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Developmental Biology - Cell Size

What Controls Cell Size?

Biologists, engineers and physicists uncover origin of precise cell size...

Working with bacteria, a multidisciplinary team at the University of California San Diego has provided new insight into a longstanding question in science: What are the underlying mechanisms that control the size of cells?

Nearly five years ago a team led by Suckjoon Jun, a biophysicist at UC San Diego, discovered that cell size is controlled by a fundamental process known as "the adder," a function guiding cells to grow by a fixed added size from birth to 1st division. Yet mysteries remained about the mechanisms behind this process, leading scientists into a race to find the answer.

Publishing their work in the May 16 issue of Current Biology, Jun, lead authors Fangwei Si and Guillaume Le Treut and their colleagues described the inner workings of the adder.
The adder process, aka size homeostasis, requires two components:

(1) balance of ingredients specific to cell division
(2) enough proteins accumulated to begin process

"It is a very robust mechanism because each cell is guaranteed to reach its target cell size whether born large or small. The bottom line is that we found the adder is exclusively determined by some key proteins involved in cell division."

Suckjoon Jun PhD, Associate Professor, Division of Biological Science's, Molecular Biology and Division of Physical Sciences', Department of Physics, University of California San Diego, USA.

Although researchers discovered the mechanisms in bacteria Escherichia coli (E. coli) and Bacillus subtilis (B. subtilis), they believe the process is applicable across many life forms. Jun adds that the research team, made up of biologists, physicists and engineers, cracked the adder case after years of attempting an array of investigative methods and experimental approaches.

He continues: "Cell size homeostasis is a fundamental biological question and to our knowledge this is the first time we finally understand its mechanistic origin. We would not have been able to solve this with pure physics or pure biology. It was a very multi-disciplinary approach." They are now investigating whether the quantitative and mechanistic framework underlying adder applies to other models such as yeast and cancer cells.

• The adder requires accumulation of division proteins to a threshold for division
• The adder requires constant production of division proteins during cell elongation
• In E. coli and B. subtilis, initiation and division are independently controlled
• In E. coli and B. subtilis, cell division exclusively drives size homeostasis

Evolutionarily divergent bacteria share a common phenomenological strategy for cell-size homeostasis under steady-state conditions. In the presence of inherent physiological stochasticity, cells following this “adder” principle gradually return to their steady-state size by adding a constant volume between birth and division, regardless of their size at birth. However, the mechanism of the adder has been unknown despite intense efforts. In this work, we show that the adder is a direct consequence of two general processes in biology: (1) threshold—accumulation of initiators and precursors required for cell division to a respective fixed number—and (2) balanced biosynthesis—maintenance of their production proportional to volume growth. This mechanism is naturally robust to static growth inhibition but also allows us to “reprogram” cell-size homeostasis in a quantitatively predictive manner in both Gram-negative Escherichia coli and Gram-positive Bacillus subtilis. By generating dynamic oscillations in the concentration of the division protein FtsZ, we were able to oscillate cell size at division and systematically break the adder. In contrast, periodic induction of replication initiator protein DnaA caused oscillations in cell size at initiation but did not alter division size or the adder. Finally, we were able to restore the adder phenotype in slow-growing E. coli, the only known steady-state growth condition wherein E. coli significantly deviates from the adder, by repressing active degradation of division proteins. Together, these results show that cell division and replication initiation are independently controlled at the gene-expression level and that division processes exclusively drive cell-size homeostasis in bacteria.

Fangwei Si, Guillaume Le Treut, John T. Sauls, Stephen Vadia, Petra Anne Levin and Suckjoon Jun.

The authors are deeply grateful to Willie Donachie for invaluable discussions while completing this work. They thank Dongyang Li, Rodrigo Reyes-Lamothe, Tsutomu Katayama, Anders Løbner-Olesen, Harold Erickson, William Margolin, and Paul Wiggins for providing the strains. This work was supported by the Paul G. Allen Family Foundation, Pew Charitable Trust, NSF CAREER grant MCB-1253843, and NIH grants R01 GM118565-01 (to S.J.) and R35-400 GM127331 (to P.A.L.).

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May 24 2019   Fetal Timeline   Maternal Timeline   News  

E. coli cells expressing fluorescent fusion proteins of the replisome in two colors. The replisome is a complex molecular machine that carries out replication of DNA - by first unwinding double stranded DNA into two single strands. Each of these single strands is now a new sequence of combined DNA.
CREDIT Jun Lab, UC San Diego.

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