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Gumeni 2017 Abstract MITOEAGLE Barcelona - Revision history
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Nirschl Lisa at 12:37, 12 January 2018
2018-01-12T12:37:35Z
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Impact of mitochondrial dynamics on the proteostasis network and longevity in ''Drosophila melanogaster''</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Impact of mitochondrial dynamics on the proteostasis network and longevity in ''Drosophila melanogaster''</div></td></tr>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|year=2017</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|year=2017</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|event=<del style="font-weight: bold; text-decoration: none;">MITOEAGLE </del>Barcelona 2017</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|event=<ins style="font-weight: bold; text-decoration: none;">MitoEAGLE </ins>Barcelona 2017</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Mitochondria are essential organelles for cell function as they provide metabolites and energy [1]. They are highly dynamic organelles that undergo continuous cycles of fusion and fission to mix and distribute their contents [1]. These processes depend on the function of four conserved GTPases, the mitofusins Mfn1 and Mfn2 along with Optic Atrophy 1 (OPA1) which are implicated in fusion, as well as the dynamin-related protein 1 (Drp1) that is involved in fission[1]. Beyond the organelle dynamics, the constant interaction with the ubiquitin-proteasome-system (UPS) has become an emerging aspect of healthy mitochondria [2]. Mitochondrial dysfunction and impairment of UPS have been described as two hallmarks of ageing and they are implicated in many age-related diseases [3,4]. Herein, we present our analyses of the implication of mitochondrial dynamics in the molecular processes of ageing and their functional cross talk with the UPS and the autophagy-lysosome systems. Our ''in vivo'' studies in ''Drosophila'' have shown that impairment of fusion decreased muscle strength in flies and accelerated ageing. Alterations in mitochondrial dynamics impact on proteasome functionality, increased ROS levels and activated lysosomal cathepsins. We further found that loss of Opa1 in flies caused sterility, increased sensitivity to CO<sub>2</sub> exposure and reduction of lifespan. Interestingly, loss of proteasome in Opa1 RNAi flies enhanced these toxic and deleterious effects, underlying the role of proteasome in alleviating the impact of loss of mitostasis. Our findings suggest the existence of extensive cross-talk and functional wiring between mitostatic and proteostatic modules; this cross talk is likely operating through a circuit of sensors that modulate proteolytic machineries in case of mitostasis disruption.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Mitochondria are essential organelles for cell function as they provide metabolites and energy [1]. They are highly dynamic organelles that undergo continuous cycles of fusion and fission to mix and distribute their contents [1]. These processes depend on the function of four conserved GTPases, the mitofusins Mfn1 and Mfn2 along with Optic Atrophy 1 (OPA1) which are implicated in fusion, as well as the dynamin-related protein 1 (Drp1) that is involved in fission[1]. Beyond the organelle dynamics, the constant interaction with the ubiquitin-proteasome-system (UPS) has become an emerging aspect of healthy mitochondria [2]. Mitochondrial dysfunction and impairment of UPS have been described as two hallmarks of ageing and they are implicated in many age-related diseases [3,4]. Herein, we present our analyses of the implication of mitochondrial dynamics in the molecular processes of ageing and their functional cross talk with the UPS and the autophagy-lysosome systems. Our ''in vivo'' studies in ''Drosophila'' have shown that impairment of fusion decreased muscle strength in flies and accelerated ageing. Alterations in mitochondrial dynamics impact on proteasome functionality, increased ROS levels and activated lysosomal cathepsins. We further found that loss of Opa1 in flies caused sterility, increased sensitivity to CO<sub>2</sub> exposure and reduction of lifespan. Interestingly, loss of proteasome in Opa1 RNAi flies enhanced these toxic and deleterious effects, underlying the role of proteasome in alleviating the impact of loss of mitostasis. Our findings suggest the existence of extensive cross-talk and functional wiring between mitostatic and proteostatic modules; this cross talk is likely operating through a circuit of sensors that modulate proteolytic machineries in case of mitostasis disruption.</div></td></tr>
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Nirschl Lisa
https://wiki.oroboros.at/index.php?title=Gumeni_2017_Abstract_MITOEAGLE_Barcelona&diff=132467&oldid=prev
Gnaiger Erich at 12:14, 19 March 2017
2017-03-19T12:14:23Z
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|organism=Drosophila</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|organism=Drosophila</div></td></tr>
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Gnaiger Erich
https://wiki.oroboros.at/index.php?title=Gumeni_2017_Abstract_MITOEAGLE_Barcelona&diff=132379&oldid=prev
Kandolf Georg at 08:43, 17 March 2017
2017-03-17T08:43:16Z
