# Mannose receptor RpMR1 of Manila clam (Ruditapes philippinarum) defense against Vibrio anguillarum infection

## TL;DR

This study identifies and characterizes the mannose receptor RpMR1 in Manila clams, showing its role in defending against bacterial infection.

## Contribution

The first functional evidence of mannose receptor-mediated immunity in mollusks is provided.

## Key findings

- RpMR1 significantly reduces mortality in Manila clams infected with Vibrio anguillarum.
- RpMR1 exhibits antibacterial activity against Gram-negative bacteria but not Gram-positive bacteria.
- RpMR1 interacts with TLR4 in the immune response, as shown by gene silencing and expression analysis.

## Abstract

The mannose receptor (MR) is a member of the C-type lectin superfamily and a type I transmembrane protein that functions as a pattern recognition receptor (PRR) in immune responses. In this study, we identified 13 MR genes (RpMR1-13) in the genome of Ruditapes philippinarum and investigated their expression profiles following Vibrio anguillarum challenge. Notably, RpMR1, RpMR2, RpMR3, and RpMR4 exhibited peak expression at 72 h post-infection. We successfully purified the recombinant RpMR1 protein and demonstrated its antibacterial activity against three Gram-negative bacteria (V. splendidus, V. alginolyticus, and V. anguillarum), though it had no effect on Gram-positive bacteria. Furthermore, in vivo injection of RpMR1 significantly reduced mortality in R. philippinarum following V. anguillarum infection. To explore role of RpMR1 in immune signaling, we performed RNA interference (dsRNA-RpMR1) and observed successful gene silencing. Subsequent qRT-PCR analysis revealed that RpMR1 knockdown significantly suppressed TLR4 expression (P< 0.05) under V. anguillarum stress, confirming an interaction between RpMR1 and TLR4 in the immune response. This study provides the first functional evidence of mannose receptor-mediated immunity in mollusks, offering new insights into the molecular defense mechanisms of R. philippinarum against bacterial infection.

The online version contains supplementary material available at 10.1007/s44307-025-00075-7.