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SUMMARY:NFYB-1 regulates mitochondrial function and longevity via lysosoma
 l prosaposin
DTSTART:20190619T103000
DTEND:20190619T113000
DTSTAMP:20260407T042205Z
UID:10d059b85505d509fd937a7070b1241c2efedcad7d6933e6ad72a3c3
CATEGORIES:Conferences - Seminars
DESCRIPTION:Rebecca George Tharyan\, Ph.D\, Molecular Genetics of Ageing (
 Antebi Lab)\, Max-Planck-Institut for Biology of Ageing\, Cologne\, Germa
 ny\nSEMINAR of the LAUSANNE INTEGRATIVE METABOLISM and NUTRITION ALLIANCE 
 (LIMNA)\n\nAbstract:\nMitochondrial activity is critical for cellular vita
 lity and organismal longevity\, yet underlying regulatory mechanisms in me
 tazoans remain elusive. To identify mitochondrial regulators\, we performe
 d an RNAi screen leveraging the remarkable mitochondrial changes in C. ele
 gans upon recovery from adult reproductive diapause. We discovered NFYB-1\
 , a subunit of the NF-Y transcriptional complex\, as a crucial regulator o
 f mitochondrial function. Loss of NFYB-1 leads to reduced mitochondrial ge
 ne expression\, mitochondrial fragmentation\, and abolition of longevity t
 riggered by mitochondrial impairment. Moreover\, NFYB-1 deletion disrupts 
 mitochondrial UPRmt factors and mitochondrial-to-cytosolic stress response
  (MCSR). Multi-omics analysis indicates that NFYB-1 serves as a potent rep
 ressor of several ER genes and the ER stress response\, as well as lysosom
 al prosaposin. Downstream of NFYB-1\, limiting prosaposin expression alter
 s ceramide and cardiolipin pools\, restores mitochondrial fusion\, gene ex
 pression and longevity. Thus\, the NFYB-1/PSAP axis coordinates lysosomal 
 to mitochondrial communication to prolong life.\n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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