Burt, M. A. | bioRxiv Science

bioRxiv2026

Experimental landscape connectivity decreases temporal variability in communities over 24 years of assembly

Landscape connectivity is a key regulator of dispersal, which is an important process in community assembly. Theory predicts that connectivity may influence spatial and temporal patterns of community assembly; however, empirically evaluating the role of connectivity is nearly impossible due to the need to isolate its influence over long time frames and large spatial extents. We overcome these challenges through a large-scale, long-term connectivity experiment to test how connectivity affects plant community turnover and directionality of change over 24 years of assembly. Plant communities within connected patches had lower temporal variability in composition compared to plant communities within unconnected patches. Differences in composition between patches and the directionality of compositional changes were driven more by the amount of edge habitat in a patch and the time since the start of assembly. All community responses to connectivity were stronger for species with wind or unassisted dispersal compared to those with seeds dispersed by animals. Connectivitys role in regulating local community dynamics is critical for understanding community assembly and increasingly relevant in an era of anthropogenic land-use change. Significance StatementConnectivity between habitat patches facilitates dispersal to localities, yet the impact of connectivity on local species assemblages is exceptionally challenging to isolate from other spatial changes over time. In a 24-year experiment, we found that connectivity stabilized local community composition as a higher number of species persisted across years within patches connected by corridors. Independent of connectivity, edge effects were more important for driving compositional differences between patches. Importantly, these patterns would not have been captured with short-term data or without controlling for confounding spatial changes. Our findings have broad conservation relevance. Anthropogenic landscape changes that result in a loss of connectivity or increased edge effects may disrupt local community assembly over time.

ecology↗

bioRxiv2021

BSG/CD147 and ACE2 receptors facilitate SARS-CoV-2 infection of human iPS cell-derived kidney podocytes

BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the Coronavirus disease 2019 (COVID-19), which was declared a pandemic by the World Health Organization (WHO) in March 2020. The disease has caused more than 5.1 million deaths worldwide. While cells in the respiratory system are frequently the initial target for SARS-CoV-2, clinical studies suggest that COVID-19 can become a multi-organ disease in the most severe cases. Still, the direct affinity of SARS-CoV-2 for cells in other organs such as the kidneys, which are often affected in severe COVID-19, remains poorly understood. MethodIn this study, we employed a human induced pluripotent stem (iPS) cell-derived model to investigate the affinity of SARS-CoV-2 for kidney glomerular podocytes. We studied uptake of the live SARS-CoV-2 virus as well as pseudotyped viral particles by human iPS cell derived podocytes using qPCR, western blot, and immunofluorescence. Global gene expression and qPCR analyses revealed that human iPS cell-derived podocytes express many host factor genes (including ACE2, BSG/CD147, PLS3, ACTR3, DOCK7, TMPRSS2, CTSL CD209, and CD33) associated with SARS-CoV-2 binding and viral processing. ResultInfection of podocytes with live SARS-CoV-2 or spike-pseudotyped lentiviral particles revealed viral uptake by the cells at low Multiplicity of Infection (MOI of 0.01) as confirmed by RNA quantification and immunofluorescence studies. Our results also indicate that direct infection of human iPS cell-derived podocytes by SARS-CoV-2 virus can cause cell death and podocyte foot process retraction, a hallmark of podocytopathies and progressive glomerular diseases including collapsing glomerulopathy observed in patients with severe COVID-19 disease. Additionally, antibody blocking experiments identified BSG/CD147 and ACE2 receptors as key mediators of spike binding activity in human iPS cell-derived podocytes. ConclusionThese results show that SARS-CoV-2 can infect kidney glomerular podocytes in vitro. These results also show that the uptake of SARS-CoV-2 by kidney podocytes occurs via multiple binding interactions and partners, which may underlie the high affinity of SARS-CoV-2 for kidney tissues. This stem cell-derived model is potentially useful for kidney-specific antiviral drug screening and mechanistic studies of COVID-19 organotropism. Significant statementMany patients with COVID19 disease exhibit multiorgan complications, suggesting that SARS-CoV-2 infection can extend beyond the respiratory system. Acute kidney injury is a common COVID-19 complication contributing to increased morbidity and mortality. Still, SARS-Cov-2 affinity for specialized kidney cells remain less clear. By leveraging our protocol for stem cell differentiation, we show that SARS-CoV-2 can directly infect kidney glomerular podocytes by using multiple Spike-binding proteins including ACE2 and BSG/CD147. Our results also indicate that infection by SARS-CoV-2 virus can cause podocyte cell death and foot process effacement, a hallmark of podocytopathies including collapsing glomerulopathy observed in patients with severe COVID-19 disease. This stem cell-derived model is potentially useful for kidney-specific antiviral drug screening and mechanistic studies of COVID-19 organotropism.

bioengineering↗