Shen Qing, Samu Shihabdeen Madiha Natchi, Harata Ken, Naqvi Naweed I
Temasek Life Sciences Laboratory, 1 Research Link, Singapore, Singapore.
Department of Plant Life Science, Ryukoku University, Seta, Shiga, Japan.
Front Plant Sci. 2025 Jun 5;16:1576086. doi: 10.3389/fpls.2025.1576086. eCollection 2025.
Lipid peroxidation and iron-dependent cell death, Ferroptosis, in conidia plays a crucial role in ensuring proper infection structure formation and function in the rice blast fungus . However, the distribution of such important cation(s) in regulating precise developmental cell death remains unexplored. Here, we characterized the role of an iron-copper chaperone (Ict1) and a copper transporter (Ccc2) in growth and pathogenesis in . These Heavy-Metal-Associated domain containing proteins, particularly Ict1, were found to be important for Ferroptosis in rice blast conidia. Loss of Ict1 or Ccc2 induced significant viability in the three conidial cells in contrast to the sequential demise therein in the wild-type Furthermore, an increased accumulation of oxidized lipids at the plasma membrane was evident in wild-type, but not in the Δ or δ conidial cells undergoing pathogenic differentiation. The δ showed a lack of iron accumulation in conidia at the crucial time points, and such defects in cation homeostasis and cell death were suppressed significantly upon exogenous provision of ferric ions, and to a minor extent with copper. Interestingly, the δ conidia exhibited diminished mitophagy and in turn led to a profound increase in mitochondrial membrane potential and stability suggestive of enhanced organellar function that correlates negatively with conidial cell death via Ferroptosis. Lastly, Ict1-GFP was found to be predominantly cytosolic and excluded from the vacuoles during the vegetative and infection-related development in rice blast.
脂质过氧化和铁依赖性细胞死亡，即铁死亡，在稻瘟病菌的分生孢子中对于确保适当的感染结构形成和功能起着关键作用。然而，这种重要阳离子在调节精确的发育性细胞死亡中的分布仍未得到探索。在这里，我们表征了一种铁铜伴侣蛋白（Ict1）和一种铜转运蛋白（Ccc2）在稻瘟病菌生长和致病过程中的作用。发现这些含有重金属相关结构域的蛋白质，特别是Ict1，对稻瘟病菌分生孢子中的铁死亡很重要。与野生型分生孢子中三个分生孢子细胞依次死亡相反，Ict1或Ccc2的缺失导致分生孢子细胞显著存活。此外，野生型分生孢子细胞膜上氧化脂质的积累增加明显，但在进行致病分化的Δ或δ分生孢子细胞中则不明显。δ在关键时间点的分生孢子中显示铁积累缺乏，并且在外源提供铁离子后，这种阳离子稳态和细胞死亡的缺陷得到显著抑制，而铜的抑制作用较小。有趣的是，δ分生孢子表现出线粒体自噬减少，进而导致线粒体膜电位和稳定性显著增加，这表明细胞器功能增强，而这与通过铁死亡的分生孢子细胞死亡呈负相关。最后，在稻瘟病菌营养生长和与感染相关的发育过程中，发现Ict1-GFP主要位于细胞质中，并且被排除在液泡之外。
