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SUMMARY:Cytoskeleton club - Magda Magiera
DTSTART:20260109T100000Z
DTEND:20260109T113000Z
DTSTAMP:20261010T150200Z
UID:indico-event-29@indico.i2bc.paris-saclay.fr
DESCRIPTION:Speaker: Magda Magiera - Genome Integrity\, RNA and Cancer (UM
 R3348)\, Curie Institute\, Orsay\nTitle: Microtubule polyglutamylation is 
 a key player in neuronal homeostasis and causes neurodegeneration if dysre
 gulated\nAbstract: I will talk about tubulin polyglutamylation\, a posttra
 nslational modification of microtubules\, and its role in neuronal functio
 n and homeostasis. Microtubules are present in every eukaryotic cell where
  they exert a wide variety of functions. This functional diversity require
 s a continuous readjustment of microtubule functions\, especially in highl
 y differentiated\, complex and long-lived cells such as neurons. We have s
 hown that polyglutamylation\, a prominent tubulin modification of neuronal
  microtubules\, can cause neurodegeneration when upregulated\, both in hum
 ans and in a mouse model closely replicating the human disease. Moreover\,
  our recent results revealed that reduced levels of polyglutamylation also
  lead to degenerative phenotypes. Together these two findings highlight th
 e importance of tightly controlled levels of this modification for neurona
 l survival. On the cellular level\, polyglutamylation regulates axonal tra
 nsport: increased polyglutamylation down-regulates cargo traffic\, while r
 educed levels of this modification have an inverse effect. To decipher und
 erlying molecular mechanisms\, we developed a medium-throughput approach t
 o measure how polyglutamylation affects the interactions of a broad range 
 of microtubule-associated proteins\, which showed that neuronal MAPs are s
 ensitive to this modification. We are currently exploring the effects of t
 hese perturbations on cellular functions such as autophagy\, neuronal acti
 vity and other aspects of neuronal physiology. I will also discuss how pol
 yglutamylation\, by controlling the behaviour of the microtubule-associate
 d protein tau\, could be involved in human late-onset neurodegenerative di
 sorders. \n\nhttps://indico.i2bc.paris-saclay.fr/event/29/
LOCATION:B22-N0-001 - Salle de Conférences (I2BC CNRS Gif)
URL:https://indico.i2bc.paris-saclay.fr/event/29/
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