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Bioindication, evaluating biological responses to environmental disturbances, is crucial for assessing the ecological status of an ecosystem. While historical bioindication relied on macroscopic organisms, the introduction of environmental DNA (eDNA) techniques allows the application of protists without the necessity of morphological identification. In this study, we propose a novel bioindication methodology utilizing Arcellinida, a group of top predators among protists, as bioindicators of freshwater ecosystems. For that purpose, we first characterized the Arcellinida diversity over 1 year at three different points of Lake Sanabria, an ancient glacier lake known to be subjected to anthropogenic disturbances. We compared this diversity with an undisturbed control site. Second, we characterized the Arcellinida diversity in other ecosystems to generate the ecological background to test the connectivity between them. Results indicate limited connectivity between the different ecosystems and an edge effect between terrestrial and aquatic ecosystems. Disturbed freshwater ecosystems exhibited reduced Arcellinida diversity at both specific and infraspecific levels, providing valuable insight into recent disturbances. Arcellinida‐based bioindication provides a sensitive, accurate and easy‐to‐interpret protocol for monitoring disturbances in freshwater ecosystems. It represents a valuable tool for environmental assessments and conservation strategies. [ABSTRACT FROM AUTHOR]

Astydamia latifolia is the only species of the genus Astydamia, which forms an early‐diverging lineage of Apiaceae, subfamily Apioideae. This species is subendemic to the Canary Islands and one of the most representative species of the coastal environments of this archipelago. Astydamia displays diplochory, that is, diaspores with two long‐distance dispersal (LDD) syndromes. In particular, A. latifolia has both anemochorous and thalassochorous fruit traits (corky and winged mericarps). Although we expect this species to have a high dispersal capacity, there is no genetic study addressing it. The divergence time of this species from its sister taxon is also unknown. In this study, we aimed (i) to unveil the phylogenetic relationships and divergence times of A. latifolia; (ii) to reconstruct its phylogeographic structure across the Canary Islands; and (iii) to estimate the number of inter‐island colonization events. To these ends, we first sequenced the internal transcribed spacer (ITS) region for A. latifolia, reconstructed the phylogenetic relationships of Astydamia and Apiaceae relatives and estimated divergence times. Then, two plastid DNA regions (psaI‐aacD and psbK‐trnS) were sequenced for 158 individuals (from 36 Canarian population and one NW African population) to reconstruct a haplotype network. The recently developed method Phylogeographic Analysis of Island Colonization Events (PAICE) was used to estimate the number of inter‐island colonization events. Results show that A. latifolia is a phylogenetically isolated lineage that diverged from the most closely related genus (Molopospermum) in the Eocene–Miocene. It displays a low plastid DNA diversity (only four haplotypes detected), which is accompanied by a high degree of haplotype sharing between islands and highly linear rarefaction curves of colonization obtained in PAICE. These findings suggest a high colonization ability for this species, most likely related to the availability of two LDD syndromes. [ABSTRACT FROM AUTHOR]

During hemolysis, macrophages in the liver phagocytose damaged erythrocytes to prevent the toxic effects of cell-free hemoglobin and heme. It remains unclear how this homeostatic process modulates phagocyte functions in inflammatory diseases. Using a genetic mouse model of spherocytosis and single-cell RNA sequencing, we found that erythrophagocytosis skewed liver macrophages into an antiinflammatory phenotype that we defined as [Marco.sup.hi][Hmox.sup.hi]MHC class [II.sup.lo] [degrees] erythrophagocytes. This phenotype transformation profoundly mitigated disease expression in a model of an anti-CD40-induced hyperinflammatory syndrome with necrotic hepatitis and in a nonalcoholic steatohepatitis model, representing 2 macrophage-driven sterile inflammatory diseases. We reproduced the antiinflammatory erythrophagocyte transformation in vitro by heme exposure of mouse and human macrophages, yielding a distinctive transcriptional signature that segregated heme-polarized from M1- and M2-polarized cells. Mapping transposase-accessible chromatin in single cells by sequencing defined the transcription factor NFE2L2/NRF2 as a critical driver of erythrophagocytes, and Nfe2l2/Nrf2 deficiency restored heme-suppressed inflammation. Our findings point to a pathway that regulates macrophage functions to link erythrocyte homeostasis with innate immunity., Introduction The archetypical functions of macrophages are their roles as sensors, effectors, and resolvers of inflammation and tissue damage (1). Historically defined as inflammatory M1-like and antiinflammatory M2-like, macrophage phenotypes [...]