BEGIN:VCALENDAR VERSION:2.0 PRODID:icalendar-ruby CALSCALE:GREGORIAN METHOD:PUBLISH BEGIN:VTIMEZONE TZID:Europe/Vienna BEGIN:DAYLIGHT DTSTART:20200329T030000 TZOFFSETFROM:+0100 TZOFFSETTO:+0200 RRULE:FREQ=YEARLY;BYDAY=-1SU;BYMONTH=3 TZNAME:CEST END:DAYLIGHT BEGIN:STANDARD DTSTART:20201025T020000 TZOFFSETFROM:+0200 TZOFFSETTO:+0100 RRULE:FREQ=YEARLY;BYDAY=-1SU;BYMONTH=10 TZNAME:CET END:STANDARD END:VTIMEZONE BEGIN:VEVENT DTSTAMP:20260404T052400Z UID:1600351200@ist.ac.at DTSTART:20200917T160000 DTEND:20200917T170000 DESCRIPTION:Speaker: Angelika Amon\nhosted by Tom Henzinger and Anton Zeili nger\nAbstract: In collaboration with the Austrian Academy of Sciences\, i t is a pleasure to announce the fifth annual ÖAW-IST Austria Lecture.Pl ease note that this lecture will take place online on Zoom.  All registe red participants will receive a link to join the lecture within 24 hours b efore it begins.  To register\, please click on the button below.  Abst ract:Cellular senescence\, a condition where cells lose their ability to p roliferate and enter a permanent G1 arrest\, is thought to be a cause of o rganismal aging. Why senescent cells experience functional decline and los e their ability to proliferate is poorly understood. I will discuss our wo rk that could explain cellular senescence. We have known since Hayflick’ s seminal studies in the 1960s that senescent cells are exceedingly large but their DNA content does not increase. These old observations prompted u s to investigate whether a decrease in DNA:cytoplasm ratio causes senescen ce. We found this to be the case both in yeast and mammalian cells\; young cells grown large in the absence of a corresponding increase in DNA copy number exhibit many of the phenotypes observed in senescent cells. These o bservations lead us to propose a simple model of why eukaryotic cells sene sce: It has long been known that when cell cycle progression is halted\, c ells increase in size because cell growth is not tightly coupled to cell d ivision. As cells experience damage such as DNA damage cell cycle progress ion is halted to allow for the damage to be repaired before cell division resumes. During this transient arrest cell growth continues and cells incr ease in size without a corresponding increase in DNA copy number. As cells encounter frequent cellular damage over their lifetime\, cells eventually become too large leading to functional decline and senescence due to DNA becoming limiting. More recently we have begun to investigate whether mech anisms are in place to prevent excessive growth during cell cycle arrest. I will discuss these efforts and their implication for the development of anti-aging strategies.Authors: Jette Lengefeld\, Gabriel Neurohr\, Allegr a Terhorst and Angelika Amon (Koch Institute for Integrative Cancer Resea rch\, Howard Hughes Medical Institute\, Massachusetts Institute of Techn ology)Bio:Angelika Amon received her B.S. and Ph.D. from the University of Vienna. She completed a two-year post-doctoral fellowship with Ruth Lehma nn at the Whitehead Institute and was subsequently named a Whitehead Fello w for three years. In 1999\, she joined the MIT Koch Institute for Integra tive Cancer Research and the Department of Biology where she holds the Kat hleen and Curtis Marble Chair for Cancer Research. Dr. Amon’s honors inc lude the 2003 Alan T. Waterman Award\, the 2007 Paul Marks Prize\, the 200 8 National Academy of Sciences Molecular Biology Award\, the 2013 Ernst Ju ng Prize for Medicine\, the 2018 Breakthrough Prize in Life Science and th e 2019 Vilcek Prize in Biomedical Science. Dr. Amon is a Member of the How ard Hughes Medical Institute\, the National Academy of Sciences\, the Aust rian Academy of Science\, and a Foreign Associate to EMBO.At the Koch Inst itute Dr. Amon studies the molecular mechanisms that control cell growth a nd division. Dr. Amon also studies how errors in this process lead to dise ases such as cancer and Down Syndrome and how they impact the aging proces s. She uses the budding yeast S. cerevisiae as a model system to study the se questions and probes discoveries made in yeast in the mouse and human c ells. LOCATION:Online\, ISTA ORGANIZER:arinya.eller@ist.ac.at SUMMARY:Angelika Amon: [Online] Why big is bad: Decrease in DNA - cytoplasm ratio is a cause of senescence URL:https://talks-calendar.ista.ac.at/events/2840 END:VEVENT END:VCALENDAR