Abstract
Mitochondria are abundant and important organelles present in nearly all eukaryotic cells, which maintain metabolic communication with the cytosol through mitochondrial carriers. The mitochondrial membrane localized phosphate transporter (MPT) plays vital roles in diverse development and signaling processes, especially the ATP biosynthesis. Among the three MPT genes in Arabidopsis genome, AtMPT3 was proven to be a major member, and its overexpression gave rise to multiple developmental defects including curly leaves with deep color, dwarfed stature, and reduced fertility. Transcript profiles revealed that genes involved in plant metabolism, cellular redox homeostasis, alternative respiration pathway, and leaf and flower development were obviously altered in AtMPT3 overexpression (OEMPT3) plants. Moreover, OEMPT3 plants also accumulated higher ATP content, faster respiration rate and more reactive oxygen species (ROS) than wild type plants. Overall, our studies showed that AtMPT3 was indispensable for Arabidopsis normal growth and development, and provided new sights to investigate its possible regulation mechanisms.
Highlights
Mitochondria are important organelles that can integrate numerous metabolic pathways, including energy homeostasis, redox balance, cellular growth and stress adaptation [1, 2]
We found no visible differences between the wild type and the OEMPT3 plants under normal growth conditions
We provide evidence that overexpression of AtMPT3 exhibited multiple morphological and physiological changes, such as curly leaf, abnormal flower, dwarfism, higher ATP content and respiration rate, which was due to mitochondrial dysfunction (Figs 1, 2 and 5)
Summary
Mitochondria are important organelles that can integrate numerous metabolic pathways, including energy homeostasis, redox balance, cellular growth and stress adaptation [1, 2]. The drastic expression fluctuation of mitochondrion associated genes would disturb mitochondrial function, which had significant effects on growth and development. Overexpression of the unedited form of the subunit 9 of ATP synthase gene (35S::u-atp9) caused mitochondrial dysfunction, dwarf morphology and male sterility [3]. Loss of the mitochondrial Mg2+ transporter AtMGT5 led to pollen abortion and male sterility [4]. PLOS ONE | DOI:10.1371/journal.pone.0129717 June 15, 2015
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