Cox25 Teams Up with Mss51, Ssc1, and Cox14 to Regulate Mitochondrial Cytochrome c Oxidase Subunit 1 Expression and Assembly in Saccharomyces cerevisiae
Cox25 Teams Up with Mss51, Ssc1, and Cox14 to Regulate Mitochondrial Cytochrome c Oxidase Subunit 1 Expression and Assembly in Saccharomyces cerevisiae
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DOI：
10.1074/jbc.m110.188805
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发表时间：
2011-01-07
影响因子：
4.8
通讯作者：
Barrientos, Antoni
中科院分区：
文献类型：
--
作者：
Fontanesi, Flavia;Clemente, Paula;Barrientos, Antoni
在酿酒酵母中，线粒体细胞色素 c 氧化酶 (COX) 的生物发生受到翻译调节。 Mss51 是一种特定的 COX1 mRNA 翻译激活剂和 Cox1 伴侣，驱动调节机制。在翻译期间和翻译后，新合成的 Cox1 与涉及 Ssc1、Mss51 和 Cox14 的蛋白质复合物发生物理相互作用，最终将 Cox1 交给组装途径。这一步骤可能是由 Shy1 等组装伴侣催化的，该过程与复合物中 Ssc1-Mss51 的释放相结合。 COX 组装受损会导致 Mss51 被捕获在复合物中，从而限制其 COX1 mRNA 翻译的可用性。一个例外是 COX14 中的无效突变，它不会影响 Cox1 合成，因为 Mss51 捕获复合物变得不稳定，并且 Mss51 易于翻译。在这里，我们提供的证据表明 Cox25 是一种新的重要 COX 组装因子，其作用与 Cox14 类似。 COX25 的无效突变本身或与其他 COX 突变组合不会影响 Cox1 合成。 Cox25 是一种线粒体内膜内在蛋白，其亲水性 C 末端突出到基质中。 Cox25 是包含新合成的 Cox1、Ssc1、Mss51 和 Cox14 的复合物的重要组成部分。此外，还发现 Cox25 在不含 Mss51 的复合物中与 Shy1 和 Cox5 相互作用。这些结果表明，一旦 Ssc1-Mss51 从 Cox1 稳定复合物中释放出来，Cox25 就会继续与 Cox14 和 Cox1 相互作用，以促进多亚基 COX 组装中间体的形成。
In the yeast Saccharomyces cerevisiae, mitochondrial cytochrome c oxidase (COX) biogenesis is translationally regulated. Mss51, a specific COX1 mRNA translational activator and Cox1 chaperone, drives the regulatory mechanism. During translation and post-translationally, newly synthesized Cox1 physically interacts with a complex of proteins involving Ssc1, Mss51, and Cox14, which eventually hand over Cox1 to the assembly pathway. This step is probably catalyzed by assembly chaperones such as Shy1 in a process coupled to the release of Ssc1-Mss51 from the complex. Impaired COX assembly results in the trapping of Mss51 in the complex, thus limiting its availability for COX1 mRNA translation. An exception is a null mutation in COX14 that does not affect Cox1 synthesis because the Mss51 trapping complexes become unstable, and Mss51 is readily available for translation. Here we present evidence showing that Cox25 is a new essential COX assembly factor that plays some roles similar to Cox14. A null mutation in COX25 by itself or in combination with other COX mutations does not affect Cox1 synthesis. Cox25 is an inner mitochondrial membrane intrinsic protein with a hydrophilic C terminus protruding into the matrix. Cox25 is an essential component of the complexes containing newly synthesized Cox1, Ssc1, Mss51, and Cox14. In addition, Cox25 is also found to interact with Shy1 and Cox5 in a complex that does not contain Mss51. These results suggest that once Ssc1-Mss51 are released from the Cox1 stabilization complex, Cox25 continues to interact with Cox14 and Cox1 to facilitate the formation of multisubunit COX assembly intermediates.