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

作　　者：Zhanqi Dong Nachuan Liao Yan Luo Ya Zhang Liang Huang Peng Chen Cheng Lu Minhui Pan 

机构地区：[1]State Key Laboratory of Resource Insects,Southwest University,Chongqing,China [2]Key Laboratory of Sericultural Biology and Genetic Breeding,Ministry of Agriculture and Rural Affairs,Southwest University,Chongqing,China

出　　处：《Insect Science》2025年第1期193-208,共16页昆虫科学(英文版)

基　　金：funded by the National Natural Science Foundation of China(31902214);the earmarked fund for CARS(CARS-18);the National Key R&D Program of China(2022YFD1601908).

摘　　要：ATAD3A 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 and Caenorhabditis elegans.To delve into the mechanism underlying ATAD3A defects and their impact on development,we constructed a Bombyx 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 the BmATAD3A 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 that BmATAD3A knockout inhibits amino acid biosynthesis through the regulation of mitochondrial ribosomal protein expression.Simultaneously,our findings indicate that BmATAD3A knockout impeded mitochondrial activity and ATPase synthesis and suppressed the mitochondrial oxidative phosphorylation pathway through B.mori mitochondrial ribosomal protein L11(BmmRpL11).These results provide novel insights into the molecular mechanisms involved in the inhibition of development caused by ATAD3A deficiency,offering a potential direction for targeted therapy in diseases associated with abnormal ATAD3A expression.

关 键 词：ATAD3A ATPASE BmmRpL1l Bombyx mori mitochondrial ribosomal protein 

分 类 号：Q96[生物学—昆虫学]