Activity-induced diffusion recovery in crowded colloidal suspensions.

We show that the forces generated by active enzyme molecules are strong enough to influence the dynamics of their surroundings under artificial crowded environments. We measured the behavior of polymer microparticles in a quasi-two-dimensional system under aqueous environment, at various area fraction values of particles. In the presence of enzymatic activity, not only was the diffusion of the suspended particles enhanced at shorter time-scales, but the system also showed a transition from subdiffusive to diffusive dynamics at longer time-scale limits. Similar observations were also recorded with enzyme-functionalized microparticles. Brownian dynamics simulations have been performed to support the experimental observations.

Electrochemical Energy Harvesting Using Microbial Active Matter.

With the continuous growth in world population and economy, the global energy demand is increasing rapidly. Given that non-renewable energy sources will eventually deplete, there is increasing need for clean, alternative renewable energy sources, which will be inexpensive and involve minimum risk of environmental pollution. In this paper, harnessing the activity of cupric reductase NDH-2 enzyme present in Escherichia coli bacterial cells, we demonstrate a simple and efficient energy harvesting strategy within an electrochemical chamber without the requirement of any external fuels or force fields. The transduction of energy has been demonstrated with various strains of E. coli, indicating that this strategy could, in principle, be applicable for other microbial catalytic systems. We offer a simple mechanism of the energy transduction process considering the bacterial enzyme-mediated redox reaction occurring over the working electrode of the electrochemical cell. Also, the amount of energy generated has been found to be depending on the motility of bacteria within the experimental chamber, suggesting possible opportunities for developing microbial motility-controlled small scale power generators. Finally, we show that the Faradaic electrochemical energy harvested is large enough to power a commercial light emitting diode connected to an amplifier circuit. We expect the present study to generate sufficient interest within soft condensed matter and biophysics communities, and offer useful platforms for controlled energy generation at the small scales.

Active matter dynamics in confined microfluidic environments.

The field of active matter is a nascent area of research in soft condensed matter physics, which is drawing on the expertise of researchers from diverse disciplines. Small scale active particles-both inorganic and biological-display non-trivial emergent dynamics and interactions that could help us understand complex biological processes and phenomena. Recently, using microfluidic technologies, several research groups have performed important experimental and theoretical studies to understand the behavior of self-propelled particles and molecular active matter within confined environments-to glean a fundamental understanding of the cellular processes occurring under ultra-low Reynolds number conditions. In this chapter, we would like to review applications of microfluidics in active matter research, highlighting a few important theoretical and experimental investigations. We will conclude the discussion with a note on the future of this field mentioning a few open questions that are at the forefront of our minds.

Cigarette smoke affects ESCRT-mediated vacuolar activity in Saccharomyces cerevisiae.

Cigarette smoking is a risk factor for developing chronic obstructive pulmonary disease and protein aggresome formation is considered to be a hallmark event for the disease. Since dysfunction of lysosome-mediated protein degradation leads to enhanced accumulation of misfolded proteins and subsequent aggresome formation, we examined the effect of cigarette smoke extract (CSE) on ESCRT-mediated sorting in S. cerevisiae as this process is necessary for the functioning of the vacuole, the lysosomal equivalent in yeast. An operational ESCRT pathway is essential for ion homeostasis and our observation that exposure to CSE caused increased sensitivity to LiCl indicated CSE-induced impairment of ESCRT function. To confirm the inhibition of ESCRT function, the targeting of carboxypeptidase S (CPS), which reaches the vacuole lumen via the ESCRT pathway, was examined. Treatment with CSE resulted in the mislocalization of GFP-tagged CPS to the vacuolar membrane, instead of the vacuolar lumen, confirming defective functioning of the ESCRT machinery in CSE-treated cells. Further analysis revealed that CSE-treatment inhibited the recruitment of the ESCRT-0 component, Vps27, to the endosome surface, which is a key event is for the functioning of the ESCRT pathway. This lack of endosomal recruitment of Vps27 most likely results from a depletion of the endosomally-enriched lipid, phosphatidylinositol 3-phosphate (PI3-P), which is the target of Vps27. This is supported by our observation that the presence of excess leucine, a known activator of the lipid kinase responsible for the generation of PI3-P, Vps34, in the medium can rescue the CSE-induced ESCRT misfunctioning. Thus, the current study provides an insight into CSE-induced aggresome formation as it documents that CSE treatment compromises vacuolar degradation due to an impairment of the ESCRT pathway, which likely stems from the inhibition of Vps34. It also indicates that leucine has the potential to attenuate the CSE-induced accumulation of misfolded proteins.

Leucine and its transporter provide protection against cigarette smoke-induced cell death: A potential therapy for emphysema.

Cigarette smoke (CS) is a major risk factor for emphysematous changes in the lungs and the underlying mechanism involves CS-induced cell death. In the present study we investigated the ability of nutrients to rescue CS-induced cell death. We observed that pre-treatment with excess leucine can partially rescue CS extract-induced cell death in Saccharomyces cerevisiae and alveolar epithelial A549 cells. Excess dietary leucine was also effective in alleviating effects of CS in guinea pig lungs. Further investigation to understand the underlying mechanism showed that CS exposure causes downregulation of leucine transporter that results in inactivation of mTOR, which is a positive regulator of protein synthesis and cell proliferation. Notably, leucine supplemented diet ameliorated even existing CS-induced emphysematous changes in guinea pig lung, a condition hitherto thought to be irreversible. Thus the current study documents a new mechanism by which CS affects cellular physiology wherein leucine transporter is a key target.