Open AccessEffector and regulator: Diverse functions of C. elegans C-type lectin-like domain proteins
Author(s) -
Barbara Pees,
Wentao Yang,
Anke Kloock,
Carola Petersen,
Lena Peters,
Liancheng Fan,
Meike Friedrichsen,
Sabrina Butze,
Alejandra Zárate-Potes,
Hinrich Schulenburg,
Katja Dierking
Publication year - 2021
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1009454
Subject(s) - effector , mutant , biology , caenorhabditis elegans , c type lectin , gene , pathogen , microbiology and biotechnology , function (biology) , genetics , immune system
In C . elegans , 283 clec genes encode a highly diverse family of C-type lectin-like domain (CTLD) proteins. Since vertebrate CTLD proteins have characterized functions in defense responses against pathogens and since expression of C . elegans clec genes is pathogen-dependent, it is generally assumed that clec genes function in C . elegans immune defenses. However, little is known about the relative contribution and exact function of CLEC proteins in C . elegans immunity. Here, we focused on the C . elegans clec gene clec-4 , whose expression is highly upregulated by pathogen infection, and its paralogs clec-41 and clec-42 . We found that, while mutation of clec-4 resulted in enhanced resistance to the Gram-positive pathogen Bacillus thuringiensis MYBt18247 (Bt247), inactivation of clec-41 and clec-42 by RNAi enhanced susceptibility to Bt247. Further analyses revealed that enhanced resistance of clec-4 mutants to Bt247 was due to an increase in feeding cessation on the pathogen and consequently a decrease in pathogen load. Moreover, clec-4 mutants exhibited feeding deficits also on non-pathogenic bacteria that were in part reflected in the clec-4 gene expression profile, which overlapped with gene sets affected by starvation or mutation in nutrient sensing pathways. However, loss of CLEC-4 function only mildly affected life-history traits such as fertility, indicating that clec-4 mutants are not subjected to dietary restriction. While CLEC-4 function appears to be associated with the regulation of feeding behavior, we show that CLEC-41 and CLEC-42 proteins likely function as bona fide immune effector proteins that have bacterial binding and antimicrobial capacities. Together, our results exemplify functional diversification within clec gene paralogs.