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UID:1117@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20220802T130000

DTEND;TZID=Asia/Jerusalem:20220802T140000

DTSTAMP:20220818T115705Z

URL:https://biology.technion.ac.il/en/seminars/phd-graduate-seminar-jessy-
 safieh/

SUMMARY:PhD Graduate Seminar-Jessy Safieh [No Categories]
DESCRIPTION:Location:   \n Affiliation: \n Host:\n &nbsp\;\n\nThe mechanist
 ic origin of p53 selectivity and functionalityOne of the master transcript
 ional regulation hubs of every human cell is the transcription factor (TF)
  p53 protein. p53 is activated in response to cellular stress\, and is inv
 olved in the regulation of many cellular outcomes. To initiate transcripti
 on of downstream genes\, p53 binds in a sequence-specific manner to many s
 ites on the genome\, called response elements (REs). Even after almost 40 
 years of intensive research in the field of p53\, the fundamental question
  concerning how p53 activates its p53-dependent genes in response to the s
 everity of the stress signal and consequently coordinates the functional o
 utcome in a timely manner is still poorly understood. In this research\, w
 e showed that p53-dependent functional outcome groups can be differentiate
 d by their RE flexibility. p53-dependent genes belonging to pathways activ
 ated early upon stress (e.g. DNA damage response) contain REs that are mor
 e flexible than REs of genes involved in pathways that are likely to be mo
 re strictly regulated\, or that should occur at late stages in the respons
 e to stress (e.g. intrinsic apoptosis\, p53 negative regulation). Moreover
 \, based on data of chosen REs\, genes that are part of outcome categories
  in which a response is needed immediately\, timewise\, have REs that are 
 capable of transactivating the genes at a faster rate and at low levels of
  p53\, because they are flexible. Thus\, the flexibility of p53 RE contrib
 utes to the time-wise expression of p53 target genes and thereby plays a k
 ey role in cell-faith decisions in the p53 circuity. In addition\, we have
  indications\, using SELEX-seq technique\, that the mechanistic source of 
 selectivity in p53/REs interactions is encoded in the kinetic of p53/REs i
 nteractions\, rather than in the thermodynamics of the interaction. 

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