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. 2021 Mar 4;17(3):e1009298.
doi: 10.1371/journal.ppat.1009298. eCollection 2021 Mar.

Ferroptosis and microbial pathogenesis

Qing Shen  1 , Naweed I Naqvi  1
Affiliations

Ferroptosis and microbial pathogenesis

Qing Shen et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Ferroptosis occurs sequentially in the 3-celled conidium and is essential for pathogenesis in Magnaporthe oryzae.
In M. oryzae, ferroptosis initiates first in the terminal conidial cell distal to the infection structure (appressorium). Within this cell, lipid peroxides are generated via the iron-dependent NADPH oxidase activity that accrues in the plasma membrane and trigger cell death as assessed by nuclear and cellular degradation. The reduced GSH-dependent GPX function acts as a negative regulator of such death-inducing lipid peroxides. Ferroptosis subsequently spreads to the middle and proximal conidial cells and the germ tube prior to appressorium maturation. The ferroptosis-enabling iron is acquired from intracellular source(s) in M. oryzae and is transported via autophagy, although the nature of such iron source is still unclear. The ferroptosis inhibitor Lip-1 is a lipophilic antioxidant that acts as a potent suppressor of conidial ferroptosis in rice blast. Nuclei and lipid peroxides are indicated as blue circles and orange dashes, respectively, in the conidial cell(s) undergoing ferroptosis. GPX, glutathione peroxidase; GSH, glutathione; Lip-1, liproxstatin-1; ROS, reactive oxygen species.
See this image and copyright information in PMC

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