Petra Levin

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Microbiologist, mom, runner with delusions of completing a marathon. This Week in Microbiology co-host (https://www.microbe.tv/twim/). Website: https://sites.wustl.edu/levinlab/. Views my own.

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Nominate them for the TOP prize in prokaryotic molecular biology, the Nat L. Sternberg Award!

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Sternberg Thesis Prize | Molecular Genetics of Bacteria and Phages Meeting

And 3. Perhaps most importantly, even under “steady state” conditions” there is a large (3X ish) variation in single cell growth rate (i.e. not really steady-state) and a wide variation in multifork replication frequency. I.e. all cells are not the same.

Based on population data Cooper and Helmstetter postulated that there are 2 growth regimes: slow & fast.

In the slow regime, the initiation & elongation phases of DNA replication & division are pegged to mass doubling time (MDT).

In the fast regime, C-period, the time required to complete a round of replication becomes fixed. This is a problem when C-period > MDT. To deal with this, C & H proposed cells start new rounds of replication prior to finishing old ones—>multifork replication.

Population-based data washes out all this variation, which leads to models that do not reflect what is happing inside individual cells. This is obviously a problem if you are a molecular biologist whose job description is to try and understand what is happening inside cells.
Rather than double in mass each generation, bacteria add the same amount of material. This phenomenon, known as adder, ensure that population size is maintained despite a high degree of stochasticity in size at birth (From Taheri et al, 2015)