Howe G, Mets L, Merchant S
Department of Chemistry and Biochemistry, UCLA 90024-1569.
Mol Gen Genet. 1995 Jan 20;246(2):156-65. doi: 10.1007/BF00294678.
Chlamydomonas reinhardtii uses two c-type cytochromes for photosynthetic electron transfer: the thylakoid membrane-bound cytochrome f of the cytochrome b6f complex and the soluble cytochrome c6. Previously, a class of photosynthesis-minus, acetate-requiring mutants was identified which were deficient in both c-type cytochromes, and biochemical analyses of cytochrome c6 biosynthesis in these strains indicated that they were each blocked at the step of heme attachment to apocytochrome c6. In order to demonstrate that the deficiency in cytochrome f results from the same biochemical and genetic defect, cytochrome f biosynthesis was examined in the B6 mutant (a representative of this phenotypic class) and in spontaneous suppressor strains derived from B6. Pulse-radiolabeling experiments show that B6 synthesizes a form of cytochrome f that is rapidly degraded in vivo. This polypeptide is membrane associated and migrates with an electrophoretic mobility identical to that of standard apocytochrome f produced in vitro but slightly greater than that of standard holocytochrome f produced in vivo by wild-type cells. These findings suggest that the B6 strain is unable to convert apocytochrome f to holocytochrome f and that apocytochrome f is unstable in vivo. In the suppressed strains, accumulation of both holocytochrome f and holocytochrome c6 is restored. One suppressor mutation (strain B6R) displays uniparental inheritance whereas another (B6T3) displays Mendelian inheritance. In both cases, the three phenotypes, photosynthesis-plus, b6f+ and cyt c6+ co-segregate in genetic crosses. This study therefore confirms that the dual cyt b6f-/cytc6- deficiency in B6 results from a single mutation that affects a step in holocytochrome formation that is common to the biosynthetic pathways of both plastidic c-type cytochromes. The study also confirms that pre-apocytochrome f synthesis, processing and association with the membrane is not dependent on heme attachment. Synthesis of cytochrome f does, however, appear to be dependent on heme availability. In cells depleted of tetrapyrrole pathway intermediates by gabaculine treatment, cytochrome f synthesis was significantly reduced. Since gabaculine treatment did not affect the stability of cytochrome f nor the accumulation of cytochrome f-encoding transcripts, the reduction is attributed to post-transcriptional regulation of preapocytochrome f synthesis via a pathway that is sensitive to the availability of heme or a tetrapyrrole pathway intermediate.
莱茵衣藻利用两种c型细胞色素进行光合电子传递:细胞色素b6f复合物中与类囊体膜结合的细胞色素f和可溶性细胞色素c6。此前,已鉴定出一类光合作用缺陷、需要乙酸盐的突变体,它们在两种c型细胞色素中均有缺陷,对这些菌株中细胞色素c6生物合成的生化分析表明,它们在血红素与脱辅基细胞色素c6结合的步骤中均被阻断。为了证明细胞色素f的缺陷是由相同的生化和遗传缺陷引起的,对B6突变体(该表型类别的代表)和源自B6的自发抑制菌株中的细胞色素f生物合成进行了研究。脉冲放射性标记实验表明,B6合成了一种在体内迅速降解的细胞色素f形式。该多肽与膜相关,其电泳迁移率与体外产生的标准脱辅基细胞色素f相同,但略大于野生型细胞在体内产生的标准全细胞色素f。这些发现表明,B6菌株无法将脱辅基细胞色素f转化为全细胞色素f,并且脱辅基细胞色素f在体内不稳定。在抑制菌株中,全细胞色素f和全细胞色素c6的积累均得以恢复。一个抑制突变(B6R菌株)表现出单亲遗传,而另一个(B6T3)表现出孟德尔遗传。在这两种情况下,光合作用增强、b6f+和细胞色素c6+这三种表型在遗传杂交中共同分离。因此,这项研究证实,B6中细胞色素b6f-/细胞色素c6-的双重缺陷是由一个单一突变引起的,该突变影响了全细胞色素形成中的一个步骤,这是两种质体c型细胞色素生物合成途径共有的。该研究还证实,前脱辅基细胞色素f的合成、加工以及与膜的结合不依赖于血红素的附着。然而,细胞色素f的合成似乎依赖于血红素的可用性。在用加巴喷丁处理使四吡咯途径中间体耗尽的细胞中,细胞色素f的合成显著减少。由于加巴喷丁处理不影响细胞色素f的稳定性,也不影响细胞色素f编码转录本的积累,因此这种减少归因于通过对血红素或四吡咯途径中间体的可用性敏感的途径对前脱辅基细胞色素f合成的转录后调控。