Biology subjects

Colin, J.

Publications and source records attributed to Colin, J..

4 recordsLinked to original sources

bioRxiv2025

Skin Resident T Cell Interactions with NPY1R+ Neurons During Wound Repair Are Impaired by Obesity

Wound repair involves complex cellular interactions to induce efficient healing. Skin resident {gamma}{delta} T cells regulate keratinocyte function and inflammatory responses in wound healing through the secretion of growth factors and cytokines. Some of these cytokines are involved in the neuroimmune axis, so we aimed to ascertain if {gamma}{delta} T cells and neurons exhibit crosstalk during wound repair. We identified a prevalent NPY1R+ peripheral neuron subset in the skin. {gamma}{delta} T cells interact with NPY1R+ neurons in the epidermis and dermis of both nonwounded and wounded murine skin. To determine the impact of the {gamma}{delta} TCR on NPY1R+ neuron interactions in wound healing, we compared epidermal T cell-neuron interactions in TCR{delta}-/- mice during wound repair. We found a decrease in interactions between epidermal {beta} T cells and NPY1R+ neurons in TCR{delta}-/- mice, suggesting {gamma}{delta} T cells communicate with NPY1R+ neurons more frequently than {beta} T cells in the epidermis, regardless of wound repair. In contrast, dermal T cell-neuron interactions in wildtype and TCR{delta}-/- mice during wound repair were similar between {beta} T cells and {gamma}{delta} T cells, suggesting both T cell types mediate communications with neurons in the dermis. In obese mice there are fewer NPY1R+ neurons and diminished neuron-T cell interactions indicative of neuropathy. Together these findings elucidate a neuroimmune crosstalk during wound repair that becomes disrupted in obesity.

immunology↗

bioRxiv2023

The Cryptocococcus extracellular vesicle transcriptome

Extracellular vesicles (EVs) are now recognized as key players in the biology of numerous organisms, including pathogenic fungi. However, studying EVs in these organisms remains challenging. The recent implementation of new protocols to purify EVs in the pathogenic yeast Cryptococcus neoformans has resulted in a more detailed description of their structure and protein composition. Although a few publications describing RNA molecules associated with EVs have already been published, we reasoned that these new protocols would be beneficial for gaining a deeper understanding of the EV transcriptome. We thus purified EVs and confirmed that some RNAs were associated with these EV extracts. Iodixanol gradient analyses also revealed that these RNAs co-sedimented with EVs. We then sequenced these RNAs in parallel with RNAs extracted from the very cells producing these EVs using different types of sequencing libraries. Our data confirm the presence of siRNAs and tRFs associated with EVs, some of which are enriched. We also identified some snoRNAs, which in Cryptococcus are mostly borne by coding gene or lncRNA introns.

microbiology↗

bioRxiv2023

Tur1 regulates alternative TSS usage in Cryptococcus

Alternative transcription start site (TSS) usage regulation has been identified as a major means of gene expression regulation in metazoans. However, in fungi, its impact remains elusive as its study has thus far been restricted to model yeasts. Here, we first re-analysed TSS-seq data to define genuine TSS clusters in two species of pathogenic Cryptococcus. We identified two types of TSS clusters associated with specific DNA sequence motifs. Our analysis also revealed that alternative TSS usage regulation in response to environmental cues is widespread in Cryptococcus, altering gene expression and protein targeting. Importantly, we performed a forward genetic screen to identify a unique transcription factor (TF) named Tur1, which regulates alternative TSS (altTSS) usage genome-wide when cells switch from exponential phase to stationary phase. ChiP-Seq and DamID-Seq analyses suggest that at some loci the role of Tur1 might be direct. Tur1 has been previously shown to be essential for virulence in C. neoformans. We demonstrated here that a tur1{Delta} mutant strain is more sensitive to superoxide stress and phagocytosed more efficiently by macrophages than the wild-type (WT) strain.

molecular biology↗

bioRxiv2019

Linking alpha oscillations, attention and inhibitory control in adult ADHD with EEG neurofeedback

Abnormal patterns of electrical oscillatory activity have been repeatedly described in adult ADHD. In particular, the alpha rhythm (8-12 Hz), known to be modulated during attention, has previously been considered as candidate biomarker for ADHD. In the present study, we asked adult ADHD patients to self-regulate their own alpha rhythm using neurofeedback (NFB), in order to examine the modulation of alpha oscillations on attentional performance and brain plasticity. Twenty-five adult ADHD patients and 22 healthy controls underwent a 64-channel EEG-recording at resting-state and during a Go/NoGo task, before and after a 30 min-NFB session designed to reduce (desynchronize) the power of the alpha rhythm. Alpha power was compared across conditions and groups, and the effects of NFB were statistically assessed by comparing behavioral and EEG measures pre-to-post NFB. Firstly, we found that relative alpha power was attenuated in our ADHD cohort compared to control subjects at baseline and across experimental conditions, suggesting a signature of cortical hyper-activation. Both groups demonstrated a significant and targeted reduction of alpha power during NFB. Interestingly, we observed a post-NFB increase in resting-state alpha (i.e. rebound) in the ADHD group, which restored alpha power towards levels of the normal population. Importantly, the degree of post-NFB alpha normalisation during the Go/NoGo task correlated with individual improvements in motor inhibition (i.e. reduced commission errors and slower reaction times in NoGo trials) only in the ADHD group. Overall, our findings offer novel supporting evidence implicating alpha oscillations in inhibitory control, as well as their potential role in the homeostatic regulation of cortical excitatory/inhibitory balance.\n\nHighlightsO_LIResting alpha power is reduced in adult ADHD suggesting cortical hyper-activation\nC_LIO_LIAdult ADHD patients successfully reduce alpha power during neurofeedback\nC_LIO_LIA post-neurofeedback rebound normalizes alpha power in adult ADHD\nC_LIO_LIAlpha power rebound correlates with improvement of inhibitory control in adult ADHD\nC_LI

neuroscience↗