Biology subjects

Bouchoucha, M.

Publications and source records attributed to Bouchoucha, M..

3 recordsLinked to original sources

bioRxiv2025

Expanding on the portuarization syndrome from an ecological perspective: eDNA reveals rich diversity, non-indigenous hotspots, and biotic homogenization in ports

Ports are well-known entry points for marine non-indigenous species (NIS), which arrive as hitchhikers on ships. Ports are also expected to be gateways for the spread of NIS in the wild and resemble each other more than communities outside due to their singular characteristics. However, the uniqueness of species assemblages in ports and how they differ from natural habitats have only been marginally investigated, notably at regional scale. Using eDNA metabarcoding, we obtained a comprehensive and standardized overview of metazoan community diversity in 12 paired ports and adjacent natural areas along the northwestern Mediterranean Sea. As expected, we found that NIS are more abundant in ports than in natural habitats, and that the species assemblages in ports differ from those in natural habitats. In addition, we observed that communities in ports are far more homogeneous than their natural counterparts. This finding supports the hypothesis of biotic homogenization in highly anthropized habitats. We also observed a pattern that had previously been documented mainly in fish, but that we identified here in every phylum studied except Arthropoda: species richness detected in ports is comparable to, and in some case even greater than, that observed in natural habitats. Overall, our findings broaden, through an ecological perspective, the "portuarization syndrome" concept, which originally defined ports as unique replicated environments that promote specific evolutionary processes.

ecology↗

bioRxiv2025

Impact of port conditions and acclimation capacity of common two-banded seabream juveniles in the bay of Toulon: implications for nursery rehabilitation efforts

Ports are heavily anthropized coastal environments characterized by intense pollution and habitat alterations, creating challenging living conditions for marine organisms, particularly juvenile fish that rely on these areas as nurseries. While recent rehabilitation efforts of the nursery function in ports have focused on structural modifications, the impacts of port chemical and physical pollution are currently disregarded. Using field sampling and caging experiments, we examined the physiological (growth, lipid content, CYP1A-dependent biotransformation activity) and molecular (RNA-seq) responses of juvenile two-banded sea bream (Diplodus vulgaris) by comparing one port site with two adjacent sites from outside of the port, assessing their potential for short-term acclimation to port conditions. Results from individuals sampled in the field revealed distinct physiological and transcriptomic profiles in port juveniles, indicating specific responses to this environment. Notably, alterations related to lipid accumulation, detoxification, hypoxia, and circadian regulation were observed. After one month of caging all the individuals from different locations in the port, juveniles originating from outside the port exhibited stronger transcriptional responses compared to individuals that grew within the port, with higher expression of genes involved in detoxification and lipid metabolism, and a strong overexpression of oncogenes, while individuals originating from the port upregulated genes involved in energy metabolism, suggesting some capacity for short-term acclimation in port-resident juvenile fish. These findings highlight the potential impact of port conditions on juvenile fish health, with implications for the effectiveness of rehabilitation efforts. This study emphasizes the need for further research to inform nursery rehabilitation strategies in polluted ports.

physiology↗

bioRxiv2025

The Olfactory Epithelium: A Critical Gateway for Pathological Tau Propagation and a Target for Mitigating Tauopathy in the Central Nervous System

Olfactory impairment is a recognized early indicator of neurodegenerative diseases (NDs), such as Alzheimers disease (AD). Intracellular aggregates of hyperphosphorylated tau protein, referred to as neurofibrillary tangles (NFTs), are a hallmark of AD. NFTs are found in the olfactory bulb (OB) and entorhinal cortex (EC), both crucial for processing olfactory information. We explored the hypothesis that typical tau lesions could appear early and progress along olfactory regions to reach connected areas critically affected in AD (e.g. EC and hippocampal formation). To that end, we used transgenic PS19 mice expressing mutated human tau protein (1N4R isoform, P301S mutation). They recapitulate major phenotypes of AD, such as accumulation of NFTs, synaptic dysfunction, cognitive impairment, and neuronal loss. The presence of pathological hyperphosphorylated human tau protein (pTau) was monitored in olfactory regions: olfactory epithelium (OE), OB, piriform cortex (PC), and in connected regions of the hippocampal formation (hippocampus and EC). pTau was detected in the OEs middle stratum and in the OBs olfactory nerve layer (ONL) at 1.5 months. At 6 months of age, tau accumulations were found in the PC and EC, along with the CA3 region and dentate gyrus of the hippocampus. We found that olfactory function remained unaffected in PS19 mice, despite the presence of tau pathology in key regions of the olfactory system. Complete stripping of the OE by intranasal administration of ZnSO4 led to a significant reduction in pretangle-like tau pathology within the PC, amygdala, and EC of 6-month-old PS19 mice. Finally, we observed in human post-mortem samples that pTau signal was present in the olfactory regions (OE and OB) of patients at early Braak stages (I/II). Based on these observations, we propose that pTau could appear, due to ageing or environmental agents, in the OE and subsequently spread in a prion-like manner to the hippocampal formation along neuroanatomical connections. These findings also indicate the interest of the OE as a target for intervention aimed at mitigating the progression of tauopathy in the CNS.

neuroscience↗