Abstract
The fall armyworm (Spodoptera frugiperda), a globally invasive pest, poses substantial threats to corn in China. Microsporidia are a group of obligate intracellular parasitic fungi and are considered to have great potential in biological control. In this article, we investigated the pathology of Nosema sp. infection in S. frugiperda larvae at the organismal, cellular, and molecular levels. At the organism level, this microsporidian significantly prolonged the developmental duration of the host, reduced its body weight, caused molting failure, and led to a high mortality rate at 98.9%, 97.8%, and 64.0%, respectively, in 5 × 10(5), 5 × 10(4), 5 × 10(3) spores/larva doses. Microsporidia infection caused severe damage to midgut cells, including the formation of vacuoles in the cytoplasm, mitochondria, and intercellular spaces, destruction of goblet cells, and partial encapsulation of spores by mitochondria. Transcriptomic profiling revealed significant alterations in gene expression profiles in S. frugiperda larvae following microsporidian infection. The expression levels of genes associated with the chitin synthesis pathway (CHS1, G6PI, GFAT, GNPNA, PAGM, UAP) were inhibited, which may contribute to the effects of Nosema sp. on the growth and development of S. frugiperda.