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RNA m6A methylation suppresses insect juvenile hormone degradation to minimize fitness costs in response to a pathogenic attack

ABSTRACT: Bioinsecticides and transgenic crops based on the bacterial pathogen Bacillus thuringiensis (Bt) can effectively control diverse agricultural insect pests, nevertheless, insect resistance evolution without causing obvious fitness costs has seriously eroded the sustainable use of these Bt products. Recently, we have discovered that an increased titer of juvenile hormone (JH) favors an insect host (Plutella xylostella) to enhance fitness whilst resisting the Bt pathogen, however, the underlying regulatory mechanisms of the increased JH titer is obscure. Here, we define the involvement of N6-methyladenosine (m6A) RNA modification in modulating the availability of JH in this process. Specifically, we found that two m6A methyltransferase subunit genes, PxMettl3 and PxMettl14, repressed the expression of a key JH-degrading enzyme JH esterase (JHE) to induce an increased JH titer, mitigating the fitness costs associated with a robust defense against the Bt pathogen. This study identifies an as-yet uncharacterized m6A-mediated epigenetic regulator of insect hormones for maintaining fitness during pathogen defense and unveils an emerging Bt resistance-related m6A methylation atlas in insects, which further expands the functional landscape of m6A modification and showcases the pivotal role of epigenetic regulation in host-pathogen interactions.

ORGANISM(S): Plutella xylostella

PROVIDER: GSE247107 | GEO | 2023/11/10

REPOSITORIES: GEO

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Project description:Juvenile hormone (JH) and 20-hydroxy-ecdysone (20E) are highly versatile hormones, coordinating development, growth, and reproduction in insects. Pulses of 20E provide key signals for initiating developmental and physiological transitions, while JH promotes or inhibits these signals in a stage-specific manner. Previous evidence suggests that JH and 20E might modulate innate immunity, but whether and how these hormones interact to regulate the immune response remains unclear. Here we show that JH and 20E have antagonistic effects on the expression of antimicrobial peptides (AMPs) in Drosophila melanogaster. In S2* cells challenged with bacterial peptidoglycans, 20E induces promoter activity and expression of AMPs in a dose-dependent manner, while JH III and its synthetic analogs (JHa) methoprene and pyriproxyfen abolish this 20E-dependent response. Using microarrays and GFP reporter gene assays in adult flies, we confirm that JH is a hormonal immuno-suppressor in vivo. When silencing both partners of the ecdysone receptor (EcR ) / ultraspiracle (USP) heterodimer with RNAi in S2* cells, 20E fails to activate Diptericin (Dpt) expression, suggesting that 20E regulates expression of this gene through EcR / USP signaling. In contrast, silencing methoprene-tolerant (MET), a candidate JH receptor, does not impair the immuno-suppressive action of JH III and JHa, indicating that in this context MET does not function as a JH receptor. Our results suggest that the balance of 20E and JH is a major determinant of immune homeostasis in insects. Experiment Overall Design: To examine the transcriptional response of y, w flies to treatment with exogenous JH, we performed a microarray experiment on females treated with JH or solvent (control). Flies were grown on regular yeast diet, switched to no-yeast food within one hour of eclosion, and yeast-starved for 5 days posteclosion to lower their endogenous JH titer and to synchronize their physiology (cf. Tu and Tatar, 2003; Gershman et al., 2007). Subsequently, we anesthetized flies on ice and topically treated them with 0.1 ïl of 187 mM JH III in acetone or with 0.1ï ïl 100% acetone (control) using a 1 ïl Hamilton syringe with a repeating dispenser. 12 hours after hormone administration, samples were snap-frozen in liquid nitrogen and stored at -80Â°C. RNA was isolated from samples (2 JH samples, 2 control samples, each with 30 females) by lysis, as described in Gershman et al. (2007). cDNA products were hybridized at the Brown University Genomics Core Facility to Affymetrix GeneChip Drosophila_1 Genome Arrays (2 replicate chips per treatment). The dataset consisted of 14,009 probe sets, with 6,142 probe sets annotated. Expression data were analyzed for significant over- or underrepresentation of gene ontology (GO) terms with the web application FatiGO (Al-Shahrour et al., 2004), using a two-fold change criterion. To test whether JH treatment significantly suppresses expression of AMPs we used t-tests implemented in JMP IN 5.1.

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RNA m6A methylation suppresses insect juvenile hormone degradation to minimize fitness costs in response to a pathogenic attack

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