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Kodama, S.

Publications and source records attributed to Kodama, S..

2 recordsLinked to original sources

Inferring the Demographic History of Japanese Eel (Anguilla japonica) from Genomic Data: Insights for Conservation and Fisheries Management

O_LIAssessing the status or population size of species is a key task for wildlife conservation and the sustainable management of harvested species. In particular, assessing historical changes in population size provides an evolutionary perspective on current population dynamics and can help distinguish between anthropogenic and natural causes for population decline. C_LIO_LIJapanese eel (Anguilla japonica) is an endangered yet commercially important catadromous fish species. Here we assess the demographic history of Japanese eel using the pairwise and multiple sequentially Markovian coalescent methods. C_LIO_LIThe analyses indicate a reduction in effective population size (Ne) from 38 000 to 10 000 individuals between 4 and 1 Ma, followed by an increase to 80 000 individuals, between 1 Ma and 22-30 kya. Approximately 22-30 kya there is evidence for a reduction in Ne to approximately 60 000 individuals. These events are likely due to changes in environmental conditions, such as sea level and oceanic currents, especially around the last glacial maximum (19-33 kya). C_LIO_LIThe results of this study suggest that Japanese eel has experienced at least two population bottlenecks, interspersed by a period of population growth. This pattern of demographic history may make Japanese eel sensitive to current and future population declines. Conservation management of Japanese eel should focus on practical ways to prevent further population decline and the loss of genetic diversity that is essential for the species to adapt to changing environmental conditions such as climate change. C_LI

evolutionary biology↗

CCN2 activates ERK-signaling via integrin αv and enhances the interaction of ERK and DUSP6 in lymphatic endothelial cells

Cellular communication network factor 2 (CCN2, also known as CTGF), is a modular and matricellular protein and a well-known angiogenic factor in physiological and pathological angiogenesis. However, its roles in lymphangiogenesis and intracellular signaling in lymphatic endothelial cells (LECs) remain unclear. Here, we investigated CCN2 signaling in LECs and its effects on lymphangiogenesis. In primary cultured LECs, gene expressions of lymphatic endothelial markers lymphatic vessel endothelial hyaluronan receptor 1 (Lyve1), Podoplanin and prospero homeobox 1 (Prox1) and lymphangiogenic factors vascular endothelial cell growth factor c (Vegfc), vascular endothelial cell growth factor d (Vegfd) and fms-related tyrosine kinase 4 (Flt4, also known as Vegfr3) were upregulated by CCN2. Subsequently, we found that CCN2 induced phospho-ERK and that was decreased by suppression of integrin v. CCN2 slightly decreased the growth of LECs due to enhancement of the interaction of ERK and dual specific protein phosphatase 6 (DUSP6), and knockdown of DUSP6 increased CCN2-induced phospho-ERK levels. In in vivo Matrigel plug assays, the number of Podoplanin-positive vessels was increased by exogenous CCN2, and phospho-ERK-positive LEC and DUSP6-positive LEC were detected in CCN2 plugs. These results suggest that CCN2-related lymphangiogenesis is regulated by DUSP6, which enables negative modulation of ERK-signaling.

cell biology↗