ATAD3A is a mitochondrial membrane protein in the ATPase family containing an AAA+ domain, which is widely involved in mitochondrial metabolism, protein transport, cell growth, development, and other important life processes. It has previously been reported that the deletion of ATAD3A causes individual growth and development defects in humans, mice, and Caenorhabditis elegans. To further analyze the mechanism of ATAD3A defects affecting individual development, we constructed a BmATAD3A defect model in silkworm larvae to provide a reference for ATAD3A genetic diseases and molecular regulation mechanisms. The results showed that knockout of the BmATAD3A gene could significantly affect individual weight, survival rate, ATPase production, and mitochondrial metabolism after 24 h of individual incubation. Metabonomics and transcriptomics combined analysis further showed that knockout of BmATAD3A could inhibit individual amino acid biosynthesis by regulating mitochondrial ribosomal protein expression. Meanwhile, the knockout of BmATAD3A could block mitochondrial activity and ATPase synthesis through the mitochondrial ribosomal protein BmmRPL11 and thereby inhibit mitochondrial oxidative phosphorylation. These results could provide new insights into the inhibition of individual development caused by ATAD3A deficiency, thus allowing the identification of new directions for the targeted therapy of diseases caused by abnormal expression of ATAD3A.