bioRxiv preprint doi: https://doi.org/10.1101/2020.11.20.390153; this version posted November 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Inactivation of mitochondrial Complex I stimulates chloroplast ATPase in Physcomitrella (Physcomitrium patens). Marco Mellon a, Mattia Storti a, Antoni Mateu Vera Vives a, David M. Kramer b, Alessandro Alboresi a and Tomas Morosinotto a a. Department of Biology, University of Padova, 35121 Padova, Italy b. MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, MI 48824, United States of America; Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, United States of America. Corresponding author: Tomas Morosinotto, Dipartimento di Biologia, Università di Padova, Via Ugo Bassi 58B, 35121 Padova, Italy. Tel. +390498277484, Email:
[email protected] Abstract While light is the ultimate source of energy for photosynthetic organisms, mitochondrial respiration is still fundamental for supporting metabolism demand during the night or in heterotrophic tissues. Respiration is also important for the metabolism of photosynthetically active cells, acting as a sink for excess reduced molecules and source of substrates for anabolic pathways. In this work, we isolated Physcomitrella (Physcomitrium patens) plants with altered respiration by inactivating Complex I of the mitochondrial electron transport chain by independent targeting of two essential subunits. Results show that the inactivation of Complex I causes a strong growth impairment even in fully autotrophic conditions in tissues where all cells are photosynthetically active.