Is there a transgenerational inheritance of host resistance against pathogens? Lessons from the <i>Galleria mellonella</i>-<i>Bacillus thuringiensis</i> interaction model

Bierne, Hélène; Nielsen-LeRoux, Christina

doi:10.1080/21505594.2017.1356538

Cited by 4 publications

(2 citation statements)

References 27 publications

(35 reference statements)

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“…Although the intestinal microbiota and epigenetic mechanisms mentioned above can promote the development of insect resistance, it, like a coin, has two sides. To wrestle against the host, Bt may enhance the toxicity of Cry toxins by exploiting the intestinal microbiota ( Broderick et al, 2009 ; Paramasiva et al, 2014 ) or by interfering with the epigenetic mechanism of the insect host to affect the expression of immune and development-related genes ( Bierne and Nielsen-LeRoux, 2017 ; Baradaran et al, 2019 ; Özbek et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Which Is Stronger? A Continuing Battle Between Cry Toxins and Insects

Luo

et al. 2021

Front. Microbiol.

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In this article, we review the latest works on the insecticidal mechanisms of Bacillus thuringiensis Cry toxins and the resistance mechanisms of insects against Cry toxins. Currently, there are two models of insecticidal mechanisms for Cry toxins, namely, the sequential binding model and the signaling pathway model. In the sequential binding model, Cry toxins are activated to bind to their cognate receptors in the mid-intestinal epithelial cell membrane, such as the glycophosphatidylinositol (GPI)-anchored aminopeptidases-N (APNs), alkaline phosphatases (ALPs), cadherins, and ABC transporters, to form pores that elicit cell lysis, while in the signaling pathway model, the activated Cry toxins first bind to the cadherin receptor, triggering an extensive cell signaling cascade to induce cell apoptosis. However, these two models cannot seem to fully describe the complexity of the insecticidal process of Cry toxins, and new models are required. Regarding the resistance mechanism against Cry toxins, the main method insects employed is to reduce the effective binding of Cry toxins to their cognate cell membrane receptors by gene mutations, or to reduce the expression levels of the corresponding receptors by trans-regulation. Moreover, the epigenetic mechanisms, host intestinal microbiota, and detoxification enzymes also play significant roles in the insects’ resistance against Cry toxins. Today, high-throughput sequencing technologies like transcriptomics, proteomics, and metagenomics are powerful weapons for studying the insecticidal mechanisms of Cry toxins and the resistance mechanisms of insects. We believe that this review shall shed some light on the interactions between Cry toxins and insects, which can further facilitate the development and utilization of Cry toxins.

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Section: Discussionmentioning

confidence: 99%

Which Is Stronger? A Continuing Battle Between Cry Toxins and Insects

Luo

et al. 2021

Front. Microbiol.

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“…In parasitism, one organism, referred to as the parasite or pathogen, causes harm to the other organism, the host, by either living on or inside it 5 . As a result of such interactions, adaptive multigenerational epigenetic effects encompassing both behavioral and physiological defences have been reported in a wide range of taxa, such as bees 6,7 , pipefish [8][9][10] , ragworm 11 , honeycomb moths 12 , Drosophila [13][14][15] , beetles [16][17][18][19][20] , brine shrimps 21 , C. elegans 22,23 , and mice 24 .…”

Section: Introductionmentioning

confidence: 99%

Multigenerational inheritance of parasitic stress memory inDrosophila melanogaster

Khan,

Saini,

Hamid

et al. 2023

Preprint

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SUMMARYOrganisms sense harmful environmental conditions and employ strategies to safeguard themselves. Moreover, they can communicate this experience to the next generation or beyond via non-DNA sequence-based mechanisms, referred to as intergenerational or transgenerational epigenetic inheritance, respectively. Using a specialist larval parasitoid,Leptopilina boulardi, and its host,Drosophila melanogaster, we show that the parental experience of parasitic stress results in an increased survivability of the immediate offspring of the host. Furthermore, we observe that the increased survivability in response to the parasitic stress is transmitted transgenerationally where the grandparents have been exposed to the parasitoid but not the parents. The increased survivability is primarily inherited through male parents, and at least one of the forms of the memory is better immune priming at larval stage. Our study suggests that the stress exposure during the pre-adult stage of the host has lifetime benefits for its progeny to deal with the future parasitic attack.

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