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SUMMARY:Babraham Distinguished Lecture - Endoplasmic reticulum turnover vi
 a selective autophagy - Prof. Ivan Dikic\; Director of the Institute of Bi
 ochemistry II (IBC2)\, Goethe University\, Frankfurt\, Germany
DTSTART:20181121T140000Z
DTEND:20181121T150000Z
UID:TALK99523@talks.cam.ac.uk
CONTACT:Bobbie Claxton
DESCRIPTION:The endoplasmic reticulum (ER) is the largest intracellular en
 domembrane system enabling synthesis and transport of cellular components.
  Constant ER turnover is needed to meet different cellular requirements an
 d autophagy plays an important role in this process. In mammalian cells th
 e ER is degraded via a selective autophagy pathway (called ER-phagy)\, med
 iated by specific ER-resident proteins that interacts with LC3\, via conse
 rved LC3-interacting region (LIR). Reticulon-type protein FAM134B is respo
 nsible for the turnover of ER sheets as its overexpression stimulates ER f
 ragmentation and delivery to lysosomes via the autophagy pathway. Converse
 ly\, blockade of autophagy or depletion of FAM134B triggers a marked incre
 ase in the ER volume. Mutations of FAM134B in humans are unable to act as 
 ER-phagy receptors and cause sensory neurodegeneration. We have recently i
 dentified full length reticulon 3 (RTN3) as a specific receptor for the de
 gradation of ER tubules. The major questions we are exploring at the momen
 t deal with the action of reticulone domains in banding the membranes and 
 the regulatory mechanisms of a family of co-receptors that assist FAM134B 
 or RTN3 proteins in selecting the appropriate cargoes during the ER-phagy 
 process. Taken together\, ER-phagy possesses the potential to remodel or r
 ebalance the entire ER network and – given the physical and functional c
 onnection of ER to other organelles inside the cell – ER-phagy might als
 o impact the function of other organelles as well.
LOCATION:Babraham - The Cambridge Building\; Petersfield Lecture Theatre
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