Bates, A. E. | Search bioRxiv

bioRxiv2019

Temperature-related biodiversity change across temperate marine and terrestrial systems

Climate change is reshaping global biodiversity as species respond to changing temperatures. However, the net effects of climate-driven species redistribution on local assemblage diversity remain unknown. Here, we relate trends in species richness and abundance from 21,500 terrestrial and marine assemblage time series across temperate regions (23.5-60.0{degrees}) to changes in air or sea surface temperature. We find a strong coupling between biodiversity and temperature changes in the marine realm, which is conditional on the baseline climate. We detect increases in species richness with increasing temperature that is twice as pronounced in warmer locations, while abundance declines with warming in the warmest marine locations. In contrast, we did not detect systematic temperature-related richness or abundance trends on land, despite a greater magnitude of warming. We also found no evidence for an interaction between biodiversity change and latitude, further emphasizing the importance of baseline climate in structuring assemblages. As the world is committed to further warming, significant challenges remain in maintaining local biodiversity amongst the non-uniform inflow and outflow of "climate migrants" across distinct regions, especially in the ocean.

ecology↗

bioRxiv2019

HIV-1 genome trafficking initiates APOBEC3G packaging in the cytosol

HIV-1 RNA genomes interact with diverse RNA binding proteins (RBPs) in the cytoplasm including antiviral factor APOBEC3G (A3G) that, in the absence of viral Vif proteins, is packaged into virions. Where and when HIV-1-A3G interactions are initiated for packaging inside the cell is unknown, and the relative contributions of genome vs. Gag capsid proteins to this process remains controversial. Here we visualized A3G responses to HIV-1 infection over an entire replication cycle using long-term (up to 72 h) live single cell imaging. We show that Vif-deficient HIV-1 dramatically shifts A3G and a second RNA surveillance factor, MOV10, from the cytoplasm to virus particle assembly sites with little to no net discernible effects on general markers of cytoplasmic processing bodies (DCP1A), stress granules (TIA-1), or a marker of the nonsense-mediated decay machinery (UPF1). Using a new live cell RNA-protein interaction assay based on RNA tethering (the in-cell RNA-protein interaction protocol, or IC-IP), we provide evidence that A3G- and MOV10- genome interactions are selective, strong, occur in presence or absence of Gag, and are initiated in the cytosol soon if not immediately after genome nuclear export. Finally, although Gag is sufficient to package A3G into virions even in the absence of genomes, single virion imaging indicates that selective A3G-genome interactions promote much more consistent per virion delivery of A3G to assembly sites. Collectively, these studies suggest a paradigm for early, strong, and persistent cytosolic detection of select HIV-1 RNA signatures by A3G, MOV10 and other host RBPs that are enriched in virions. IMPORTANCEHost-pathogen interactions determine the success of viral replication. While extensive work has identified many interactions between HIV-1 and cellular factors, our understanding of where these interactions in cells occur during the course of infection is incomplete. Here, we show that multiple RNA-binding proteins (including the antiviral restriction factor, APOBEC3G, and MOV10 helicase) bind HIV-1 RNA genomes in the cytoplasm and co-traffic with them into progeny virions. Furthermore, we show that these interactions with HIV-1 RNA occur in the absence of Gag and are sufficiently strong to recruit these to otherwise non-native subcellular locales. Together, these data begin to illuminate the intracellular trafficking pathways shared by host RNA binding proteins and the viral RNAs they preferentially bind.

cell biology↗