The decrotonylase FoSir5 facilitates mitochondrial metabolic state switching in conidial germination of Fusarium oxysporum.
The decrotonylase FoSir5 facilitates mitochondrial metabolic state switching in conidial germination of Fusarium oxysporum.
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DOI：
10.7554/elife.75583
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发表时间：
2021-12-20
期刊：
影响因子：
7.7
通讯作者：
Liang W
中科院分区：
文献类型：
--
作者：
Zhang N;Song L;Xu Y;Pei X;Luisi BF;Liang W
尖孢镰刀菌是最重要的病原真菌之一，具有广泛的植物和动物宿主。其感染周期的第一个关键步骤是分生孢子萌发，但支持这一过程的分子事件的信息有限。我们在这里表明，发芽是伴随着FoSir5，人类赖氨酸脱乙酰酶SIRT5的直系同源物的表达急剧下降。我们观察到，FoSir5 decrotonylates真菌丙酮酸脱氢酶复合物（FoDLAT）在K148的亚基，导致在线粒体中的复合物的活性的抑制。此外，FoSir 5使组蛋白H3K18去巴豆酰化，导致编码有氧呼吸途径的酶的转录物下调。因此，FoSir 5的活性协调不同细胞器中的调节，以通过呼吸引导代谢通量。由于ATP含量与真菌萌发呈正相关，我们推测FoSir5负调节F.尖孢菌通过其代谢影响。这些发现为FoSir5催化的脱巴豆基化的多方面作用提供了见解，该作用支持F.尖孢菌属
Fusarium oxysporum is one of the most important pathogenic fungi with a broad range of plant and animal hosts. The first key step of its infection cycle is conidial germination, but there is limited information available on the molecular events supporting this process. We show here that germination is accompanied by a sharp decrease in expression of FoSir5, an ortholog of the human lysine deacetylase SIRT5. We observe that FoSir5 decrotonylates a subunit of the fungal pyruvate dehydrogenase complex (FoDLAT) at K148, resulting in inhibition of the activity of the complex in mitochondria. Moreover, FoSir5 decrotonylates histone H3K18, leading to a downregulation of transcripts encoding enzymes of aerobic respiration pathways. Thus, the activity of FoSir5 coordinates regulation in different organelles to steer metabolic flux through respiration. As ATP content is positively related to fungal germination, we propose that FoSir5 negatively modulates conidial germination in F. oxysporum through its metabolic impact. These findings provide insights into the multifaceted roles of decrotonylation, catalyzed by FoSir5, that support conidial germination in F. oxysporum.