N6‐methyladenosine (m6A) RNA is the most abundant modification of mRNA, and has been demonstrated in regulating various post‐transcriptional processes. Many studies have shown that m6A methylation plays key roles in sex determination, neuronal functions, and embryonic development in Drosophila and mammals. Here, we analyzed transcriptome‐wide profile of m6A modification in the embryonic development of the destructive agricultural pest Spodoptera frugiperda. We found that the 2 key mRNA m6A methyltransferases SfrMETTL3 and SfrMETTL14 have high homologies with other insects and mammals, suggesting that SfrMETTL3 and SfrMETTL14 may have conserved function among different species. From methylated RNA immunoprecipitation sequencing analysis, we obtained 46 869 m6A peaks representing 8 587 transcripts in the 2‐h embryos after oviposition, and 41 389 m6A peaks representing 9 230 transcripts in the 24‐h embryos. In addition, 5 995 m6A peaks were differentially expressed including 3 752 upregulated and 2243 downregulated peaks. Functional analysis with Gene Ontology and Kyoto Encyclopedia of Genes and Genomes suggested that differentially expressed m6A peak‐modified genes were enriched in cell and organ development between the 2‐ and 24‐h embryos. By conjoint analysis of methylated RNA immunoprecipitation‐seq and RNA‐seq data, we found that RNA m6A methylation may regulate the transcriptional levels of genes related to tissue and organ development from 2‐ to 24‐h embryos. Our study reveals the role of RNA m6A epigenetic regulation in the embryonic development of S. frugiperda, and provides new insights for the embryonic development of insects.

N6-Methyladenosine (m6A), the most abundant mammalian mRNA modification, has been reported to modulate various viral infections. Although it has been confirmed that RNA modifications can also modulate the replication and development of different parasites, the role of the RNA epitranscriptome in the regulation of host response post parasite infection remains to be elucidated. Here we report host spleen m6A epitranscriptome landscapes induced by different strains of the malaria parasite Plasmodium yoelii. We found that malaria parasite infection dramatically changes host spleen m6A mRNA modification and gene expression. Additionally, malaria parasite infection reprograms host immune response pathways by regulating the m6A modification enzymes. Collectively, our study is the first characterization of host spleen m6A methylome triggered by malaria parasite infections, and our data identify m6A modifications as significant transcriptome-wide marks during host-parasite interactions. We demonstrate that host mRNA methylation machinery can sense and respond to malaria parasite infections, and provide new insights into epitranscriptomic mechanisms underlying parasite-induced pathogenesis.