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Hematopoietic stem cells (HSCs) produce all essential cellular components of the blood. Stromal cell lines supporting HSCs follow a vascular smooth muscle cell (vSMC) differentiation pathway, suggesting that some hematopoiesis-supporting cells originate from vSMC precursors. These pericyte-like precursors were recently identified in the aorta-gonad-mesonephros (AGM) region; however, their role in the hematopoietic development in vivo remains unknown. Here, we identify a subpopulation of NG2 + Runx1 + perivascular cells that display a sclerotome-derived vSMC transcriptomic profile. We show that deleting Runx1 in NG2 + cells impairs the hematopoietic development in vivo and causes transcriptional changes in pericytes/vSMCs, endothelial cells and hematopoietic cells in the murine AGM. Importantly, this deletion leads also to a significant reduction of HSC reconstitution potential in the bone marrow in vivo. This defect is developmental, as NG2 + Runx1 + cells were not detected in the adult bone marrow, demonstrating the existence of a specialised pericyte population in the HSC-generating niche, unique to the embryo., (© 2024. The Author(s).)

Planktonic heterotrophic prokaryotes (HProks) are a pivotal functional group in marine ecosystems and are highly sensitive to environmental variability and climate change. This study aimed to investigate the short-term effects of increasing carbon dioxide (CO 2 ), ultraviolet radiation (UVR), and temperature on natural assemblages of HProks in the Ria Formosa coastal lagoon during winter. Two multi-stressor microcosm experiments were used to evaluate the isolated and combined effects of these environmental changes on HProk abundance, production, growth, and mortality rates. The isolated and combined effects of increased CO 2 on HProks were not significant. However, HProk production, cellular activity, instantaneous growth rate, and mortality rate were negatively influenced by elevated UVR and positively influenced by warming. Stronger effects were detected on HProk mortality in relation to specific growth rate, leading to higher HProk net growth rates and abundance under elevated UVR and lower values under warming conditions.

Water quality and quantity problems in the Guadiana estuary due to a recently built dam have been predicted, including an enhancement of cyanobacteria blooms. The main goal of this work was thus to describe the present phytoplankton dynamics in relation to its environmental drivers and to evaluate the effects of damming on phytoplankton in the Guadiana estuary. Sampling campaigns were conducted during 2007-2009 in 4 locations of the Guadiana estuary, covering the salinity gradient. Phytoplankton-related and physical-chemical variables were analyzed. Throughout our study, light availability was mainly controlled by suspended sediments and it was much lower than saturating intensities described for phytoplankton growth. Therefore, light was probably limiting to phytoplankton growth throughout the year, especially in the middle and upper estuarine zones. Nitrogen limitation of phytoplankton growth occurred occasionally throughout the study period, especially during spring and summer. Overall, light and nutrient availability were mainly controlled by river flow; anthropogenic sources of nutrients to the estuary were negligible. Phytoplankton showed a unimodal cycle with biomass maximum in late spring/early summer, and the typical seasonal succession of freshwater phytoplankton (diatoms, green algae, cyanobacteria) was observed. Diatoms were the main component of the phytoplankton community and their variability closely followed nitrate and river flow variability. The relative abundance of the main phytoplankton groups changed in relation to the period before dam construction, with a decrease on cyanobacteria contribution to total abundance. The environmental perturbation induced by dam construction has now stabilized and resulted in an overall decrease in nutrient concentrations, an increase in light availability and a decrease in cyanobacteria abundance., (Copyright © 2011 Elsevier B.V. All rights reserved.)