The disulphide cleavage derivative (C42-4) of 11′-deoxyverticillin A (C42) fails to induce apoptosis and genomic instability in HeLa cells

Hou, Bolin; Yang, Huaiyi; Li, Erwei; Jiang, Xuejun

doi:10.1080/21501203.2023.2248168

Cited by 1 publication

(1 citation statement)

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“…In line with these results, some evidence indicates that the presence of the oxidized disulfide bridge is crucial for gliotoxin entry into cells (Schrettl et al ., 2010). Furthermore, recently Hou et al (2023) showed that the reduction of the disulfide bridge of Deoxyverticillin A, another ETP metabolite produced by Clonostachys rogersoniana , fails to induce apoptosis and genomic instability in HeLa cells. These findings suggest that the disulfide bridge is essential for toxins belonging to the ETP group to enter the host cells and to react with proteins.…”

Section: Discussionmentioning

confidence: 99%

Unveiling the Virulence Mechanism ofLeptosphaeria maculansin theBrassica napusInteraction: The Key Role of Sirodesmin PL in Cell Death Induction

Pombo,

Rosli,

Maiale

et al. 2024

Preprint

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SummaryLeptosphaeria maculansis the causal agent of blackleg disease inBrassica napus, leading to substantial yield losses. Sirodesmin PL, the principal toxin produced byL. maculans, has been implicated in the infective process in plants. However, the precise molecular and physiological mechanisms governing its effects remain elusive. This study investigates the changes induced by Sirodesmin PL at the transcriptomic, physiological, and morphological levels inB. napuscotyledons. Sirodesmin PL treatment upregulates genes associated with plant defense processes, including response to chitin, sulfur compound biosynthesis, toxin metabolism, oxidative stress response, and jasmonic acid/ethylene synthesis and signaling. Validation of these transcriptomic changes is evidenced by several typical defense response processes, such as the accumulation of reactive oxygen species (ROS) and callose deposition. Concomitantly, oxidized Sirodesmin PL induces concentration- and exposure duration-dependent cell death. This cellular death is likely attributed to diminished activity of photosystem II and a reduction in the number of chloroplasts per cell. In agreement, a down-regulation of genes associated with the photosynthesis process is observed following Sirodesmin PL treatment. Thus, it is plausible thatL. maculansexploits Sirodesmin PL as a virulence factor to instigate cell death inB. napusduring its necrotrophic stage, favoring the infective process.HighlightSirodesmin PL, the principal toxin produced by Leptosphaeria maculans, induces cell death and defense mechanisms inBrassica napus, disrupting photosynthesis and facilitating the infective process

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Section: Discussionmentioning

confidence: 99%