Abstract: SGT1 (Suppressor of G2 allele of SKP1) acts as an essential regulatory factor that coordinates the balance between autophagy and apoptosis, and maintains the protein homeostasi in higher animals. However, the- immune functions of SGT1 in invertebrates remain unclear. Here, we investigate the molecular characteristics and antibacterial role of SGT1 in the giant freshwater prawn Macrobrachium rosenbergii, with particular emphasis on its modulation of autophagic and apoptotic signaling. The full-length M. rosenbergii SGT1 transcript (MrSGT1) was amplified by PCR and subjected to comprehensive bioinformatic analyses to delineate its sequence characteristics, domain organization, and phylogenetic affiliation. The expression changes of MrSGT1 were quantified by qRT-PCR under basal conditions and following challenge with Aeromonas hydrophila or lipopolysaccharide (LPS). The function of MrSGT1 was performed by RNA interference coupled with qRT-PCR, Western blotting, and enzymatic assays to assess the impact of MrSGT1 silencing on autophagy, apoptosis, and antioxidant capacity. The results showed that, the open reading frame (ORF) of MrSGT1 was 687 bp encoding a peptide of 228 amino acids with CS and SGS domains. The predicted molecular weight of MrSGT1 protein was 25.41 ku with an isoelectric point of 5.54. Sequence homology analysis and phylogenetic analysis showed that the amino acid sequence of MrSGT1 shared 95.61% similarity with that of SGT1 from M. nipponense, and clustered with crustaceans, indicating that the protein has evolved relatively conservatively in crustaceans. MrSGT1 was ubiquitously expressed in all examined tissues, with maximal expression in hepatopancreas, where its expression level is 18.33-fold higher than that in hemolymph.. The relative expression of MrSGT1 in the hepatopancreas and gills of M. rosenbergii increased significantly after challenge with A. hydrophila and LPS, indicating its involvement in the prawn’s antibacterial immune response. Following A. hydrophila stimulation, the peak levels of MrSGT1 in the hepatopancreas and gill tissues were 5.51-fold and 5.15-fold higher than those of the control group, respectively, while the peak levels of MrSGT1 were 1.74-fold and 5.23-fold higher than the control group after LPS stimulation, respectively. Knockdown of MrSGT1 in combination with A. hydrophila infection resulted in a significant change in autophagic activity, an increase in apoptosis, and a decrease in antioxidant enzyme levels in M. rosenbergii. These findings revealed that MrSGT1 fortifies the antioxidant defenses of M. rosenbergii against pathogenic invasion by modulating the dynamic interplay between autophagy and apoptosis. These results provide pivotal foundational data to guide future investigations into the antibacterial defense mechanisms of M. rosenbergii.