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Fujino, M.

Publications and source records attributed to Fujino, M..

2 recordsLinked to original sources

Predator-driven local convergence fosters global microbial community divergence

Understanding the rules that govern microbial community assembly is essential for predicting ecosystem function. While microbial predators are key biotic agents that shape bacterial communities through predation, yet their ecological consequences have been studied mostly in isolated and in vitro systems1-3. In contrast, large-scale studies of microbial diversity have primarily emphasized abiotic factors as drivers of community assembly 4-7, while the role of microbial predators modulating global microbial divergence and convergence patterns remains largely neglected. Here, we show that bacterivorous protists (predators) exert dual, scale-dependent effects on microbial communities: promoting local convergence by suppressing dominant bacterial taxa, while generating global divergence through species-specific predation effects. By integrating global meta-analyses, controlled field experiments, and reconstructions of natural and synthetic communities, we find that predator identity and prey susceptibility jointly determine convergence outcomes. Communities dominated by predator-resistant taxa exhibit reduced convergence under predation pressure, revealing a predictable trait-based filtering mechanism. This framework reconciles previous contradictory findings3,8-11 and highlights predators as selective, context-dependent agents of microbial biogeography. Predator-driven convergence suggests new opportunities for microbiome engineering 12: targeted use of predators may steer microbial communities toward functional configurations that enhance soil health, disease suppression, carbon cycling, and ecosystem resilience 2,13,14.

ecology↗

Amyloid-β fibrils accumulated in preeclamptic placentas suppress syncytialization of cytotrophoblasts

Cerebral deposition of fibrillar amyloid-{beta} (A{beta}) is a pathological hallmark of Alzheimers disease. While A{beta} is present in human placentas and accumulates in preeclamptic placentas characterized by poor placentation, the production and role of A{beta} in the human placenta remain unclear. Because hypoxia in mid-to-late pregnancy is a risk for preeclampsia, we found that levels of hypoxia-inducible factor 1- and {beta}-secretase (BACE-1) increased concurrently with placental A{beta} deposition in late stage preeclamptic placentas. We also found that a human cytotrophoblast (CTB) model, BeWo cells, actually produced A{beta} species, and that hypoxia increased A{beta} production and BACE-1 protein levels. A{beta}42 fibrils inhibited CTB syncytialization, a critical step in maintaining pregnancy, by inducing loss of membrane localization of cell-cell adhesion molecules. Primary human CTBs confirmed these observations. Taken together, our results suggest that increased A{beta} production in CTBs by hypoxia may lead to the formation of A{beta} fibrils, which inhibit syncytiotrophoblast formation and are detrimental to pregnancy. Thus, our results reveal the novel role of A{beta} fibrils in the pathogenesis of preeclampsia.

biochemistry↗