The Roles of Distinct Transcriptional Factors in the Innate Immunity of C. elegans

Abstract

Deleterious molecules or factors produced by pathogens can hinder the normal physiological functioning of organisms. In response to these survival challenges, organisms rely on innate immune signaling as their first line of defense, which regulates immune-responsive genes and antimicrobial peptides to protect against pathogenic infections. These genes are under the control of transcription factors, which are known to regulate the transcriptional activity of genes after binding to their regulatory sequences. Previous studies have employed Caenorhabditis elegans as a host-pathogen interaction model to demonstrate the essential role of different transcription factors in the innate immunity of worms. In this review, we summarize the advances made regarding the functioning of distinct transcription factors in the innate immune response upon pathogen infection. Finally, we discuss the open questions in the field, whose resolutions have the potential to expand our understanding of the mechanisms underlying the innate immunity of organisms.

Keywords: GATA TFs; WH-FORKHEAD TFs; bZIP TFs; host–pathogen interaction; innate immunity; transcription factors.

Figure 1

Members of the WH-FORKHEAD, bZIP, and GATA transcription factor families are required to mediate immune responses in C. elegans. (A–C): DAF-16 (A), ZIP-2 (B), and ELT-2 (C), as central members of the WH-FORKHEAD, bZIP, and GATA families, respectively, which regulate the immune response individually and in coordination with other transcripts.

Figure 2

Illustrative model showing research gaps related to intercellular signaling, stress response (heat stress, starvation, and chemical stress), immunosenescence, metabolism, aging, and conserved function in humans. The question mark indicates areas for further exploration.