skip to main content

Search for: All records

Creators/Authors contains: "Schulz, Vincent"

Note: When clicking on a Digital Object Identifier (DOI) number, you will be taken to an external site maintained by the publisher. Some full text articles may not yet be available without a charge during the embargo (administrative interval).
What is a DOI Number?

Some links on this page may take you to non-federal websites. Their policies may differ from this site.

  1. Summary

    Mitochondria play critical roles in generating ATP through oxidative phosphorylation (OXPHOS) and produce both damaging and signaling reactive oxygen species (ROS). They have reduced genomes that encode essential subunits of the OXPHOS machinery. Mitochondrial Transcription tERmination Factor‐related (mTERF) proteins are involved in organelle gene expression, interacting with organellar DNA or RNA.

    We previously found that mutations inArabidopsis thaliana mTERF18/SHOT1enable plants to better tolerate heat and oxidative stresses, presumably due to low ROS production and reduced oxidative damage.

    Here we discover thatshot1mutants have greatly reduced OXPHOS complexes I and IV and reveal that suppressor ofhot1‐41 (SHOT1) binds DNA and localizes to mitochondrial nucleoids, which are disrupted inshot1. Furthermore, three homologues of animal ATPase family AAA domain‐containing protein 3 (ATAD3), which is involved in mitochondrial nucleoid organization, were identified as SHOT1‐interacting proteins. Importantly, disrupting ATAD3 function disrupts nucleoids, reduces accumulation of complex I, and enhances heat tolerance, as is seen inshot1mutants.

    Our data link nucleoid organization to OXPHOS biogenesis and suggest that the common defects inshot1mutants and ATAD3‐disrupted plants lead to critical changes in mitochondrial metabolism and signaling that result in plant heat tolerance.

    more » « less