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 08:43, 17 March 2017</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Abstract</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{Abstract</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|title=[[File:MITOEAGLE-representation.jpg|left|60px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|title=[[File:MITOEAGLE-representation.jpg|left|60px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Impact of mitochondrial dynamics on the proteostasis network and longevity in ''Drosophila melanogaster''</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|info=[[MITOEAGLE]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|info=[[MITOEAGLE]]</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>|authors=</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>|authors=<ins style="font-weight: bold; text-decoration: none;">Gumeni S, Evangelakou Z, Tsakiri EN, Debattisti V, Papassideri IS, Scorrano L, Trougakos IP</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|year=2017</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|year=2017</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|event=MITOEAGLE Barcelona 2017</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|event=MITOEAGLE Barcelona 2017</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]</div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">Mitochondria are essential organelles for cell function as they provide metabolites and energy [1]. They are highly dynamic organelles that undergo continuous cycles of fusion and fission to mix and distribute their contents [1]. These processes depend on the function of four conserved GTPases, the mitofusins Mfn1 and Mfn2 along with Optic Atrophy 1 (OPA1) which are implicated in fusion, as well as the dynamin-related protein 1 (Drp1) that is involved in fission[1]. Beyond the organelle dynamics, the constant interaction with the ubiquitin-proteasome-system (UPS) has become an emerging aspect of healthy mitochondria [2]. Mitochondrial dysfunction and impairment of UPS have been described as two hallmarks of ageing and they are implicated in many age-related diseases [3,4]. Herein, we present our analyses of the implication of mitochondrial dynamics in the molecular processes of ageing and their functional cross talk with the UPS and the autophagy-lysosome systems. Our ''in vivo'' studies in ''Drosophila'' have shown that impairment of fusion decreased muscle strength in flies and accelerated ageing. Alterations in mitochondrial dynamics impact on proteasome functionality, increased ROS levels and activated lysosomal cathepsins. We further found that loss of Opa1 in flies caused sterility, increased sensitivity to CO<sub>2</sub> exposure and reduction of lifespan. Interestingly, loss of proteasome in Opa1 RNAi flies enhanced these toxic and deleterious effects, underlying the role of proteasome in alleviating the impact of loss of mitostasis. Our findings suggest the existence of extensive cross-talk and functional wiring between mitostatic and proteostatic modules; this cross talk is likely operating through a circuit of sensors that modulate proteolytic machineries in case of mitostasis disruption.</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|editor=[[Kandolf G]],</ins></div></td></tr>
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<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">{{Labeling</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|area=mt-Structure;fission;fusion</ins></div></td></tr>
<tr><td colspan="2"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">|organism=Drosophila</ins></div></td></tr>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Affiliations ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Affiliations ==</div></td></tr>
</table>
Kandolf Georg
https://wiki.oroboros.at/index.php?title=Gumeni_2017_Abstract_MITOEAGLE_Barcelona&diff=132371&oldid=prev
Kandolf Georg: Created page with "{{Abstract |title=COST Action MITOEAGLE |info=MITOEAGLE |authors= |year=..."
2017-03-17T08:28:05Z
<p>Created page with "{{Abstract |title=<a href="/index.php/File:MITOEAGLE-representation.jpg" title="File:MITOEAGLE-representation.jpg">left|60px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE</a> |info=<a href="/index.php/MITOEAGLE" class="mw-redirect" title="MITOEAGLE">MITOEAGLE</a> |authors= |year=..."</p>
<p><b>New page</b></p><div>{{Abstract<br />
|title=[[File:MITOEAGLE-representation.jpg|left|60px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]<br />
|info=[[MITOEAGLE]]<br />
|authors=<br />
|year=2017<br />
|event=MITOEAGLE Barcelona 2017<br />
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]<br />
}}<br />
== Affiliations ==<br />
:::: Gumeni S(1), Evangelakou Z(1), Tsakiri EN(1), Debattisti V(2), Papassideri IS(1), Scorrano L(2), Trougakos IP(1)<br />
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::::#Dept Cell Biology Biophysics, Fac Biol, National Kapodistrian Univ Athens, Greece <br />
::::#Dulbecco-Telethon Inst, Venetian Inst Molecular Medicine Dept Biol, Univ Padua, Italy<br />
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== References ==<br />
:::#Newmeyer DD, Ferguson-Miller S (2003) Mitochondria: releasing power for life and unleashing the machineries of death. Cell 112:481-90.<br />
:::#Gumeni S, Trougakos IP (2016) Cross talk of proteostasis and mitostasis in cellular homeodynamics, ageing, and disease. Oxid Med Cell Longev 2016:4587691.<br />
:::#Chan DC (2006) Mitochondria: dynamic organelles in disease, aging, and development. Cell 125:1241-52. <br />
:::#Koga H, Kaushik S, Cuervo AM (2011) Protein homeostasis and aging: The importance of exquisite quality control. Ageing Res Rev 2:205-15.</div>
Kandolf Georg