Biology subjects

Wiech, M.

Publications and source records attributed to Wiech, M..

3 recordsLinked to original sources

bioRxiv2025

Genetics in the ocean's twilight zone: Population structure of the Mueller's pearlside across its distribution range

The large estimates of mesopelagic fish biomass have fuelled harvesting interests in the relatively untouched oceans twilight zone. The Muellers pearlside, one of the most abundant species inhabiting the north Atlantic mesopelagic layer, is a candidate to such fisheries despite its enormous ecological importance and the insufficient knowledge about its population genetic structure. To shed light on the latter, 863 individuals sampled across the North Atlantic and Mediterranean were genotyped using 170 genome-wide SNPs. Analyses revealed habitat-driven differentiation in three units: Mediterranean Sea, oceanic samples, and Norwegian fjords. These groups were not completely isolated to each other as a cline of Mediterranean admixture was detected in the Eastern Atlantic facade up to 47{degrees}N in an otherwise genetically homogeneous oceanic cluster. Temperature seemed to modulate the differentiation patterns, and in the Mediterranean added to the complicated topography of the Greek Seas to shape genetic structure. In the Norwegian coastline, sills did not hamper genetic exchange among fjords ranging 200 km apart, probably due to the position of the species in the water column together with its swimming capacity. This genetic information should be combined with demographic properties to outline the management of this species prior to any eventual fishery attempt.

genetics↗

bioRxiv2024

Five millennia of mitochondrial introgression in Atlantic bluefin tuna identified using ancient DNA

Mitogenomic (MT) introgression between species is readily documented in marine fishes. Such introgression events may either be long-term natural phenomena or the result of human-driven shifts in spatial distributions of previously separated species. Determining the drivers behind MT introgression is stymied by the difficulty of directly observing patterns of interbreeding over long timescales. Using ancient DNA spanning five millennia, we here investigate the long-term presence of MT introgression from Pacific bluefin tuna (Thunnus orientalis) and albacore (Thunnus alalunga) into Atlantic bluefin tuna (Thunnus thynnus), a species with extensive exploitation history and observed shifts in abundance, and demographic distribution. Comparing ancient (n=130) and modern (n=78) mitogenomes of specimens covering most of the range of Atlantic bluefin tuna we detect no significant spatial or temporal population structure. This lack of spatiotemporal genomic differentiation is indicative of ongoing gene flow between populations and large effective population sizes over millennia. Moreover, we identify introgressed MT genomes in ancient specimens up to 5000 years old and find that this rate of introgression has remained similar through time. We therefore conclude that MT introgression in the Atlantic bluefin tuna is to date unaffected by anthropogenic impacts. By providing the oldest example of directly observed MT introgression in the marine environment, our results highlight the utility of ancient DNA to obtain temporal insights in the long-term persistence of such phenomena.

evolutionary biology↗

bioRxiv2021

Targeting Integrated Stress Response by ISRIB combined with imatinib attenuates STAT5 signaling and eradicates therapy-resistant Chronic Myeloid Leukemia cells

Integrated Stress Response (ISR) facilitates cellular adaptation to variable environmental conditions by reprogramming cellular response. Activation of ISR was reported in neurological disorders and solid tumours, but its function in hematological malignancies remains largely unknown. Previously we showed that ISR is activated in chronic myeloid leukemia (CML) CD34+ cells, and its activity correlates with disease progression and imatinib resistance. Here we demonstrate that inhibition of ISR by small molecule ISRIB, but not by PERK inhibitor GSK2656157, restores sensitivity to imatinib and eliminates CM Blast Crisis (BC) D34+ resistant cells. We found that in Patient Derived Xenograft (PDX) mouse model bearing CD34+ imatinib/dasatinib-resistant CML blasts with PTPN11 gain-of-function mutation, combination of imatinib and ISRIB decreases leukemia engraftment. Furthermore, genes related to SGK3, RAS/RAF/MAPK, JAK2 and IFN{gamma} pathways were downregulated upon combined treatment. Remarkably, we confirmed that ISRIB and imatinib combination decreases STAT5 phosphorylation and inhibits expression of STAT5-target genes responsible for proliferation, viability and stress response. Thus, our data point to a substantial effect of imatinib and ISRIB combination, that results in transcriptomic deregulation and eradication of imatinib-resistant cells. Our findings suggest such drug combination might improve therapeutic outcome of TKI-resistant leukemia patients exhibiting constitutive STAT5 activation.

cancer biology↗