BmATAD3A mediates mitochondrial ribosomal protein expression to maintain the mitochondrial energy metabolism of the silkworm, Bombyx mori

BmATAD3A knockout could inhibit the synthesis of mitochondrial ribosomal protein, leading to mitochondrial dysfunction that affects the mitochondrial membrane potential, inhibits the expression levels of oxidative phosphorylation subunit complexes  I (BmND4,BmND5), III (BmCYTB), IV (BmCOX2) and V (BmATP6), and reduces ATPase activity. AbstractATAD3A is a mitochondrial membrane protein belonging to the ATPase family that contains the AAA+ domain. It 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 growth and development defects in humans, mice andCaenorhabditis elegans. To delve into the mechanism underlying ATAD3A defects and their impact on development, we constructed aBombyx mori ATAD3A (BmATAD3A) defect model in silkworm larvae. We aim to offer a reference for understanding ATAD3A genetic defects and elucidating the molecular regulatory mechanisms. The results showed that knockout of theBmATAD3A gene significantly affected the weight, survival rate, ATPase production and mitochondrial metabolism of individuals after 24  h of incubation. Combined metabolomics and transcriptomics analysis further demonstrated thatBmATAD3A knockout inhibits amino acid biosynthesis through the regulation of mitochondrial ribosomal protein expression. Simultaneously, our findings indicate thatBmATAD3A knockout impeded mitochondrial activity and ATPa...
Source: Insect Science - Category: Biology Authors: Tags: ORIGINAL ARTICLE Source Type: research