Effective diffusion of a tracer in active bath: a path-integral approach

We investigate the effective diffusion of a tracer immersed in an active particle bath consisting of self-propelled particles. Utilising the Dean's method developed for the equilibrium bath and extending it to the nonequilibrium situation, we derive a generalized Langevin equation (GLE) for the tracer particle. The complex interactions between the tracer and bath particles are shown as a memory kernel term and two colored noise terms. To obtain the effective diffusivity of the tracer, we use path integral technique to calculate all necessary correlation functions. Calculations show the effective diffusion decreases with the persistent time of active force, and has rich behavior with number density of bath particles, depending on different activity. All theoretical results regarding the dependence of such diffusivity on bath parameters have been confirmed by direct computer simulation.Comment: 11pages, 4figure

Motility-induced phase separation is reentrant

Active systems made of self-propelled units are widespread in nature, and Active Brownian particles (ABPs) are one of the simplest such system The authors theoretically and numerically investigate the collective assembly of ABPs finding a new re-entrant phase that enables motility-induced phase separation, which is dependent solely on activity

Macrophage LMO7 deficiency facilitates inflammatory injury via metabolic-epigenetic reprogramming

Inflammatory bowel disease (IBD) is a formidable disease due to its complex pathogenesis. Macrophages, as a major immune cell population in IBD, are crucial for gut homeostasis. However, it is still unveiled how macrophages modulate IBD. Here, we found that LIM domain only 7 (LMO7) was downregulated in pro-inflammatory macrophages, and that LMO7 directly degraded 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) through K48-mediated ubiquitination in macrophages. As an enzyme that regulates glycolysis, PFKFB3 degradation led to the glycolytic process inhibition in macrophages, which in turn inhibited macrophage activation and ultimately attenuated murine colitis. Moreover, we demonstrated that PFKFB3 was required for histone demethylase Jumonji domain-containing protein 3 (JMJD3) expression, thereby inhibiting the protein level of trimethylation of histone H3 on lysine 27 (H3K27me3). Overall, our results indicated the LMO7/PFKFB3/JMJD3 axis is essential for modulating macrophage function and IBD pathogenesis. Targeting LMO7 or macrophage metabolism could potentially be an effective strategy for treating inflammatory diseases

New insights into the non-enzymatic function of HDAC6

Histone deacetylase 6 (HDAC6) is a class IIb histone deacetylase that contains two catalytic domains and a zinc-finger ubiquitin binding domain (ZnF-UBP) domain. The deacetylation function of HDAC6 has been extensively studied with common substrates such as α-tubulin, cortactin, and Hsp90. Apart from its deacetylase activity, HDAC6 ZnF-UBP binds to unanchored ubiquitin of specific sequences and serves as a carrier for transporting aggregated proteins. As a result, aggresomes are formed and protein degradation is facilitated by the autophagy-lysosome pathway. This HDAC6-dependent microtubule transport can be used by cells to assemble and activate inflammasomes, which play a critical role in immune regulation. Even viruses can benefit from the carrier of HDAC6 to assist in uncoating their surfaces during their infection cycle. However, HDAC6 is also capable of blocking virus invasion and replication in a non-enzymatic manner. Given these non-enzymatic functions, HDAC6 is closely associated with various diseases, including neurodegeneration, inflammasome-associated diseases, cancer, and viral infections. Small molecule inhibitors targeting the ubiquitin binding pocket of HDAC6 have been investigated. In this review, we focus on mechanisms in non-enzymatic functions of HDAC6 and discuss the rationality and prospects of therapeutic strategies by intervening the activation of HDAC6 ZnF-UBP in concrete diseases