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Abstract Although the type‐I interferon (IFN‐I) response is considered vertebrate‐specific, recent findings about the Intracellular Pathogen Response (IPR) in nematodeCaenorhabditis elegansindicate that there are similarities between these two transcriptional immunological programs. The IPR is induced during infection with natural intracellular fungal and viral pathogens of the intestine and promotes resistance against these pathogens. Similarly, the IFN‐I response is induced by viruses and other intracellular pathogens and promotes resistance against infection. Whether the IPR and the IFN‐I response evolved in a divergent or convergent manner is an unanswered and exciting question, which could be addressed by further studies of immunity against intracellular pathogens inC. elegansand other simple host organisms. Here we highlight similar roles played by RIG‐I‐like receptors, purine metabolism enzymes, proteotoxic stressors, and transcription factors to induce the IPR and IFN‐I response, as well as the similar consequences of these defense programs on organismal development.
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Immune activation during Pseudomonas infection causes local cell wall remodeling and alters AGP accumulation
Significance Statement Although potentiating resilience is foundational to crop improvement, and despite the notion that cell wall (CW) protects against pathogens, the extent of pathogen‐induced CW changes and the CW composition requirements for a successful defense are largely unknown. By investigating the bacteria‐induced impact on the Arabidopsis CW, we found changes exclusively in infected leaves with the remodeling of distinct CW polysaccharides, including arabinogalactan proteins, whose loss is detrimental to defense, highlighting specific requirements for antagonizing pathogens and potentiating plant defenses.
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- Award ID(s):
- 1714561
- PAR ID:
- 10451753
- Date Published:
- Journal Name:
- The Plant Journal
- ISSN:
- 0960-7412
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Journal Article:
- https://doi.org/10.1111/tpj.16393
