Biology subjects

Wang, G. Z.

Publications and source records attributed to Wang, G. Z..

3 recordsLinked to original sources

bioRxiv2026

Loss of ASIC1A-dependent inhibitory neuron activity in basolateral amygdala is associated with increased CO2-evoked jumping

BackgroundResponding appropriately to threats is critical for survival. Dysregulated defensive responses are core features of psychiatric illnesses including panic disorder and post-traumatic stress disorder. Carbon dioxide (CO2) inhalation evokes defensive behaviors in both humans and mice. Here we investigated the role of acid-sensing ion channels (ASICs) in CO2-evoked jumping in mice. MethodsDefensive behaviors (jumping and freezing) were assessed in response to CO2 inhalation and basolateral amygdala (BLA) acidification. We tested the role of ASICs using global knockout mice and Asic1aloxP/loxP mice transduced with AAV-CMV-Cre or AAV-CaMKII-Cre in the BLA. Effects of CO2 on single neuron firing and local field potentials were studied via BLA microwire arrays. ResultsASIC1A disruption increased CO2-evoked jumping while reducing freezing, paralleled by increased BLA c-Fos induction. Acidification of the BLA recapitulated these effects. Virus-mediated ASIC1A disruption in BLA did not resolve the locus of ASIC1A action in jumping. CO2 inhalation suppressed firing in most BLA neurons, though a small number increased firing. ASIC1A disruption enhanced CO2-induced suppression of narrow waveform neurons (putative interneurons), and facilitated excitation of wide waveform neurons (putative principal neurons). Additionally, CO2 produced concentration-dependent broadband power suppression with selective theta enhancement, effects that were augmented by ASIC1A disruption. ConclusionsTogether, these findings suggest that ASIC1A promotes interneuron activity during acidosis and that its loss may reduce inhibition of principal neuron output, shifting defensive responses from freezing toward jumping. These results advance our understanding of how brain pH and ASICs regulate defensive behavior, with potential implications for understanding dysregulated defensive responses.

neuroscience↗

bioRxiv2025

Histone H1 Promotes Silencing of Unintegrated HIV-1 DNA

In eukaryotic cells, genomic DNA is packaged into chromatin with nucleosomes formed by core histones H2A, H2B, H3, and H4, and further stabilized by the linker histone H1. During the early stages of retroviral infection, such as with murine leukemia virus (MLV) and human immunodeficiency virus type 1 (HIV-1), host core and H1 histones are rapidly deposited onto unintegrated viral DNAs upon nuclear entry. These unintegrated viral DNAs are transcriptionally silenced through histone post-translational modifications (PTMs), including high levels of H3K9 trimethylation and low levels of H3 acetylation. Linker histone H1 is closely associated with chromatin compaction and histone PTMs, suggesting a potential role in regulating retroviral DNA fate. In this study, we demonstrate that simultaneous knockdown of four somatic H1 variants (H1.2, H1.3, H1.4, and H1.5) in K562 cells reverses the silencing of unintegrated HIV-1 DNA, resulting in increased viral expression. Notably, this effect was specific to HIV-1, as the same H1 depletion did not alter the silencing of MLV unintegrated DNA. These results reveal distinct roles of H1 in regulating HIV-1 and MLV unintegrated DNA expression.

microbiology↗

bioRxiv2023

Staphylococcal secreted cytotoxins are competition sensing signals for Pseudomonas aeruginosa

Coinfection with two notorious opportunistic pathogens, the Gram-negative Pseudomonas aeruginosa and Gram-positive Staphylococcus aureus, dominates chronic pulmonary infections. While coinfection is associated with poor patient outcomes, the interspecies interactions responsible for such decline remain unknown. Here, we dissected molecular mechanisms of interspecies sensing between P. aeruginosa and S. aureus. We discovered that P. aeruginosa senses S. aureus secreted peptides and, counterintuitively, moves towards these toxins. P. aeruginosa tolerates such a strategy through "competition sensing", whereby it preempts imminent danger/competition by arming cells with type six secretion (T6S) and iron acquisition systems. Intriguingly, while T6S is predominantly described as weaponry targeting Gram-negative and eukaryotic cells, we find that T6S is essential for full P. aeruginosa competition with S. aureus, a previously undescribed role for T6S. Importantly, competition sensing was activated during coinfection of bronchial epithelia, including T6S islands targeting human cells. This study reveals critical insight into both interspecies competition and how antagonism may cause collateral damage to the host environment.

microbiology↗