Translocase of the Outer Mitochondrial Membrane 40 Is Required for Mitochondrial Biogenesis and Embryo Development in Arabidopsis

Abstract

In eukaryotes, mitochondrion is an essential organelle which is surrounded by a double membrane system, including the outer membrane, intermembrane space and the inner membrane. The translocase of the outer mitochondrial membrane (TOM) complex has attracted enormous interest for its role in importing the preprotein from the cytoplasm into the mitochondrion. However, little is understood about the potential biological function of the TOM complex in Arabidopsis . The aim of the present study was to investigate how AtTOM40 , a gene encoding the core subunit of the TOM complex, works in Arabidopsis. As a result, we found that lack of AtTOM40 disturbed embryo development and its pattern formation after the globular embryo stage, and finally caused albino ovules and seed abortion at the ratio of a quarter in the homozygous tom40 plants. Further investigation demonstrated that AtTOM40 is wildly expressed in different tissues, especially in cotyledons primordium during Arabidopsis embryogenesis. Moreover, we confirmed that the encoded protein AtTOM40 is localized in mitochondrion, and the observation of the ultrastructure revealed that mitochondrion biogenesis was impaired in tom40-1 embryo cells. Quantitative real-time PCR was utilized to determine the expression of genes encoding outer mitochondrial membrane proteins in the homozygous tom40-1 mutant embryos, including the genes known to be involved in import, assembly and transport of mitochondrial proteins, and the results demonstrated that most of the gene expressions were abnormal. Similarly, the expression of genes relevant to embryo development and pattern formation, such as SAM (shoot apical meristem), cotyledon, vascular primordium and hypophysis, was also affected in homozygous tom40-1 mutant embryos. Taken together, we draw the conclusion that the AtTOM40 gene is essential for the normal structure of the mitochondrion, and participates in early embryo development and pattern formation through maintaining the biogenesis of mitochondria. The findings of this study may provide new insight into the biological function of the TOM40 subunit in higher plants.

Chromosome-scale assemblies of the male and female Populus euphratica genomes reveal the molecular basis of sex determination and sexual dimorphism

“…The best hit for TRANSLOCASE OF THE OUTER MITOCHONDRIAL MEMBRANE 40 ( TOM40 ) in P. euphratica ( PeuTM14G01682 and PeuTF14G0787 ) exhibited a 2.6-fold higher expression in male leaves than in female leaves. TOM40 is a core subunit of the TOM complex and is required for mitochondrial biogenesis and embryo development 53 .

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Genome wide association analysis for yield related traits in maize

“…TOM40 was relatively conservative and had homologous genes in rice and maize. In Arabidopsis , AtTOM40 was essential for the normal structure of the mitochondrion, and participated in early embryo development and pattern formation through maintaining the biogenesis of mitochondria [ 41 ]. The candidate gene GRMZM2G304745 of SNP 2_23576028 encoded a leucine-rich repeat protein kinase family protein, overexpression of LRK (leucine-rich repeat receptor kinase) gene could increase the yield of rice [ 42 ].…”

“…TOM40 was relatively conservative and had homologous genes in rice and maize. In Arabidopsis, AtTOM40 was essential for the normal structure of the mitochondrion, and participated in early embryo development and pattern formation through maintaining the biogenesis of mitochondria [41].…”

Rapid Single-Step Affinity Purification of HA-Tagged Plant Mitochondria

“…Recently, analyses of mitochondrial proteome content, complexome composition, posttranslational modifications, energy metabolism, OXPHOS complex formation and function, protein translocation, and metabolite shuttles have been conducted to further our understanding of mitochondrial metabolism in Arabidopsis (König et al, 2014;Fromm et al, 2016;De Col et al, 2017;Rao et al, 2017;Senkler et al, 2017;Porcelli et al, 2018;Hu et al, 2019;Kolli et al, 2019;Meyer et al, 2019;Nickel et al, 2019). Many of these analyses required the isolation of intact mitochondria.…”