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UID:1041@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20220103T130000

DTEND;TZID=Asia/Jerusalem:20220103T140000

DTSTAMP:20220104T070153Z

URL:https://biology.technion.ac.il/en/seminars/dr-maya-maor-nof-department
 -of-genetics-stanford-university-school-of-medicine/

SUMMARY:Dr. Maya Maor-Nof\, Department of Genetics\, Stanford University Sc
 hool of Medicine [No Categories]
DESCRIPTION:Location:   \n Affiliation: \n Host:\n Title: The diverse cell
 ular and molecular mechanisms driving neuronal and axonal degenerationZoom
 : https://technion.zoom.us/j/98391777547Abstract: Aberrations in protein 
 folding\, processing and degradation are common features of neurodegenerat
 ive diseases\, resulting in their accumulation. Amyotrophic lateral sclero
 sis (ALS) and frontotemporal dementia(FTD) are two neurodegenerative disea
 ses that share genetic and neuropathological features. The most common gen
 etic cause of both ALS and FTD is a hexanucleotide repeat expansion in the
  C9orf72 gene. In both diseases aggregation of the protein TDP-43 is the m
 ajor pathological hallmark. How theC9orf72 hexanucleotide repeat expansion
  and the TDP-43 protein accumulations contribute to neurodegeneration is l
 argely unknown. To study the cellular mechanisms driving neurodegeneratio
 n\, I developed a platform to interrogate the chromatin accessibility land
 scape and transcriptional program within neurons in response to pathogenic
  protein accumulation. I provide evidence that neurons expressing the dipe
 ptide repeat protein poly(proline-arginine)\, translated from the C9orf72 
 nucleotide repeat expansion\, activate a highly specific transcriptional p
 rogram\, exemplified by a single transcription factor p53. Ablating p53 in
  mice completely rescued neurons from cell death and axonal degeneration a
 nd markedly increased survival in a C9orf72 mouse model. Furthermore\, p53
  reduction was sufficient to rescueC9orf72 ALS patient iPSC-derived motor 
 neurons from degeneration. Mechanistically\, p53 is stabilized\, binds to 
 DNA and activates a downstream transcriptional program\, including Puma\, 
 which drives neurodegeneration. These data demonstrate neurodegenerative m
 echanisms are dynamically regulated through transcription factor binding e
 vents controlling gene expression programs and provide a framework to appl
 y chromatin accessibility and transcription program profiles to neurodegen
 eration.Host: Prof. Benjamin Podbilewicz 

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