Biology subjects

Morin, P.

Publications and source records attributed to Morin, P..

6 recordsLinked to original sources

bioRxiv2025

Experimental community ecology in decline: A call to embrace technology

Community dynamics are complex and thus challenging to infer from observational data alone. Experiments, with their ability to control variables and isolate mechanisms, are a powerful tool for uncovering the causal processes that drive community dynamics. They therefore allow us to move beyond correlations and to directly test theoretical predictions. Yet, because experiments are often logistically demanding and resource-intensive, they are less frequently employed than observational approaches in community ecology. Here, we trace the past three decades of experimental research in community ecology through a systematic literature review. We focus on the motivation behind experiments, their links to ecological theory, the types of questions they address, their scale, and the methods used to do this. Our results corroborate the historically tight relationship between experiments and ecological theory and document a gradual increase in experimental complexity --particularly related to the use of molecular methods. However, persistent gaps remain in the taxa and ecosystems studied, with aquatic ecosystems, fungi, and microbes still underrepresented compared to terrestrial plants and animals. Moreover, experiments are still limited in their spatial and temporal scale; they are typically short-term, local, and reliant on manual methods. The integration of high-throughput technologies with experimental workflows is still in its infancy, even though they are increasingly common in biomonitoring. To illustrate the potential of such tools in experimental research, we present a proof-of-concept study. It shows how automated technologies can be incorporated at different stages of the experimental workflow to expand the scale of experiments while reducing the reliance on human labor and potentially lowering financial costs. We conclude that many of the long-lasting biases and challenges in experimental community ecology could be addressed by combining technological innovations with broader collaboration among research groups. Coordinated networks, standardized protocols, and the integration of long-term and large-scale experimental designs can substantially improve in situ replication as well as cross-site comparability. Such efforts are essential for developing a more comprehensive mechanistic understanding of community dynamics across diverse ecosystems.

ecology↗

bioRxiv2025

Synaptotoxic forms of amyloid-b and a-synuclein act through a common pathway.

It has been suggested that -synuclein (Syn), a major player in Parkinsons disease (PD), plays a role in Alzheimers disease (AD). Several reports have also concluded that Syn and amyloid-{beta} (A{beta}) are mechanistically linked, although how is unclear. Synapse loss is an early feature in both PD and AD and held to be the driver of both diseases. We have previously uncovered a signalling pathway required for A{beta}-driven dendritic spine loss - a non-canonical branch of Wnt signalling known as the Wnt/Planar Cell Polarity (Wnt/PCP) pathway. We asked if a synaptotoxic form of Syn known to impact dendritic spines, the A53T autosomal dominant PD mutant form of Syn (A53T-Syn), might act on synapses through the same pathway. Here, by blocking all Wnt activity with the porcupine inhibitor IWP2, we show that A53T-Syn-driven spine loss is Wnt-dependent. By silencing Daam1, which is unique to Wnt/PCP, we show that A53T-Syn spine loss is Daam1-dependent. Finally, using the pan-ROCK inhibitor fasudil indicates the mechanism also involves ROCK1/2, which Daam1 signals to via RhoA to modulate actin cytoskeletal dynamics within dendritic spines. Together, these observations indicate that A53T-Syn-driven spine loss involves the Wnt/PCP pathway, the same pathway that mediates A{beta} synaptotoxicity. This indicates that A{beta} and Syn are mechanistically connected and that a common pathway is responsible for synapse loss in AD and PD. It also begins to explain why this group of neurodegenerative diseases have many features in common and suggests that drugs which target Wnt/PCP could be of benefit for both AD and PD.

neuroscience↗

bioRxiv2022

Application of Quasimetagenomics Methods to Define Microbial Diversity and Subtype Listeria monocytogenes in Dairy and Seafood Production Facilities

Microorganisms frequently colonize surfaces and equipment within food production facilities. Listeria monocytogenes is a ubiquitous foodborne pathogen widely distributed in food production environments and is the target of numerous control and prevention procedures. Detection of L. monocytogenes in a food production setting requires culture dependent methods, but the complex dynamics of bacterial interactions within these environments and their impact on pathogen detection remains largely unexplored. To address this challenge, we applied both 16S rRNA and shotgun quasimetagenomic (enriched microbiome) sequencing of swab culture enrichments from seafood and dairy production environments. Utilizing 16S rRNA amplicon sequencing, we observed variability between samples taken from different production facilities and a distinctive microbiome for each environment. With shotgun quasimetagenomic sequencing, we were able to assemble L. monocytogenes metagenome assembled genomes (MAGs) and compare these MAGSs to their previously sequenced whole genome sequencing (WGS) assemblies, which resulted in two polyphyletic clades (lineages I and II). Using these same datasets together with in silico downsampling to produce a titration series of proportional abundances of L. monocytogenes, we were able to begin to establish limits for Listeria detection and subtyping using shotgun quasimetagenomics. This study contributes to the understanding of microbial diversity within food production environments and presents insights into how many reads or relative abundance is needed in a metagenome sequencing dataset to detect, subtype, and source track at a SNP level, as well as providing an important foundation for utilizing metagenomics to mitigate unfavorable occurrences along the farm to fork continuum. IMPORTANCEIn developed countries, the human diet is predominantly food commodities, which have been manufactured, processed, and stored in a food production facility. It is well known that the pathogen Listeria monocytogenes is frequently isolated from food production facilities and can cause serious illness to susceptible populations. Multistate outbreaks of L. monocytogenes over the last 10 years have been attributed to food commodities manufactured and processed in production facilities, especially those dealing with dairy products such as cheese and ice cream. A myriad of recalls due to possible L. monocytogenes contamination have also been issued for seafood commodities originating from production facilities. It is critical to public health that the means of growth, survival and spread of Listeria in food production ecosystems is investigated with developing technologies, such as 16S rRNA and quasimetagenomic sequencing, to aid in the development of effective control methods.

