Abstract
Toll-like receptors (TLRs) recognize conserved pathogen-associated molecular patterns (PAMPs) and are an ancient and well-conserved group of pattern recognition receptors (PRRs). The isolation of the Antarctic continent and its unique teleost fish and microbiota prompted the present investigation into Tlr evolution. Gene homologues of tlr members in teleosts from temperate regions were present in the genome of Antarctic Nototheniidae and the non-Antarctic sister lineage Bovichtidae. Overall, in Nototheniidae apart from D. mawsoni, no major tlr gene family expansion or contraction occurred. Instead, lineage and species-specific changes in the ectodomain and LRR of Tlrs occurred, particularly in the Tlr11 superfamily that is well represented in fish. Positive selective pressure and associated sequence modifications in the TLR ectodomain and within the leucine-rich repeats (LRR), important for pathogen recognition, occurred in Tlr5, Tlr8, Tlr13, Tlr21, Tlr22, and Tlr23 presumably associated with the unique Antarctic microbiota. Exposure to lipopolysaccharide (Escherichia coli O111:B4) Gram negative bacteria did not modify tlr gene expression in N. rossii head–kidney or anterior intestine, although increased water temperature (+4°C) had a significant effect.
Highlights
The innate immune system is a defense mechanism present in all metazoans and provides a rapid and nonspecific cellular and humoral response against a wide range of viruses, bacteria, fungi, and parasites [1]
We reveal that apart from D. mawsoni, no major gene family expansion or contraction occurred in Nototheniidae, and the tlr gene complement was conserved across most teleosts
Within the leucine-rich repeat (LRR) motif of the ectodomain, which recognize pathogen molecules, positive selection was detected in Tlr5, Tlr8, Tlr13, Tlr22, and Tlr23 across all the analyzed Antarctic Notothenioids
Summary
The innate immune system is a defense mechanism present in all metazoans and provides a rapid and nonspecific cellular and humoral response against a wide range of viruses, bacteria, fungi, and parasites [1]. The molecular elements of innate immunity include soluble mediators (such as cytokines, chemokines, antimicrobial peptides, lytic enzymes, and growth inhibitors) and innate immune cells such as granulocytes and phagocytes and innate immune host-cell receptors [2, 3]. Tissues such as the thymus and head–kidney (primary immune organs) and the spleen, liver, and mucosa-associated lymphoid tissues, such as the skin and intestine (secondary immune organs), play a major role in innate immunity [4]. TLRs are characterized by a highly conserved Toll/interleukin-1 receptor (TIR) intracellular domain that, after receptor interaction with PAMPs, triggers the intracellular signaling cascade that leads to an inflammatory response [23,24,25,26,27,28]
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