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Iron deficiency leads to repression of a non-canonical methionine salvage pathway in Schizosaccharomyces pombe.
Molecular Microbiology ( IF 2.6 ) Pub Date : 2020-02-23 , DOI: 10.1111/mmi.14495 Ariane Brault 1 , Simon Labbé 1
Molecular Microbiology ( IF 2.6 ) Pub Date : 2020-02-23 , DOI: 10.1111/mmi.14495 Ariane Brault 1 , Simon Labbé 1
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The methionine salvage pathway (MSP) regenerates methionine from 5′‐methylthioadenosine (MTA). Aerobic MSP consists of six enzymatic steps. The mug14+ and adi1+ genes that are involved in the third and fifth steps of the pathway are repressed when Schizosaccharomyces pombe undergoes a transition from high‐ to low‐iron conditions. Results consistently show that methionine auxotrophic cells (met6Δ ) require iron for growth in the presence of MTA as the sole source of methionine. Inactivation of the iron‐using protein Adi1 leads to defects in the utilization of MTA. In the case of the third step of the pathway, co‐expression of two distinct proteins, Mta3 and Mde1, is required. These proteins are interdependent to rescue MTA‐dependent growth deficit of met6Δ cells. Coimmunoprecipitation experiments showed that Mta3 is a binding partner of Mde1. Meiotic met6Δ cells co‐expressing mta3+ and mde1+ or mta3+ and mug14+ produce comparable levels of spores in the presence of MTA, revealing that Mde1 and Mug14 share a common function when co‐expressed with Mta3 in sporulating cells. In sum, our findings unveil several novel features of MSP, especially with respect to its regulation by iron and the discovery of a non‐canonical third enzymatic step in the fission yeast.
中文翻译：
缺铁导致粟酒裂殖酵母中非规范的蛋氨酸抢救途径受到抑制。
蛋氨酸抢救途径（MSP）从5'-甲硫基腺苷（MTA）再生蛋氨酸。有氧MSP包含六个酶促步骤。的mug14 + 和ADI1 + 时所涉及的途径中的第三个和第五步的基因被抑制裂殖酵母经历从高至低铁条件的转变。结果一致表明，蛋氨酸营养缺陷型细胞（met6Δ）需要铁才能在MTA作为蛋氨酸唯一来源的情况下生长。铁蛋白Adi1的失活导致MTA利用方面的缺陷。在该途径的第三步中，需要同时表达两种不同的蛋白质Mta3和Mde1。这些蛋白质相互依赖，可以挽救MTA依赖的met6Δ细胞的生长缺陷。免疫共沉淀实验表明Mta3是Mde1的结合伴侣。共表达mta3 +和mde1 +或mta3 +和mug14 +的减数分裂met6Δ细胞 在MTA存在下可产生相当水平的孢子，这表明Mde1和Mug14在孢子形成细胞中与Mta3共表达时具有共同的功能。总而言之，我们的发现揭示了MSP的几个新颖特征，特别是在铁的调控下以及在裂变酵母中发现了非典型的第三酶促步骤。
更新日期：2020-02-23
中文翻译：
缺铁导致粟酒裂殖酵母中非规范的蛋氨酸抢救途径受到抑制。
蛋氨酸抢救途径（MSP）从5'-甲硫基腺苷（MTA）再生蛋氨酸。有氧MSP包含六个酶促步骤。的mug14 + 和ADI1 + 时所涉及的途径中的第三个和第五步的基因被抑制裂殖酵母经历从高至低铁条件的转变。结果一致表明，蛋氨酸营养缺陷型细胞（met6Δ）需要铁才能在MTA作为蛋氨酸唯一来源的情况下生长。铁蛋白Adi1的失活导致MTA利用方面的缺陷。在该途径的第三步中，需要同时表达两种不同的蛋白质Mta3和Mde1。这些蛋白质相互依赖，可以挽救MTA依赖的met6Δ细胞的生长缺陷。免疫共沉淀实验表明Mta3是Mde1的结合伴侣。共表达mta3 +和mde1 +或mta3 +和mug14 +的减数分裂met6Δ细胞 在MTA存在下可产生相当水平的孢子，这表明Mde1和Mug14在孢子形成细胞中与Mta3共表达时具有共同的功能。总而言之，我们的发现揭示了MSP的几个新颖特征，特别是在铁的调控下以及在裂变酵母中发现了非典型的第三酶促步骤。
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