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UID:1038@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20220117T130000

DTEND;TZID=Asia/Jerusalem:20220117T140000

DTSTAMP:20220117T111604Z

URL:https://biology.technion.ac.il/en/seminars/dr-noa-lamm-shalem-sydney-m
 edical-school-sydney-university-childrens-medical-research-institute-sydne
 y/

SUMMARY:Dr. Noa Lamm-Shalem\, Sydney Medical School\, Sydney University. Ch
 ildren's Medical Research Institute\, Sydney [No Categories]
DESCRIPTION:Location:  In hybrid format: Auditorium + Zoom (see link below)
   \n Affiliation: \n Host:\n Title: Filamentous actin drives nuclear arch
 itectural changes to maintain genome stability\n\nZOOM:  https://technio
 n.zoom.us/j/91878900904\n\nAbstract: Cell proliferation requires efficien
 t and accurate DNA replication. The complexity of replication\, however\, 
 renders genome copying susceptible to endogenous and exogenous threats. An
 y process hindering replication is referred to as “replication stress\,
 ” and the cellular processes that countervail replication threats are th
 e “replication stress response”. Most of the genome instability that d
 rives oncogenesis results from replication stress\, and consequently\, can
 cer cells typically suffer from endogenous replication stress and are susc
 eptible to replication stress response challenges.\n\nActin is a cytoskele
 tal protein that polymerizes from monomeric to filamentous form(F-actin) t
 o provide cells with mechanical support\, transport pathways\, and a drivi
 ng force for movement. While actin is traditionally considered a cytoplasm
 ic protein\, nuclear actin polymerization was recently identified to contr
 ibute to various nuclear functions.\n\nI employed live-cell and super-reso
 lution imaging\, chromatin fiber analysis\, biochemistry\, and cell and mo
 lecular biology to discover a novel replication stress response pathway wh
 ere polymerization of nucleus-specific filamentous actin (F-actin) promote
 s replication stress repair. In this pathway\, nuclear F-actin cables incr
 ease nuclear volume and sphericity and enhance the mobility of replication
  stressed chromatin. This includes directed movement of stressed replicati
 on foci along F-actin towards the nuclear periphery where replication stre
 ssed loci interact with nuclear pore complexes to promote their repair. Th
 ese data substantially broaden our understanding of the nucleus as a dynam
 ic environment shaped by nuclear actin forces. This is a conceptual advanc
 e in nuclear biology only beginning to be explored.\n\nHost: Prof. Benjam
 in Podbilewicz 
LOCATION: In hybrid format: Auditorium + Zoom (see link below)

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