Biology subjects

Parks, S.

Publications and source records attributed to Parks, S..

4 recordsLinked to original sources

bioRxiv2025

Detection, communication, and individual identification with deep audio embeddings: A case study with North Atlantic right whales

Anthropogenic noise has increased ambient sound levels across the globe, both underwater and on land. Among its many negative impacts, heightened noise can impair communication in vocal animals through acoustic masking. Conceptually, noise reduces the animals communication space - the area in which an individual animal can effectively convey information to a conspecific listener. Previous studies have estimated the communication space using sound propagation models and/or behavioral studies. However, studies frequently equate signal recognition with signal detection - a necessary but not sufficient precondition - thereby persistently overestimating spatial coverage and underestimating anthropogenic impacts. Measuring communication is inherently difficult, and varies with taxa, call type, and context, leading to significant data gaps in key parameters. We propose that deep learning creates an opportunity to estimate biologically-relevant communication, even for data-limited species. In particular, we present a case study with the critically endangered North Atlantic right whale (Eubalaena glacialis; hereafter NARW). Prior research has demonstrated that the upcall - a low-frequency contact call produced across ages and sexes - encodes individual identity. We therefore consider a dataset of NARW vocalizations recorded with on-animal archival tags, spanning 234 samples across 11 individuals from 3 sites. First, we demonstrate that audio embeddings from the BirdNET model can robustly distinguish individual right whales. Then, we simulate the effect of varying ambient noise levels to estimate signal excess for both signal detection and individual identification. Altogether, we hope this work provides both a methodological advance for individual identification and a framework for better understanding anthropogenic impacts on vocal wildlife.

ecology↗

bioRxiv2025

LSD Restores Synaptic Plasticity in VTA of Morphine-Treated Mice and Disrupts Morphine-Conditioned Place Preference

Psychedelics are emerging as a promising treatment option for a range of neuropsychiatric disorders, including substance use disorders. One potential mechanism underlying their therapeutic benefits may involve a reversal of maladaptive plasticity induced by drug exposure. Here, we identify physiological, behavioral, and epigenetic impacts of lysergic acid diethylamide (LSD) on morphine-treated male and female mice. Morphine was selected due to the high leverage capacity to address the opioid epidemic. A single treatment of LSD, or 4 microdoses of LSD, cause accelerated extinction of morphine-induced conditioned place preference. Whole-cell electrophysiology revealed that excitatory synaptic plasticity, which was eliminated in VTA GABA neurons following morphine exposure, was restored 24 hours after a single high dose of LSD. To explore the impact of LSD treatment on potential epigenetic changes, whole-brain DNA methylation analysis in morphine-treated mice that received either saline or LSD post-morphine treatment revealed significant differences in methylation profiles associated with LSD treatment. Collectively, these findings suggest that LSD may reverse or prevent morphine-induced changes in reward circuit plasticity and attenuate measures of morphine-preference.

neuroscience↗

bioRxiv2021

Parasitic nematode fatty acid- and retinol-binding proteins compromise host immunity by interfering with host lipid signaling pathways

Parasitic nematodes cause significant morbidity and mortality globally. Excretory/secretory products (ESPs) such as fatty acid- and retinol- binding proteins (FARs) are hypothesized to suppress host immunity during infection, yet little is known about their interactions with host tissues. Leveraging the insect parasitic nematode, Steinernema carpocapsae, we provide the first in vivo study that shows FARs modulate animal immunity, causing an increase in susceptibility to bacterial infection. Next we determined that FARs dampen various aspects of the fly immune response including the phenoloxidase cascade and antimicrobial peptide (AMP) production. Finally, we found that FARs deplete lipid signaling precursors in vivo as well as bind to these fatty acids in vitro, suggesting that FARs elicit their immunomodulatory effects by altering the availability of lipid signaling molecules necessary for a functional immune response. Collectively, these data reveal a complex role for FARs in immunosuppression and provide detailed mechanistic insight into parasitism in phylum Nematoda. SignificanceA central aspect of parasitic nematode success is their ability to modify host biology, including evasion and/or subversion of host immunity. Modulation of host biology and the pathology caused by parasitic nematodes is largely effected through the release of proteins and small molecules. There are hundreds of proteins released by nematodes during an infection and few have been studied in detail. Fatty acid- and retinol-binding proteins (FARs) are a unique protein family released during infection. We report that nematode FARs from S. carpocapsae, C. elegans and A. ceylanicum dampen fly immunity decreasing resistance to infection. Mechanistically, this is achieved through modulation of the phenoloxidase cascade and antimicrobial peptide production. Furthermore, FARs alter the availability of lipid immune signaling precursors in vivo and show binding specificity in vitro. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=187 SRC="FIGDIR/small/436866v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@48f582org.highwire.dtl.DTLVardef@1ee4292org.highwire.dtl.DTLVardef@1548248org.highwire.dtl.DTLVardef@13574d6_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract C_FIG

molecular biology↗

bioRxiv2020

Sorcin stimulates Activation Transcription Factor 6α (ATF6) transcriptional activity

Levels of the transcription factor ATF6, a key mediator of the unfolded protein response, that provides cellular protection during the progression endoplasmic reticulum (ER) stress, are markedly reduced in the pancreatic islet of patients with type 2 diabetes and in rodent models of the disease, including ob/ob and high fat-fed mice. Sorcin (gene name SRI) is a calcium (Ca2+) binding protein involved in maintaining ER Ca2+ homeostasis. We have previously shown that overexpressing sorcin under the rat insulin promoter in transgenic mice was protective against high fat diet-induced pancreatic beta cell dysfunction, namely preserving intracellular Ca2+ homeostasis and glucose-stimulated insulin secretion during lipotoxic stress. Additionally, sorcin overexpression was apparently activating ATF6 signalling in MIN6 cells despite lowering ER stress. Here, in order to investigate further the relationship between sorcin and ATF6, we describe changes in sorcin expression during ER and lipotoxic stress and changes in ATF6 signalling after sorcin overexpression or inactivation, both in excitable and non-excitable cells. Sorcin mRNA levels were significantly increased in response to the ER stress-inducing agents thapsigargin and tunicamycin, but not by palmitate. On the contrary, palmitate caused a significant decrease in sorcin expression as assessed by both qRT-PCR and Western blotting despite inducing ER stress. Moreover, palmitate prevented the increase in sorcin expression induced by thapsigargin. In addition, sorcin overexpression significantly increased ATF6 transcriptional activity, whereas sorcin inactivation decreased ATF6 signalling. Finally, sorcin overexpression increased levels of ATF6 immunoreactivity and FRET imaging experiments following ER stress induction by thapsigargin showed a direct sorcin-ATF6 interaction. Altogether, our data suggest that sorcin down-regulation during lipotoxicity may prevent full ATF6 activation and a normal UPR during the progression of obesity and insulin resistance, contributing to beta cell failure and type 2 diabetes.

cell biology↗