Frequency modulation of the Min-protein oscillator by nucleoid-associated factors in Escherichia coli.

In E. coli, the Min-protein oscillator, together with the nucleoid occlusion (NO), destabilizes the Z-ring assembly away from the midcell to ensure faithful septation. These two inhibitory pathways are thought to be working independently for division site placement. Even though the Min-protein oscillator has been displayed by synthetic minimal systems, it is unclear the interplays of Min proteins and compartment geometry are sufficient to bolster oscillation stability in vivo. By probing if NO plays a role in the Min oscillation, we study the oscillation frequency in the anucleate and nucleoid-perturbed cells. Surprisingly, we found that the oscillation periods of the Min-protein oscillators were seriously deviated in the anucleate and nucleoid-perturbed cells, but the oscillation frequency either went up in the anucleate or down in the nucleoid-perturbed cells. Intriguingly, enhanced stability and reduced frequency were observed in the cells expressing the NO factor SlmA higher than the native level. Our results reveal an unanticipated role of the nucleoid in modulating the frequency and stability of Min-protein system. SlmA is indicated to facilitate such modulations, potentially via directly interacting with the Min-protein system. A fresh perspective is suggested that frequency modulation of Min-protein oscillator is mediated via the act of nucleoid-associated factors.

Morphological plasticity of bacteria-Open questions.

Morphological plasticity of bacteria is a cryptic phenomenon, by which bacteria acquire adaptive benefits for coping with changing environments. Some environmental cues were identified to induce morphological plasticity, but the underlying molecular mechanisms remain largely unknown. Physical and chemical factors causing morphological changes in bacteria have been investigated and mostly associated with potential pathways linked to the cell wall synthetic machinery. These include starvation, oxidative stresses, predation effectors, antimicrobial agents, temperature stresses, osmotic shock, and mechanical constraints. In an extreme scenario of morphological plasticity, bacteria can be induced to be shapeshifters when the cell walls are defective or deficient. They follow distinct developmental pathways and transform into assorted morphological variants, and most of them would eventually revert to typical cell morphology. It is suggested that phenotypic heterogeneity might play a functional role in the development of morphological diversity and/or plasticity within an isogenic population. Accordingly, phenotypic heterogeneity and inherited morphological plasticity are found to be survival strategies adopted by bacteria in response to environmental stresses. Here, microfluidic and nanofabrication technology is considered to provide versatile solutions to induce morphological plasticity, sort and isolate morphological variants, and perform single-cell analysis including transcriptional and epigenetic profiling. Questions such as how morphogenesis network is modulated or rewired (if epigenetic controls of cell morphogenesis apply) to induce bacterial morphological plasticity could be resolved with the aid of micro-nanofluidic platforms and optimization algorithms, such as feedback system control.

Bacteria under the physical constraints of periodic micro-nanofluidic junctions reveal morphological plasticity and dynamic shifting of Min patterns.

Morphological plasticity is an important survival strategy for bacteria adapting to stressful environments in response to new physical constraints. Here, we demonstrate Escherichia coli morphological plasticity can be induced by switching stress levels through the physical constraints of periodic micro-nanofluidic junctions. Moreover, the generation of diverse morphological aberrancies requires the intact functions of the divisome- and elongasome-directed pathways. It is also intriguing that the altered morphologies are developed in bacteria undergoing morphological reversion as stresses are removed. Cell filamentation underlies the most dominant morphological phenotypes, in which transitions between the novel pattern formations by the spatial regulators of the divisome, i.e., the Min system, are observed, suggesting their potential linkage during morphological reversion.

Epidermal growth factor inhibits amiloride-sensitive sodium absorption in renal collecting duct cells.

The effects of the ERK pathway on electrogenic transepithelial Na(+) absorption by renal collecting duct cells were determined. Approximately 90% of the unstimulated short-circuit current (15 +/- 1 microA/cm(2), n = 10) across conditionally immortalized murine collecting duct epithelial cells (mCT1) is amiloride sensitive and is likely mediated by apical epithelial Na(+) channels. Chronic exposure (24 h) of the epithelial monolayers to either EGF (50 ng/ml) or transforming growth factor-alpha (TGF-alpha; 20 ng/ml) reduced amiloride-sensitive short-circuit current by >60%. The inhibitory effect of EGF on Na(+) absorption was not due to inhibition of basolateral Na(+)-K(+)-ATPase, because the pump current elicited by permeabilization of apical membrane with nystatin was not reduced by EGF. Chronic exposure of the mCT1 cells to EGF (20 ng/ml, 24 h) elicited a 70-85% decrease in epithelial Na(+) channel subunit mRNA levels. Exposure of mCT1 cells to either EGF (20 ng/ml) or PMA (150 nM) induced rapid phosphorylation of p42/p44 (ERK1/2) and pretreatment of the monolayers with PD-98059 (an ERK kinase inhibitor; 30 microM) prevented phosphorylation of p42/p44. Similarly, pretreatment of mCT1 monolayers with PD-98059 prevented the EGF- and PMA-induced inhibition of amiloride-sensitive Na(+) absorption. The results of these studies demonstrate that amiloride-sensitive Na(+) absorption by renal collecting duct cells is regulated by the ERK pathway. This pathway may play a role in alterations in ion transport that occur in polycystic kidney disease.