Postnatal developmental dynamics of mitochondrial complex I in mouse tissues.

TitlePostnatal developmental dynamics of mitochondrial complex I in mouse tissues.
Publication TypeJournal Article
Year of Publication2025
AuthorsSiragusa M, Yoval-Sánchez B, Guerrero I, Galkin A
JournalAm J Physiol Cell Physiol
Volume329
Issue5
PaginationC1666-C1671
Date Published2025 Nov 01
ISSN1522-1563
KeywordsAnimals, Animals, Newborn, Brain, Electron Transport Complex I, Female, Kidney, Male, Mice, Mice, Inbred C57BL, Mitochondria, Muscle, Skeletal, Myocardium, Oxidative Phosphorylation
Abstract

Although the content of mitochondrial enzymes in different tissues can vary greatly, understanding the regulation behind these differences has been hampered by a lack of quantitative knowledge in relation to postnatal development. Here we report a quantitative analysis of developing brain, heart, kidneys, and muscle tissue of C57BL/6J mice, focusing on the content of mitochondrial complex I, a key component of the respiratory chain. We found that in all tissues except kidneys, complex I content gradually increases after birth, reaching a plateau level at around 25 days. Complex I content in muscles does not change significantly until postnatal day 7-10, and then also increases. The greatest increment was found in kidneys, where a 16-fold increase in complex I level after birth was observed. We also found that content of complex I in all postnatal tissues, but muscle, is higher in males than in females. These baseline dynamics of this key mitochondrial flavoprotein serve as a reference for evaluating genetic influences on development and provide a standard for assessing mitochondrial complex I function during postnatal growth.NEW & NOTEWORTHY Mitochondrial complex I is a key enzyme of mammalian oxidative phosphorylation. Here, we provide the first quantitative map of mitochondrial complex I maturation in postnatal mouse tissues. Complex I content rises after birth with striking tissue- and sex-specific patterns, including a dramatic 16-fold increase in kidney. These findings establish a baseline for developmental bioenergetics and a reference for evaluating genetic or disease-related mitochondrial dysfunction.

DOI10.1152/ajpcell.00692.2025
Alternate JournalAm J Physiol Cell Physiol
PubMed ID41101777
PubMed Central IDPMC12700496
Grant ListS10OD030335 / / HHS | National Institutes of Health (NIH) /
R01NS131322 / / HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS) /
R01 NS131322 / NS / NINDS NIH HHS / United States
R01 NS112381 / NS / NINDS NIH HHS / United States
R01NS112381 / / HHS | National Institutes of Health (NIH) /
S10 OD030335 / OD / NIH HHS / United States