Ejima, H. | bioRxiv Science

bioRxiv2026

Metabolic reprogramming and stress mitigation of Chlamydomonas reinhardtii using protective metal-phenolic networks

Single-cell encapsulation is widely used in biotechnology to protect highly sensitive living cells from environmental stress. However, the impact of encapsulation on biological function and metabolism remains rarely explored despite its importance for understanding stress response and modulating the production of valuable metabolites. Herein, we show that coating individual cells with protective metal-phenolic networks not only improves survival against stress, but also modifies cellular metabolism. Importantly, this encapsulation technique induces a reversible state of quiescence, which enables accumulation of high-energy-density compounds through selective nutrient diffusion and the resulting carbon flux redistribution. Specifically, light exposure favors the accumulation of nearly eightfold higher starches, while incubation in darkness leads to twofold higher lipid accumulation compared to native cells. This metabolic engineering approach via individual cell encapsulation expands the cell editing toolbox and will facilitate applications in synthetic biology, bioengineering, and cell-based therapeutics. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=184 SRC="FIGDIR/small/711231v2_ufig1.gif" ALT="Figure 1"> View larger version (60K): org.highwire.dtl.DTLVardef@d27478org.highwire.dtl.DTLVardef@dc73baorg.highwire.dtl.DTLVardef@131dcaeorg.highwire.dtl.DTLVardef@8f3dc4_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

bioRxiv2024

Conditional knockout of Shank3 in the ventral CA1 by quantitative in vivo genome-editing impairs social memory

Individuals with autism spectrum disorder (ASD) have a higher prevalence of social memory impairment. A series of our previous studies revealed that hippocampal ventral CA1 (vCA1) neurons possess social memory engram and that the neurophysiological representation of social memory in the vCA1 neurons is disrupted in ASD-associated Shank3 knockout mice. However, whether the dysfunction of Shank3 in vCA1 causes the social memory impairment observed in ASD remains unclear. In this study, we found that vCA1-specific Shank3 conditional knockout (cKO) by the adeno-associated virus (AAV)- or specialized extracellular vesicle (EV)-mediated in vivo gene editing was sufficient to recapitulate the social memory impairment in male mice. Furthermore, the utilization of EV-mediated Shank3-cKO allowed us to quantitatively examine the role of Shank3 in social memory. Our results suggested that there is a certain threshold for the proportion of Shank3-cKO neurons required for social memory disruption. Thus, our study provides insight into the population coding of social memory in vCA1, as well as the pathological mechanisms underlying social memory impairment in ASD.

neuroscience↗