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Aging in Single-celled Organisms: from Bacteria to the Whole Tree of Life

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Category: Application Area Application Area: Cellular Aging

Date/Time: December 3, 2019 - December 5, 2019

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  • Jacopo Grilli (ICTP)

  • Chris Kempes (SFI)

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    Click each agenda item's title for more information.
    Monday, February 10, 2020
    8:30 am - 9:00 am Day 1 Continental Breakfast (outside SFI Collins Conference Room)
    9:00 am - 9:30 am Overview of the meeting - Jacopo Grilli (ICTP)
    9:30 am - 10:00 am More questions than answers: relations between quantittative physiology and aging in E. coli - Matteo Osella (Univ. Turin) Download Presentation
    10:45 am - 11:15 am Stochasticity, immortality, and mortality in E. coli - Lin Chao (UC San Diego)
    11:45 am - 12:15 pm Stochastic processes shape senescence, beyond genes, and environment - Uli Steiner (University of Southern Denmark)
    1:30 pm - 2:00 pm About time: Precision measurements and emergent simplicities in an individual bacterial cell's stochastic aging dynamics. - Srividya Iyer-Biswas (Purdue Univ./SFI)
    2:30 pm - 3:00 am All creatures fast and slow: senescence and longevity across the tree of life - Owen Jones (University of Southern Denmark)
    3:45 pm - 4:15 pm Toward a Molecular Understanding of Quiescence versus Senescence - Sabrina Spencer (CU Boulder)
    Tuesday, February 11, 2020
    9:15 am - 9:45 am The long and the short of it: mycobacterial aging, asymmetry, and stress tolerance - Bree Aldridge (Tufts Univ.)
    10:15 am - 10:45 am Systematic Physiology and Aging Across Diverse Organisms - Chris Kempes (SFI)
    11:30 am - 12:00 pm Time perception and the rate of cellular aging outside the human body: an energetic perspective - Martin Picard (Columbia University)
    1:30 pm - 2:00 am A time to sleep and a time to die - Geoffrey West (SFI)
    Wednesday, February 12, 2020
    9:00 am - 12:00 pm Discussion

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    Abstracts by Presenters

    Lin Chao (UC San Diego) - Stochasticity, immortality, and mortality in E. coli[edit source]

    Here we show that the bacterium Escherichia coli exhibits both lineage mortality and immortality.  The outcome depends on a whether a balance is achieved between damage accumulation and the asymmetric allocation of damage from mother to daughters. At low damage rates, both old and new daughters, which are allocated respectively more and less damage, generated immortal lineages that achieved stable growth rate equilibria. At high rates, mortality ensued because while the new daughter lineage persisted, the old daughter lineage stopped dividing.  The stoppage was found to result from an increase in the stochasticity of cell growth.

    Sabrina Spencer (CU Boulder) - Toward a Molecular Understanding of Quiescence versus Senescence[edit source]

    Cellular aging is often used synonymously with cellular senescence, a state of permanent cell-cycle exit associated with DNA damage and cytokine secretion. However, senescence is easily confused with quiescence, in large part due to lack of reliable markers.  We have found that the gold-standard senescence marker, senescence-associated beta-galactosidase activity, is unreliable in that it can stain strongly positive in cells that are actively dividing. We have also found that establishing a homogeneous population of senescent cells is quite difficult since many cells continue to cycle and out-proliferate senescent cells, despite the use of standard senescence-inducing treatments. Thus, the senescence field has a chicken/egg problem in that one cannot study senescence if no reliable markers exist to identify senescent cells, and one cannot develop a senescence marker without a truly senescent sample in hand. We are therefore developing a functional readout to identify cells that have not cycled in n days, where n is triggered and defined by the researcher and can be several months long. In this way, we can isolate a homogeneous senescent population that can be profiled and compared to quiescent cells to develop better markers for quiescence vs. senescence and to better study cellular aging.

    Post-meeting Reflection by Presenter

    Jacopo Grilli (ICTP) Link to the source page[edit source]


    Matteo Osella. Interesting idea of connecting laws of physiology (Hwa) with aging/senescence. Not trivial how to do that for single cells.

    Lin Chao. Aging and asymmetry in E. coli. Advantage of asymmetry is portfolio diversification. Somewhat optimal level of asymmetry emerges.

    Uli Steiner . Fitness as combination of fecundity and mortality. Death in the mother machine (surprisingly high): mother (early daugther) has an increased mortality rate with age, while her latest daughter has an approximately constant mortality rate. Idea: late daughter inherits the damage, while the mother was starting with minimal damage. No correlation between mother and late daughter lifespan.

    Sri Iyer-Biswas. Cool data on C crescentus and collapses. Interesting observation of memory of past conditions lasting for long time.

    Owen Jones. Senescence across the tree of life. Measure shape and pace (timescale)

    Sabrina Spencer.

    Bree Aldrige

    Chris Kempes

    Martin Picard

    Geoffrey West


    What is aging? Requires asymmetry in division and the ability to label individual with a "time stamp". In E. coli age of the pole, in mycobacteria cell wall. Senescence is the loss of function associated to aging. The question then is what is function. We have a bias for growth rate.

    It is very unclear to my whether asymmetry is adaptive or not. It is also unclear how to prove it.

    The other axis is memory. Memory (information) about the environment. Unclear how that is related with aging.

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    Post-meeting Reflection by Non-presenting Attendees

    Reference Materials by Presenting Attendees[edit source]

    Reference Materials by Non-presenting Attendees

    General Meeting Reference Material[edit source]