Difference between revisions of "Di 2011 EMBO J"
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{{Publication | {{Publication | ||
|title=Di Y, Holmes EJ, Butt A, Dawson K, Mironov A, Kotiadis VN, Gourlay CW, Jones N, Wilkinson CR (2011) H₂O₂ stress-specific regulation of S. pombe MAPK Sty1 by mitochondrial protein phosphatase Ptc4. EMBO J 31: 563-575. | |title=Di Y, Holmes EJ, Butt A, Dawson K, Mironov A, Kotiadis VN, Gourlay CW, Jones N, Wilkinson CR (2011) H₂O₂ stress-specific regulation of S. pombe MAPK Sty1 by mitochondrial protein phosphatase Ptc4. EMBO J 31: 563-575. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22139357 PMID: 22139357] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22139357 PMID: 22139357] | ||
|authors=Di Y, Holmes EJ, Butt A, Dawson K, Mironov A, Kotiadis VN, Gourlay CW, Jones N, Wilkinson CR | |authors=Di Y, Holmes EJ, Butt A, Dawson K, Mironov A, Kotiadis VN, Gourlay CW, Jones N, Wilkinson CR | ||
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|abstract=In fission yeast, the stress-activated MAP kinase, Sty1, is activated via phosphorylation upon exposure to stress and orchestrates an appropriate response. Its activity is attenuated by either serine/threonine PP2C or tyrosine phosphatases. Here, we found that the PP2C phosphatase, Ptc4, plays an important role in inactivating Sty1 specifically upon oxidative stress. Sty1 activity remains high in a ptc4 deletion mutant upon H(2)O(2) but not under other types of stress. Surprisingly, Ptc4 localizes to the mitochondria and is targeted there by an N-terminal mitochondrial targeting sequence (MTS), which is cleaved upon import. A fraction of Sty1 also localizes to the mitochondria suggesting that Ptc4 attenuates the activity of a mitochondrial pool of this MAPK. Cleavage of the Ptc4 MTS is greatly reduced specifically upon H(2)O(2), resulting in the full-length form of the phosphatase; this displays a stronger interaction with Sty1, thus suggesting a novel mechanism by which the negative regulation of MAPK signalling is controlled and providing an explanation for the oxidative stress-specific nature of the regulation of Sty1 by Ptc4. | |abstract=In fission yeast, the stress-activated MAP kinase, Sty1, is activated via phosphorylation upon exposure to stress and orchestrates an appropriate response. Its activity is attenuated by either serine/threonine PP2C or tyrosine phosphatases. Here, we found that the PP2C phosphatase, Ptc4, plays an important role in inactivating Sty1 specifically upon oxidative stress. Sty1 activity remains high in a ptc4 deletion mutant upon H(2)O(2) but not under other types of stress. Surprisingly, Ptc4 localizes to the mitochondria and is targeted there by an N-terminal mitochondrial targeting sequence (MTS), which is cleaved upon import. A fraction of Sty1 also localizes to the mitochondria suggesting that Ptc4 attenuates the activity of a mitochondrial pool of this MAPK. Cleavage of the Ptc4 MTS is greatly reduced specifically upon H(2)O(2), resulting in the full-length form of the phosphatase; this displays a stronger interaction with Sty1, thus suggesting a novel mechanism by which the negative regulation of MAPK signalling is controlled and providing an explanation for the oxidative stress-specific nature of the regulation of Sty1 by Ptc4. | ||
|keywords=oxidative stress, stress-activated MAP kinase Sty1, PP2C phosphatase Ptc4 | |keywords=oxidative stress, stress-activated MAP kinase Sty1, PP2C phosphatase Ptc4 | ||
|mipnetlab=UK Canterbury Gourlay CW, | |mipnetlab=UK Canterbury Gourlay CW, | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|injuries=RONS; Oxidative Stress, Genetic Defect; Knockdown; Overexpression | |injuries=RONS; Oxidative Stress, Genetic Defect; Knockdown; Overexpression | ||
|kinetics=z in prep | |kinetics=z in prep | ||
}} | }} | ||
Revision as of 23:54, 4 April 2012
| Di Y, Holmes EJ, Butt A, Dawson K, Mironov A, Kotiadis VN, Gourlay CW, Jones N, Wilkinson CR (2011) H₂O₂ stress-specific regulation of S. pombe MAPK Sty1 by mitochondrial protein phosphatase Ptc4. EMBO J 31: 563-575. |
Di Y, Holmes EJ, Butt A, Dawson K, Mironov A, Kotiadis VN, Gourlay CW, Jones N, Wilkinson CR (2011) EMBO J
Abstract: In fission yeast, the stress-activated MAP kinase, Sty1, is activated via phosphorylation upon exposure to stress and orchestrates an appropriate response. Its activity is attenuated by either serine/threonine PP2C or tyrosine phosphatases. Here, we found that the PP2C phosphatase, Ptc4, plays an important role in inactivating Sty1 specifically upon oxidative stress. Sty1 activity remains high in a ptc4 deletion mutant upon H(2)O(2) but not under other types of stress. Surprisingly, Ptc4 localizes to the mitochondria and is targeted there by an N-terminal mitochondrial targeting sequence (MTS), which is cleaved upon import. A fraction of Sty1 also localizes to the mitochondria suggesting that Ptc4 attenuates the activity of a mitochondrial pool of this MAPK. Cleavage of the Ptc4 MTS is greatly reduced specifically upon H(2)O(2), resulting in the full-length form of the phosphatase; this displays a stronger interaction with Sty1, thus suggesting a novel mechanism by which the negative regulation of MAPK signalling is controlled and providing an explanation for the oxidative stress-specific nature of the regulation of Sty1 by Ptc4. • Keywords: oxidative stress, stress-activated MAP kinase Sty1, PP2C phosphatase Ptc4
• O2k-Network Lab: UK Canterbury Gourlay CW
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.
HRR: Oxygraph-2k
