Leptospiral lipopolysaccharide mediated Hog1 phosphorylation in Saccharomyces cerevisiae directs activation of autophagy

Bothammal, Palanisamy; Prasad, Muthu; Muralitharan, Gangatharan; Natarajaseenivasan, Kalimuthusamy

doi:10.1016/j.micpath.2022.105840

Cited by 4 publications

(2 citation statements)

References 29 publications

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“…Prolonged exposure to CaCl 2 stress impairs mitochondrial function and triggers CN-dependent cell death (Figure 4, C-F). Mitochondrial dysfunction, as well as exposure to various environmental stressors, has been shown to increase intracellular reactive oxygen species (ROS) (Brennan and Schiestl, 1996; Davidson et al ., 1996; Granot et al ., 2003; Drakulic et al ., 2005; Du et al ., 2007; Dudgeon et al ., 2008; Yi et al ., 2018; Bothammal et al ., 2022; Trip et al ., 2022). To protect against ROS-induced damage to proteins, lipids, and nucleic acids, cells rely on the antioxidant glutathione (GSH) (Jamieson, 1998).…”

Section: Resultsmentioning

confidence: 99%

Calcineurin promotes adaptation to chronic stress through two distinct mechanisms

Flynn,

Harper,

et al. 2024

Preprint

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Adaptation to environmental stress requires coordination between stress-defense programs and cell cycle progression. The immediate response to many stressors has been well characterized, but how cells survive in challenging environments long-term is unknown. Here, we investigate the role of the stress-activated phosphatase calcineurin (CN) in adaptation to chronic CaCl2stress inSaccharomyces cerevisiae.We find that prolonged exposure to CaCl2impairs mitochondrial function and demonstrate that cells respond to this stressor using two CN-dependent mechanisms – one that requires the downstream transcription factor Crz1 and another that is Crz1-independent. Our data indicate that CN maintains cellular fitness by promoting cell cycle progression and preventing CaCl2-induced cell death. When Crz1 is present, transient CN activation suppresses cell death and promotes adaptation despite high levels of mitochondrial loss. However, in the absence of Crz1, prolonged activation of CN prevents mitochondrial loss and further cell death by upregulating glutathione (GSH) biosynthesis genes thereby mitigating damage from reactive oxygen species. These findings illustrate how cells maintain long-term fitness during chronic stress and suggest that CN promotes adaptation in challenging environments by multiple mechanisms.

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Section: Resultsmentioning

confidence: 99%

Calcineurin promotes adaptation to chronic stress through two distinct mechanisms

Flynn,

Harper,

et al. 2024

Preprint

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“…In Saccharomyces cerevisiae , PBS2 can activate HOG1 by phosphorylating specific Thr174 and Tyr176 residues in the HOG1 T-G-Y motif [ 33 ]. HOG1 phosphorylation leads to autophagy-related gene phosphorylation and activation, while loss of HOG1 leads to high levels of ROS production [ 34 ]. Therefore, HOG1 maintains intracellular ROS homeostasis and regulates autophagy.…”

Section: Discussionmentioning

confidence: 99%

Insights into the Global Transcriptome Response of Lentinula edodes Mycelia during Aging

Gao

Fan

Wei

et al. 2023

JoF

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The spawn of Lentinula edodes and other basidiomycete fungi tend to age with long-term culture. This causes heavy yield losses if aging spawn is used for propagation. In this study, we cultivated dikaryotic L. edodes mycelia in plates for 60 days to produce intrinsic aging phenotypes. We found that intracellular reactive oxygen species levels increased in contrast to mitochondrial depolarization and also observed greater DNA fragmentation with longer culture time. Transcriptome analysis of mycelia at different growth stages revealed pronounced expression differences between short- and long-term cultures. In particular, “phenylalanine, tyrosine, and tryptophan biosynthesis”, “mitophagy and autophagy”, “MAPK signaling pathway”, and “ABC transporter” were among the enriched terms in the mycelial aging process. Weighted correlation network analysis identified LeAtg8, LeHog1, LePbs2, and LemTOR as key genes during aging. Western blotting confirmed that LeATG8 and phosphorylated LeHOG1 protein levels were significantly upregulated in aging mycelia. Our combined analytical approach provides insights into the mechanisms that regulate mycelial aging, indicating that autophagy/mitophagy plays a major role in counteracting the effects of age on mycelial growth development.

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Calcineurin promotes adaptation to chronic stress through two distinct mechanisms

Flynn,

Harper,

et al. 2024

MBoC

View full text Add to dashboard Cite

Adaptation to environmental stress requires coordination between stress-defense programs and cell cycle progression. The immediate response to many stressors has been well characterized, but how cells survive in challenging environments long-term is unknown. Here, we investigate the role of the stress-activated phosphatase calcineurin (CN) in adaptation to chronic CaCl2 stress in Saccharomyces cerevisiae. We find that prolonged exposure to CaCl2 impairs mitochondrial function and demonstrate that cells respond to this stressor using two CN-dependent mechanisms – one that requires the downstream transcription factor Crz1 and another that is Crz1-independent. Our data indicate that CN maintains cellular fitness by promoting cell cycle progression and preventing CaCl2-induced cell death. When Crz1 is present, transient CN activation suppresses cell death and promotes adaptation despite high levels of mitochondrial loss. However, in the absence of Crz1, prolonged activation of CN prevents mitochondrial loss and further cell death by upregulating glutathione (GSH) biosynthesis genes thereby mitigating damage from reactive oxygen species. These findings illustrate how cells maintain long-term fitness during chronic stress and suggest that CN promotes adaptation in challenging environments by multiple mechanisms.

show abstract

Leptospiral lipopolysaccharide mediated Hog1 phosphorylation in Saccharomyces cerevisiae directs activation of autophagy

Cited by 4 publications

References 29 publications

Calcineurin promotes adaptation to chronic stress through two distinct mechanisms

Calcineurin promotes adaptation to chronic stress through two distinct mechanisms

Insights into the Global Transcriptome Response of Lentinula edodes Mycelia during Aging

Calcineurin promotes adaptation to chronic stress through two distinct mechanisms

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