Abstract
Mitochondria play a pivotal role in most eukaryotic cells, as they are responsible for the generation of energy and diverse metabolic intermediates for many cellular events. During endosymbiosis, approximately 99% of the genes encoded by the mitochondrial genome were transferred into the host nucleus, and mitochondria import more than 1000 nuclear-encoded proteins from the cytosol to maintain structural integrity and fundamental functions, including DNA replication, mRNA transcription and RNA metabolism of dozens of mitochondrial genes. In metazoans, a family of nuclear-encoded proteins called the mitochondrial transcription termination factors (mTERFs) regulates mitochondrial transcription, including transcriptional termination and initiation, via their DNA-binding activities, and the dysfunction of individual mTERF members causes severe developmental defects. Arabidopsis thaliana and Oryza sativa contain 35 and 48 mTERFs, respectively, but the biological functions of only a few of these proteins have been explored. Here, we investigated the biological role and molecular mechanism of Arabidopsis mTERF15 in plant organelle metabolism using molecular genetics, cytological and biochemical approaches. The null homozygous T-DNA mutant of mTERF15, mterf15, was found to result in substantial retardation of both vegetative and reproductive development, which was fully complemented by the wild-type genomic sequence. Surprisingly, mitochondria-localized mTERF15 lacks obvious DNA-binding activity but processes mitochondrial nad2 intron 3 splicing through its RNA-binding ability. Impairment of this splicing event not only disrupted mitochondrial structure but also abolished the activity of mitochondrial respiratory chain complex I. These effects are in agreement with the severe phenotype of the mterf15 homozygous mutant. Our study suggests that Arabidopsis mTERF15 functions as a splicing factor for nad2 intron 3 splicing in mitochondria, which is essential for normal plant growth and development.
Highlights
Mitochondria, which originated through the endosymbiosis of a-proteobacteria into ancestral host cells, are the cellular powerhouses and play vital roles in diverse eukaryotic cell processes through the production of ATP and various metabolic intermediates [1,2]
The full-length mTERF15 transcript was not detected in the homozygous mterf15 plant (Figure 1C), suggesting that all of the observed phenotypes resulted from the null mutation of the mTERF15 allele (SALK_134099)
Mutating mTERF15 impaired the normal activity of mitochondrial respiratory chain complex I (Figure 5), thereby resulting in abnormal mitochondrial development (Figure 2) and the widespread retardation of plant growth and development (Figure 1)
Summary
Mitochondria, which originated through the endosymbiosis of a-proteobacteria into ancestral host cells, are the cellular powerhouses and play vital roles in diverse eukaryotic cell processes through the production of ATP and various metabolic intermediates [1,2]. Recent studies suggest that dysfunctional mitochondria are involved in many neurodegenerative diseases such as aging and cognitive decline in a wide range of metazoans, including humans [3]. Over the course of symbiotic evolution, the majority of mitochondrial genes migrated into the nuclear genome of the original host, leaving an incomplete set of essential genes in the mitochondrial genomes of most organisms, including plants [4,5,6]. The proteins involved in these processes are predominantly encoded by the nuclear genome and are imported into mitochondria after protein synthesis. Recent studies suggested that one protein family, called the mitochondrial transcription termination factors (mTERFs), plays important roles in regulating the organellar transcription machinery
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