Welch, J. L. | bioRxiv Science

bioRxiv2025

Pelagic trophodynamics control invertebrate population dynamics

Invertebrates are increasingly targeted by commercial fisheries, yet assessment approaches designed for finfish often fail to capture their complex population dynamics. For many crustaceans, prolonged, long-distance larval dispersal decouples local recruitment from adult abundance and exposes populations to remote climate conditions overlooked in traditional models. Here we introduce a trophodynamic index that anticipates adult invertebrate population fluctuations by tracking material flows through the pelagic food web during the dispersal and early growth period. Combining primary production with the slope of zooplankton size spectra, the index reflects both productivity and trophic transfer efficiency. Applied to Bermudas Caribbean spiny lobster population, which supports both commercial and recreational fisheries that have steadily declined over the last decade, ecological forecasts based on this trophodynamic index outperform climatological, persistence, and environment-based models. This framework links pelagic ecosystem processes to invertebrate population dynamics, improving predictive capacity and supporting the development of ecosystem-based management for small-scale fisheries.

ecology↗

bioRxiv2020

N6-methyladenosine modification of HIV-1 RNA evades RIG-I-mediated sensing to suppresses type-I interferon induction in monocytic cells

N6-methyladenosine (m6A) is a prevalent RNA modification that plays a key role in regulating eukaryotic cellular mRNA functions. RNA m6A modification is regulated by two groups of cellular proteins, writers and erasers that add or remove m6A, respectively. HIV-1 RNA contains m6A modifications that modulate viral infection and gene expression in cells. However, it remains unclear whether m6A modifications of HIV-1 RNA modulate innate immune responses in cells or HIV-1-infected individuals. Here we show that m6A modification of HIV-1 RNA suppresses the expression of antiviral cytokine type-I interferon (IFN-I) in human monocytic cells. Transfection of differentiated monocytic cells with HIV-1 RNA fragments containing a single m6A-modification significantly reduced IFN-I mRNA expression relative to their unmodified RNA counterparts. We generated HIV-1 with altered RNA m6A levels by manipulating the expression of the m6A erasers or pharmacological inhibition of m6A addition in virus-producing cells. RNA transfection and viral infection of differentiated monocytic cells demonstrated that HIV-1 RNA with decreased m6A levels enhanced IFN-I expression, whereas HIV-1 RNA with increased m6A modifications had opposite effects. Our mechanistic studies revealed that m6A of HIV-1 RNA escaped the RIG-I-mediated RNA sensing and activation of the transcription factors IRF3 and IRF7 that drive IFN-I gene expression. Moreover, RNA of peripheral blood mononuclear cells from HIV-1 viremic patients showed increased m6A levels that correlated with increased IFN-I mRNA expression compared to levels from HIV-1-suppressed patients on antiretroviral therapy. Together, our results suggest that RNA m6A modifications regulate viral replication and antiviral innate immune responses in HIV-1-infected individuals. Author SummaryHIV-1 is known as a weak inducer of antiviral cytokines including IFN-I, but it is unclear how HIV-1 evades innate immunity. Different types of RNA modifications including m6A within the HIV-1 genome modulate viral replication; however, the role of m6A modifications of HIV-1 RNA in regulating innate immune responses remains elusive. In this study, we found that HIV-1 RNA modified with m6A suppresses the expression of IFN-I in differentiated monocytic cells by avoiding innate immune detection of viral RNA mediated by RIG-I, an RNA sensor in host cells. We also observed significantly increased RNA m6A modifications of peripheral blood mononuclear cells from HIV-1 viremic patients compared to virally suppressed patients on combined antiretroviral therapy, suggesting a functional link between m6A modifications and antiretroviral treatment. Investigating the functions of m6A modifications of HIV-1 RNA in regulating innate immune sensing and IFN-I induction in monocytic cells can help understand the mechanisms of HIV-1 persistence.

microbiology↗