Three STAT isoforms formed by selective splicing are involved in the regulation of anti-lipopolysaccharide factor expression in Macrobrachium nipponense during WSSV infection.

White spot syndrome virus (WSSV), a double-stranded DNA virus, is harmful in aquaculture. The signal transducer and activator of transcription (STAT) has been shown to play a role during host infection with the virus, but the exact mechanism by which it acts is unclear. In this study, three STAT isoforms (MnSTAT1, MnSTAT2, and MnSTAT3) were identified in Macrobrachium nipponense. The full-length sequence of MnSTAT1 was 3336 bp, with 2259 bp open reading frame (ORF), encoding a 852 amino acids protein. The full-length sequence of MnSTAT2 was 2538 bp, and the ORF was 2391 bp, encoding 796 amino acids. The full-length sequence of MnSTAT3 sequence was 2618 bp, and the ORF was 2340 bp, encoding 779 amino acids. MnSTAT1-3 is produced by alternative last exon. MnSTAT1-3 all contain a STAT_int, a STAT_alpha, a STAT_bind, and a SH2 structure. MnSTAT1-3 are widely expressed in various tissues tested. The expression levels of MnSTAT1-3 in the intestine of M. nipponense were upregulated at multiple time points following WSSV stimulation. The expression of seven anti-lipopolysaccharide factors (ALFs) was significantly reduced with the knockdown of MnSTATs during WSSV infection. Results showed that MnSTATs regulated the expression of intestinal ALFs and was involved in the innate immunity against WSSV of M. nipponense.