evaluated the impact of multiple electricity sources on the environmental impact of culture medium production. Energy, animal-derived materials, and expendables at the current scale, and energy, animal-derived materials, amino acids, and glucose at future scale are hotspots in the environmental impact of this culture medium production. The production of serum substitutes accounts for most of the environmental impact. As the scale shifts, the environmental impacts are expected to decrease by more than 70% in all impact categories. As the composition of electricity sources changed, the impact on certain categories decreased. However, as the share of renewable energy increased, the impact on land use also increased significantly. This study promotes the practical application of new culture-media for low-cost and low-environment-impact cultivated meat. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=108 SRC="FIGDIR/small/611339v2_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@ac6daorg.highwire.dtl.DTLVardef@1852ef4org.highwire.dtl.DTLVardef@cdbbe8org.highwire.dtl.DTLVardef@eb8703_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstract.C_FLOATNO SYNOPSIS. This study evaluated the environmental impact of culture-medium production for cultivated meat and reports that energy, animal-derived materials, expendables, amino acids and glucose are hotspots of this impact. C_FIG

ecology↗

Physiological reprogramming in vivo mediated by Sox4 pioneer factor activity

Tissue damage elicits cell fate switching through a process called metaplasia, but how the starting cell fate is silenced and the new cell fate is activated has not been investigated in animals. In cell culture, pioneer transcription factors mediate "reprogramming" by opening new chromatin sites for expression that can attract transcription factors from the starting cells enhancers. Here we report that Sox4 is sufficient to initiate hepatobiliary metaplasia in the adult liver. In lineage-traced cells, we assessed the timing of Sox4-mediated opening of enhancer chromatin versus enhancer decommissioning. Initially, Sox4 directly binds to and closes hepatocyte regulatory sequences via a motif it overlaps with Hnf4a, a hepatocyte master regulator. Subsequently, Sox4 exerts pioneer factor activity to open biliary regulatory sequences. The results delineate a hierarchy by which gene networks become reprogrammed under physiological conditions, providing deeper insight into the basis for cell fate transitions in animals.

cell biology↗