Biology subjects

Lason, W.

Publications and source records attributed to Lason, W..

3 recordsLinked to original sources

bioRxiv2025

Citizen science and detailed searches reveal widespread occurrence of hybrid-like Syrian x Great-spotted woodpeckers

The Syrian Woodpecker (hereafter SW) expansion into Europe since the end of the 19th century has enabled its hybridisation with the Great spotted Woodpecker (hereafter GW). This phenomenon, however, has generally been considered sporadic. Here, we examined the occurrence of mixed pairs and hybrids based on our own field observations and citizen science data. Interspecific pairs and individuals of SW and GW were found to be generally scarce but occurred in all parts of the area investigated, not only at the edges of the SWs range. The proportion of hybrid occurrence in woodpecker populations was found to be similar across the whole SWs range in Europe and in both urban and rural populations. However, on a local level, hybrids seemed to be more abundant in certain regions, for example, E Austria, Moravia, SE Poland, W Russia, S Ukraine, Bulgaria, E Greece and W Turkey. Generally, females were 1.4 times more frequent among hybrids. Three major phenotypical hybrid forms were identified: GW-like, SW-like, and intermediate, with first two forms being more frequent in the central and south of Europe respectively. Whereas proportion of the intermediate form was relatively constant across the whole range of hybrid occurrence. The results indicate that hybrids of the two species have become significant part of woodpecker populations and thus should be considered in research and nature conservation projects.

zoology↗

bioRxiv2024

MAIT cells protect against sterile lung injury

Mucosal-associated invariant T (MAIT) cells, the most abundant unconventional T cells in the lung, have been recently linked to tissue protection and repair. Their role, especially in sterile lung injury, is unknown. Using single cell RNA sequencing (scRNA-seq), spectral analysis and adoptive transfer in a bleomycin-induced sterile lung injury, we found that bleomycin activates murine pulmonary MAIT cells and induces an accompanying tissue repair programme, associated with a protective role against bleomycin-induced lung injury. MAIT cells drive the accumulation of type 1 conventional dendritic cells (cDC1), limiting tissue damage in a DNGR-1 dependent manner. Human scRNA-seq data revealed that MAIT cells were activated, with increased cDC populations in idiopathic pulmonary fibrosis patients. Thus, MAIT cells enhance defence against sterile lung injury by fostering cDC1-driven anti-fibrotic pathways.

immunology↗

bioRxiv2021

Pan-cancer survey of tumour mass dormancy and underlying mutational processes

Tumour mass dormancy is the key intermediate step between immune surveillance and cancer progression, yet due to its transitory nature it has been difficult to capture and characterise. Little is understood of its prevalence across cancer types and of the mutational background that may favour such a state. While this balance is finely tuned internally by the equilibrium between cell proliferation and cell death, the main external factors contributing to tumour mass dormancy are immunological and angiogenic. To understand the genomic and cellular context in which tumour mass dormancy may develop, we comprehensively profiled signals of immune and angiogenic dormancy in 9,631 cancers from the Cancer Genome Atlas and linked them to tumour mutagenesis. We find evidence for immunological and angiogenic dormancy-like signals in 16.5% of bulk sequenced tumours, with a frequency of up to 33% in certain tissues. Mutations in the CASP8 and HRAS oncogenes were positively selected in dormant tumours, suggesting an evolutionary pressure for controlling cell growth/apoptosis signals. By surveying the mutational damage patterns left in the genome by known cancer risk factors, we found that ageing-induced mutations were relatively depleted in these tumours, while patterns of smoking and defective base excision repair were linked with increased tumour mass dormancy. Furthermore, we identified a link between APOBEC mutagenesis and dormancy, which comes in conjunction with immune exhaustion and may partly depend on the expression of the angiogenesis regulator PLG as well as interferon and chemokine signals. Tumour mass dormancy also appeared to be impaired in hypoxic conditions in the majority of cancers. The microenvironment of dormant cancers was enriched in cytotoxic and regulatory T cells, as expected, but also in macrophages and showed a reduction in inflammatory Th17 signals. Finally, tumour mass dormancy was linked with improved patient survival outcomes. Our analysis sheds light onto the complex interplay between dormancy, exhaustion, APOBEC activity and hypoxia, and sets directions for future mechanistic explorations.

cancer biology↗