Positive Selection Drives the Adaptive Evolution of Mitochondrial Antiviral Signaling (MAVS) Proteins-Mediating Innate Immunity in Mammals

Abstract

The regulated production of filamentous protein complexes is essential in many biological processes and provides a new paradigm in signal transmission. The mitochondrial antiviral signaling protein (MAVS) is a critical signaling hub in innate immunity that is activated when a receptor induces a shift in the globular caspase activation and recruitment domain of MAVS into helical superstructures (filaments). It is of interest whether adaptive evolution affects the proteins involved in innate immunity. Here, we explore and confer the role of selection and diversification on mitochondrial antiviral signaling protein in mammalian species. We obtined the MAVS proteins of mammalian species and examined their differences in evolutionary patterns. We discovered evidence for these proteins being subjected to substantial positive selection. We demonstrate that immune system proteins, particularly those encoding recognition proteins, develop under positive selection using codon-based probability methods. Positively chosen regions within recognition proteins cluster in domains involved in microorganism recognition, implying that molecular interactions between hosts and pathogens may promote adaptive evolution in the mammalian immune systems. These significant variations in MAVS development in mammalian species highlights the involvement of MAVS in innate immunity. Our findings highlight the significance of accounting for how non-synonymous alterations affect structure and function when employing sequence-level studies to determine and quantify positive selection.