5th ASM Conference on Prokaryotic Cell Biology and DevelopmentJune 12-16, 2015Merck invites conference participants to join us on Monday, June 15, from 7:00 – 8:00 am for a sponsored breakfast and learn seminar entitled “Insights into Bacterial Growth: Case Studies Using the CellASIC® ONIX microfluidic platform”. This event will be held in the conference general session room, Independence Ballroom A. |
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Probing Mechanical Effects on Bacterial and Archaeal Growth
Using the CellASIC® ONIX Microfluidic Platform
Ethan Garner,Ph.D., Harvard University Speaker Bio:
Ethan became interested in self-organization during his Graduate work at UCSF with Dyche Mullins. Rather than studying eukaryotic actins, he studied bacterial polymers, and during his Ph.D. worked on plasmid segregating systems. In his postdoc, he learned how to examine bacterial polymers in vivo, working at Harvard with Tim Mitchison, Xiaowei Zhuang, and David Rudner. HIs lab at Harvard has been active since 2012.
Current Position:
Assistant Professor, Molecular and Cellular Biology. Harvard
Education:
PhD, 2008, Cell Biology, UCSF
Ethan Garner, Harvard University
Abstract:
To protect themselves from the environment, free living single celled organisms require a protective layer surrounding the cell. This protective coating can take various forms, from cross-linked peptidoglycan cell walls in gram positive bacteria, to tightly packed arrays of protein in the case of some archaea. These confining walls oppose the internal turgor pressures in within the cells. The encapsulating networks do not function alone, and these factors use binding to cations to modulate the structure and rigidity of the network. Our group has found that the shape, and growth pattern of both bacteria (Bacillus subtilis) and archaea (Halobacterium salinarum) can be modulated by the stiffness of the substrates on which they are grown, suggesting that there is feedback between the mechanics of the confining cell walls and their synthesis. Using the CellASIC® ONIX plates we are able to quickly modulate not only the induction of genes required for synthesis, but also add or deplete environmental factors that modulate cell wall rigidity, and then measure the resultant effect on cell shape. Furthermore, we can use the differential confinement in the Z direction conferred by these plates to test the feedback between cell wall synthesis and cell shape.
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For Whom The Cell Tolls
KC Huang, Ph.D.Speaker Bio:
KC Huang, Ph.D. (MIT) is an Assistant Professor of Bioengineering at Stanford University. Dr. Huang completed his postdoctoral studies with Dr. Ned Wingreen at Princeton University analyzing relationships among cell shape detection, determination, and maintenance in bacteria. The Huang group employs diverse interdisciplinary methods of inquiry to understand the interplay between intracellular organization and cellular geometry. His current interests include cell division, membrane organization, cell wall biogenesis, and collective motility of bacterial communities.
KC Huang, Stanford University
Abstract:
It has long been proposed that turgor pressure plays an essential role during bacterial growth by driving mechanical expansion of the cell wall. This hypothesis is based on analogy to plant cells, for which this mechanism has been established, and on experiments in which the growth rate of bacterial cultures was observed to decrease as the osmolarity of the growth medium was increased. To distinguish the effect of turgor pressure from pressure-independent effects that osmolarity might have on cell growth, we monitored the elongation of single Escherichia coli cells while rapidly changing the osmolarity of their media. By plasmolyzing cells, we found that cell-wall elastic strain did not scale with growth rate, suggesting that pressure does not drive cell-wall expansion. Furthermore, in response to hyper- and hypoosmotic shock, E. coli cells resumed their pre-shock growth rate and relaxed to their steady-state rate after several minutes, demonstrating that osmolarity modulates growth rate slowly, independently of pressure. Oscillatory hyperosmotic shock revealed that while plasmolysis slowed cell elongation, the cells nevertheless “stored” growth such that once turgor was re-established the cells elongated to the length that they would have attained had they never been plasmolyzed. In contrast, Bacillus subtilis cells exhibit highly regular growth oscillations in response to hypoosmotic shock that are dependent on peptidoglycan synthesis. The period of these oscillations scales linearly with the magnitude of the shock. By applying a simple mathematical theory to these data, we show that growth oscillations are initiated by mechanical-strain-induced growth arrest. This demonstrates that B. subtilis has developed an elegant system by which turgor pressure both up- and down-regulates the final steps of cell growth.
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