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Two Roles for the Tenebrio molitor Relish in the Regulation of Antimicrobial Peptides and Autophagy-Related Genes in Response to Listeria monocytogenes

Relish is a key NF-κB transcription factor of the immune-deficiency (Imd) pathway that combats infection by regulating antimicrobial peptides (AMPs). Understanding of the fundamental role of Relish ( Relish) in controlling of virulence through the regulation of both AMPs and autophagy-related (ATG)...

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Published in:Insects (Basel, Switzerland) Switzerland), 2020-03, Vol.11 (3), p.188
Main Authors: Keshavarz, Maryam, Jo, Yong Hun, Edosa, Tariku Tesfaye, Han, Yeon Soo
Format: Article
Language:English
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Summary:Relish is a key NF-κB transcription factor of the immune-deficiency (Imd) pathway that combats infection by regulating antimicrobial peptides (AMPs). Understanding of the fundamental role of Relish ( Relish) in controlling of virulence through the regulation of both AMPs and autophagy-related (ATG) genes is unclear. Here, we show that transcripts were highly abundant in the larval fat body and hemocytes compared to the gut upon infection. Furthermore, significant mortality was observed in -silenced larvae after intracellular insult. To investigate the cause of this lethality, we measured the induction of AMPs and ATG genes in the dsRNA-treated larvae. The expression of - , - , - , - , and - were suppressed in the fat body and hemocytes of ds injected larvae during infection. In addition, knockdown led to a noticeable downregulation of (a serine-threonine protein kinase) in the fat body and hemocytes of young larvae 6 h post-infection (pi). The notable increase of autophagy genes in the early stage of infection (6 h pi), suggesting autophagy response is crucial for clearance. Taken together, these results suggest that plays pivotal roles in not only regulation of AMP genes but also induction of autophagy genes in response to challenge in fat body and hemocytes of larvae. Furthermore, negative regulation of several AMPs by in the fat body, hemocytes, and gut leaves open the possibility of a crosstalk between Toll and Imd pathway.
ISSN:2075-4450
2075-4450
DOI:10.3390/insects11030188