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.
Highlights
Immune responses in mammalian cells are dependent on the exposure to conserved molecular patterns present in pathogens, such as bacterial flagellins, lipoproteins, peptidoglycans, and lipopolysaccharides, as well as viral nucleic acids [1]
We examined the conserved synteny of genomic regions adjacent to the mitochondrial antiviral signaling protein (MAVS) gene in mammalian species and discovered that it was pretty high in most of them
We examined a set of 26 MAVS proteincoding orthologs shared by the human, monkey, dog, cat, cow, mouse, and domestic yak genomes to detect positive selection signals (Supplementary Table)
Summary
Immune responses in mammalian cells are dependent on the exposure to conserved molecular patterns present in pathogens, such as bacterial flagellins, lipoproteins, peptidoglycans, and lipopolysaccharides, as well as viral nucleic acids [1]. Identification of pathogen-derived nucleic acid is an important process of the host defense cells against invading pathogens. After identifying foreign invaders, the transcription of antiviral genes results in the cellular antiviral state that arms the cells to battle and subdues the infection. The host cells’ sensors against pathogen-associated DNA and RNA exist [2]. Mitochondria are important sensors in antiviral immunity through their key role in apoptosis [3]. One of the most important defense mechanisms against viral infections is the removal of infected cells through apoptosis. Mitochondria are chief performers in antiviral immunity because of their key role in apoptosis [3]
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