Evaluation of a novel method for measurement of intracellular calcium ion concentration in fission yeast

Ogata, Fumihiko; Satoh, Ryuji; Kita, Ayako; Sugiura, Reiko; Kawasaki, Naohito

doi:10.2131/jts.42.159

Cited by 1 publication

(1 citation statement)

References 37 publications

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“…Micafungin treatment significantly increased Pmk1 phosphorylation levels in the WT cells, and this induction of Pmk1 MAPK activation was impaired in atg1 deletion cells (Figure 1A). Since micafungin was shown to induce intracellular Ca 2+ concentrations [6,7], we next investigated if the addition of CaCl2 can affect Pmk1 MAPK activation. 0.2 M CaCl2 also stimulated Pmk1 MAPK activation, and the deletion of atg1 impaired the rise in the Pmk1 phosphorylation (Figure 1B).…”

Section: Identification Of Atg1 As An Activator Of Pmk1 Mapk Signalingmentioning

confidence: 99%

Atg1, a key regulator of autophagy, functions to promote MAPK activation and cell death upon calcium overload in fission yeast

Takasaki,

Utsumi,

Shimada

et al. 2023

Microb Cell

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Autophagy promotes or inhibits cell death depending on the environment and cell type. Our previous findings suggested that Atg1 is genetically involved in the regulation of Pmk1 MAPK in fission yeast. Here, we showed that Δatg1 displays lower levels of Pmk1 MAPK phosphorylation than did the wild-type (WT) cells upon treatment with a 1,3-β-D-glucan synthase inhibitor micafungin or CaCl2, both of which activate Pmk1. Moreover, the overproduction of Atg1, but not that of the kinase inactivating Atg1D193A activates Pmk1 without any extracellular stimuli, suggesting that Atg1 may promote Pmk1 MAPK signaling activation. Notably, the overproduction of Atg1 induces a toxic effect on the growth of WT cells and the deletion of Pmk1 failed to suppress the cell death induced by Atg1, indicating that the Atg1-mediated cell death requires additional mechanism(s) other than Pmk1 activation. Moreover, atg1 gene deletion induces tolerance to micafungin and CaCl2, whereas pmk1 deletion induces severe sensitivities to these compounds. The Δatg1Δpmk1 double mutants display intermediate sensitivities to these compounds, showing that atg1 deletion partly suppressed growth inhibition induced by Δpmk1. Thus, Atg1 may act to promote cell death upon micafungin and CaCl2 stimuli regardless of Pmk1 MAPK activity. Since micafungin and CaCl2 are intracellular calcium inducers, our data reveal a novel role of the autophagy regulator Atg1 to induce cell death upon calcium overload independent of its role in Pmk1 MAPK activation.

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Section: Identification Of Atg1 As An Activator Of Pmk1 Mapk Signalingmentioning

confidence: 99%

Atg1, a key regulator of autophagy, functions to promote MAPK activation and cell death upon calcium overload in fission yeast

Takasaki,

Utsumi,

Shimada

et al. 2023

Microb Cell

Self Cite

View full text Add to dashboard Cite

show abstract

Evaluation of a novel method for measurement of intracellular calcium ion concentration in fission yeast

Cited by 1 publication

References 37 publications

Atg1, a key regulator of autophagy, functions to promote MAPK activation and cell death upon calcium overload in fission yeast

Atg1, a key regulator of autophagy, functions to promote MAPK activation and cell death upon calcium overload in fission yeast

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