microbiology↗

bioRxiv2020

A role for the autophagic receptor, SQSTM1/p62, in trafficking NF-kB/RelA to nucleolar aggresomes

Elevated NF-{kappa}B activity is a contributory factor in many haematological and solid malignancies. Nucleolar sequestration of NF-{kappa}B/RelA represses this elevated activity and mediates apoptosis of cancer cells. Here we set out to understand the mechanisms that control the nuclear/nucleolar distribution of RelA and other regulatory proteins, so that agents can be developed that specifically target these proteins to the organelle. We demonstrate that RelA accumulates in intra-nucleolar aggresomes in response to specific stresses. We also demonstrate that the autophagy receptor, SQSTM1/p62, accumulates alongside RelA in these nucleolar aggresomes. This accumulation is not a consequence of inhibited autophagy. Indeed, our data suggest nucleolar and autophagosomal accumulation of p62 are in active competition. We identify a conserved motif at the N-terminus of p62 that is essential for nucleoplasmic-to nucleolar transport of the protein. Furthermore, using a dominant negative mutant deleted for this nucleolar localisation signal (NoLS), we demonstrate a role for p62 in trafficking RelA and other aggresome-related proteins to nucleoli. Together, these data identify a novel role for p62 in trafficking nuclear proteins to nucleolar aggresomes under conditions of cell stress, thus maintaining nuclear proteostasis. They also provide invaluable information on the mechanisms that regulate the nuclear/nucleolar distribution of RelA that could be exploited for therapeutic purpose. SignificanceAberrant NF-{kappa}B activity drives many of the hallmarks of cancer and plays a key role in cancer progression. Nucleolar sequestration of NF-{kappa}B/RelA is one mechanism that switches off this activity and induces the death of cancer cells. Here we define a novel role for the autophagy receptor, SQSTM1/p62 in transport of nucleoplasmic NF-{kappa}B/RelA to nucleoli. Identification of this new trafficking mechanism opens up avenues for the development of a unique class of therapeutic agents that transport RelA and other cancer regulatory proteins to this organelle.

cell biology↗

bioRxiv2019

Killer whale genomes reveal a complex history of recurrent admixture and vicariance

Reconstruction of the demographic and evolutionary history of populations assuming a consensus tree-like relationship can mask more complex scenarios, which are prevalent in nature. An emerging genomic toolset, which has been most comprehensively harnessed in the reconstruction of human evolutionary history, enables molecular ecologists to elucidate complex population histories. Killer whales have limited extrinsic barriers to dispersal and have radiated globally, and are therefore a good candidate model for the application of such tools. Here, we analyse a global dataset of killer whale genomes in a rare attempt to elucidate global population structure in a non-human species. We identify a pattern of genetic homogenisation at lower latitudes and the greatest differentiation at high latitudes, even between currently sympatric lineages. The processes underlying the major axis of structure include high drift at the edge of species range, likely associated with founder effects and allelic surfing during post-glacial range expansion. Divergence between Antarctic and non-Antarctic lineages is further driven by ancestry segments with up to four-fold older coalescence time than the genome-wide average; relicts of a previous vicariance during an earlier glacial cycle. Our study further underpins that episodic gene flow is ubiquitous in natural populations, and can occur across great distances and after substantial periods of isolation between populations. Thus, understanding the evolutionary history of a species requires comprehensive geographic sampling and genome-wide data to sample the variation in ancestry within individuals.

evolutionary biology↗

bioRxiv2017

Activation of NF-κB by a novel, CDK4-regulated, nucleolar stress response pathway

p53 as an effector of nucleolar stress is well defined, but p53 independent mechanisms are largely unknown. Like p53, the NF-{kappa}B transcription factor plays a critical role in maintaining cellular homeostasis under stress. Many stresses that stimulate NF-{kappa}B also disrupt nucleoli. However, the link between nucleolar function and activation of the NF-{kappa}B pathway is as yet unknown. Here we demonstrate that siRNA silencing of PolI complex components stimulates NF-{kappa}B signalling. Unlike p53 nucleolar stress response, this effect does not appear to be linked to inhibition of rDNA transcription. We show that specific stress stimuli of NF-{kappa}B induce degradation of a critical component of the PolI complex, TIF-IA. This degradation precedes activation of the NF-{kappa}B pathway and is associated with an atypical nucleolar architecture. It is mimicked by CDK4 inhibition and is dependent upon upstream binding factor (UBF) and p14ARF. We show that blocking stress effects on TIF-IA blocks their ability to activate the NF-{kappa}B pathway. Finally, using ex vivo culture, we show a strong correlation between degradation of TIF-IA and activation of NF-{kappa}B in freshly resected, human colorectal tumours exposed to the chemopreventative agent, aspirin. Together, our study provides compelling evidence for a new, NF-{kappa}B nucleolar stress response pathway that has in vivo relevance and therapeutic implications.

cell biology↗