• 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 in Arabidopsis thaliana mTERF18/SHOT1 enable plants to better tolerate heat and oxidative stresses, presumably due to low ROS production and reduced oxidative damage.
• Here we discover that shot1 mutants have greatly reduced OXPHOS complexes I and IV and reveal that suppressor of hot1-4 1 (SHOT1) binds DNA and localizes to mitochondrial nucleoids, which are disrupted in shot1. 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 in shot1 mutants.
• Our data link nucleoid organization to OXPHOS biogenesis and suggest that the common defects in shot1 mutants and ATAD3-disrupted plants lead to critical changes in mitochondrial metabolism and signaling that result in plant heat tolerance.

中文翻译：

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mTERF18 和 ATAD3 是线粒体类核结构所必需的，它们的破坏赋予拟南芥耐热性

• 线粒体在通过氧化磷酸化 (OXPHOS) 生成 ATP 中发挥关键作用，并产生破坏性和信号活性氧 (ROS)。他们减少了编码 OXPHOS 机器基本亚基的基因组。线粒体转录终止因子相关 (mTERF) 蛋白参与细胞器基因表达，与细胞器 DNA 或 RNA 相互作用。
• 我们之前发现拟南芥 mTERF18/SHOT1 的突变使植物能够更好地耐受热和氧化应激，这可能是由于低 ROS 产生和减少的氧化损伤。
• 在这里，我们发现shot1突变体大大减少了 OXPHOS 复合物 I 和 IV，并揭示了hot1-4 1 (SHOT1) 的抑制因子与 DNA 结合并定位于线粒体类核，后者在shot1中被破坏。此外，参与线粒体类核组织的动物 ATP 酶家族 AAA 结构域蛋白 3 (ATAD3) 的三个同源物被鉴定为 SHOT1 相互作用蛋白。重要的是，破坏 ATAD3 功能会破坏类核，减少复合物 I 的积累，并增强耐热性，正如在shot1突变体中所见。
• 我们的数据类核组织氧化磷酸化的生物合成和链接表明，在共同的缺陷SHOT1突变体和ATAD3受到破坏的植物导致线粒体代谢和信令这一结果在植物耐热性重大变化。