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Difference between revisions of "Moisoi 2018 MiP2018a"

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{{Abstract
{{Abstract
|title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] Mitochondria-Nucleus Communication:
|title=[[Image:MoisoiN.jpg|left|90px|Nicoleta Moisoi]] Mitochondria-nucleus communication: Who talks first? Who talks louder?
Who talks First? Who Talks Louder?
|info=[[MiP2018]]
|info=[[MiP2018]]
|authors=Nicoleta Moisoi
|authors=Moisoi N
|year=2018
|year=2018
|event=MiP2018
|event=MiP2018
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]]
Mitochondrial dysfunction and DNA damage accumulation are recognised hallmarks of age related diseases. Mitochondrial dysfunction initiates protective signalling mechanisms coordinated at nuclear level particularly by modulating transcription of stress signalling factors. In turn, the cellular response to DNA lesions comprises a series of interconnected complex protective pathways, which require the energetic and metabolic support of the mitochondria. Here I will discuss how mitochondria-nucleus communication operates in physiologically relevant stress conditions to protect against neurodegeneration. Thus in mammalian cells and Drosophila subjected to both mitochondrial and genotoxic stress, mitochondrial activity slows down while maintaining the DNA integrity takes priority. Depending on the site of the initiating stress, mitochondria or the nucleus can take the lead in stress response initiation - ‘talks first’. In most situations the nucleus and its integrity appear to be a priority - ‘talks louder’. These communication phenomena have a protective role against neurodegenerative processes.
Mitochondrial dysfunction and DNA damage accumulation are recognised hallmarks of age related diseases. Mitochondrial dysfunction initiates protective signalling mechanisms coordinated at nuclear level particularly by modulating transcription of stress signalling factors. In turn, the cellular response to DNA lesions comprises a series of interconnected complex protective pathways, which require the energetic and metabolic support of the mitochondria. Here I will discuss how mitochondria-nucleus communication operates in physiologically relevant stress conditions to protect against neurodegeneration. Thus in mammalian cells and Drosophila subjected to both mitochondrial and genotoxic stress, mitochondrial activity slows down while maintaining the DNA integrity takes priority. Depending on the site of the initiating stress, mitochondria or the nucleus can take the lead in stress response initiation - ‘talks first’. In most situations the nucleus and its integrity appear to be a priority - ‘talks louder’. These communication phenomena have a protective role against neurodegenerative processes.
|editor=[[Plangger M]], [[Kandolf G]],
|editor=[[Plangger M]], [[Kandolf G]],
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{{Labeling
{{Labeling
|area=nDNA;cell genetics
|area=nDNA;cell genetics
|diseases=Aging;senescence
|diseases=Aging;senescence, Neurodegenerative
|organism=Other mammals, Drosophila
|organism=Other mammals, Drosophila
}}
}}
== Affiliations ==
== Affiliations ==
Nicoleta Moisoi
::::Leicester School Pharmacy, De Montfort Univ, United Kingdom. - [email protected]
 
Leicester School Pharmacy, De Montfort Univ, United Kingdom. - [email protected]

Latest revision as of 07:09, 13 September 2018

Nicoleta Moisoi
Mitochondria-nucleus communication: Who talks first? Who talks louder?

Link: MiP2018

Moisoi N (2018)

Event: MiP2018

COST Action MitoEAGLE

Mitochondrial dysfunction and DNA damage accumulation are recognised hallmarks of age related diseases. Mitochondrial dysfunction initiates protective signalling mechanisms coordinated at nuclear level particularly by modulating transcription of stress signalling factors. In turn, the cellular response to DNA lesions comprises a series of interconnected complex protective pathways, which require the energetic and metabolic support of the mitochondria. Here I will discuss how mitochondria-nucleus communication operates in physiologically relevant stress conditions to protect against neurodegeneration. Thus in mammalian cells and Drosophila subjected to both mitochondrial and genotoxic stress, mitochondrial activity slows down while maintaining the DNA integrity takes priority. Depending on the site of the initiating stress, mitochondria or the nucleus can take the lead in stress response initiation - ‘talks first’. In most situations the nucleus and its integrity appear to be a priority - ‘talks louder’. These communication phenomena have a protective role against neurodegenerative processes.


Bioblast editor: Plangger M, Kandolf G


Labels: MiParea: nDNA;cell genetics  Pathology: Aging;senescence, Neurodegenerative 

Organism: Other mammals, Drosophila 






Affiliations

Leicester School Pharmacy, De Montfort Univ, United Kingdom. - [email protected]