Authors: Georgina Bramwell, Aaron G. Schultz, Thomas Madsen, Frédéric Thomas, Nick Macdonald, Antoine M. Dujon, Craig D.H. Sherman, Beata Ujvari

Source: Aquaculture (Sep 2023)

Abstract

As valuable ecosystem engineers, blue mussels, are one of the most ecologically and economically important bivalve species in Australia. The need for understanding levels of genetic diversity in both wild and farmed populations of Australian mussels is ever-growing due to the increased risk of disease and decreased fitness associated with the constantly changing global environment.

This study, therefore, investigated the phylogenetic relationship, and the genetic variation of farmed blue mussels (Mytilus sp., previously noted as M. galloprovincialis, M. planulatus or a hybrid of both) at four sites along the south coast of Australia, Victoria, South Australia, Western Australia, and Tasmania.

Analyses of two genes, Cytochrome c oxidase subunit 1 gene (mtCOI) and the nuclear gene Elongation factor 1 alpha (EF1a) was completed for all mussels sampled. The phylogenetic reconstruction of mtDNA sequences was not able to cluster the samples into species. The analyses of the nuclear marker (EF1a) returned similar results, except that we could conclude the Australian samples not being M. chilensis. Furthermore, the analyses of EF1a revealed the presence of hybridisation, a pattern commonly observed in mussels.

The genetic diversity analysis of mtCOI demonstrated that samples from Victoria and Western Australia had the highest genetic diversity, while South Australia had the lowest. When analysing the nuclear EF1a sequences, mussels from Western Australian had the lowest genetic diversity, and the Victorian samples had the highest.

The study extended our knowledge on the population genetic variation of farmed blue mussels (Mytilus sp.) along the south coast of Australia. The identified genetic differences between the four southern states of Australia could be interesting for the aquaculture industry when aiming for more adaptable and profitable stocks.

Authors: Antoine M. Dujon, Jérémy Jeanjean, Orsolya Vincze, Mathieu Giraudeau, Jean-François Lemaître, Pascal Pujol, Beata Ujvari, Frédéric Thomas

Source: Ecology and Evolution (Sep 2023)

Abstract

The hygiene hypothesis, according to which the recent reduction of exposure to infectious agents in the human species would be the origin of various diseases, including autoimmune diseases and cancer, has often been proposed but not properly tested on animals.

Here, we evaluated the relevance of this hypothesis to cancer risk in mammals in an original way, namely by using information on zoo mammals. We predicted that a higher richness of parasitic cohorts in the species’ natural habitat would result in a greater occurrence of evolutionary mismatch due to the reduction of parasites in captive conditions. This, in turn, could contribute to an increased risk of developing lethal cancers.

Using a comparative analysis of 112 mammalian species, we explored the potential relationship between cancer risk and parasite species richness using generalized phylogenetic least squares regressions to relate parasite species richness to cancer risk data.

We found no strong evidence that parasite species richness increased cancer risk in zoo mammals for any of the parasite groups we tested. Without constituting definitive proof of the irrelevance of the hygienic hypothesis, our comparative study using zoo mammals does not support it, at least with respect to cancer risks.

Authors: Badreddine Bererhi, Pierre Duchesne, Tonia S. Schwartz, Beata Ujvari, Erik Wapstra, Mats Olsson

Source: Ecology and Evolution (Mar 2023)

Abstract

The harmful effects of close inbreeding have been recognized for centuries and, with the rise of Mendelian genetics, was realized to be an effect of homozygosis. This historical background led to great interest in ways to quantify inbreeding, its depression effects on the phenotype and flow-on effects on mate choice and other aspects of behavioral ecology.

The mechanisms and cues used to avoid inbreeding are varied and include major histocompatibility complex (MHC) molecules and the peptides they transport as predictors of the degree of genetic relatedness.

Here, we revisit and complement data from a Swedish population of sand lizards (Lacerta agilis) showing signs of inbreeding depression to assess the effects of genetic relatedness on pair formation in the wild. Parental pairs were less similar at the MHC than expected under random mating but mated at random with respect to microsatellite relatedness. MHC clustered in groups of RFLP bands but no partner preference was observed with respect to partner MHC cluster genotype. Male MHC band patterns were unrelated to their fertilization success in clutches selected for analysis on the basis of showing mixed paternity.

Thus, our data suggest that MHC plays a role in pre-copulatory, but not post-copulatory partner association, suggesting that MHC is not the driver of fertilization bias and gamete recognition in sand lizards.

Authors: Justine Boutry, Marie Buysse, Sophie Tissot, Chantal Cazevielle, Rodrigo Hamede, Antoine M. Dujon, Beata Ujvari, Mathieu Giraudeau, Alexander Klimovich, Frédéric Thomas & Jácint Tökölyi

Source: Scientific Reports (May 2023)

Abstract

Hydras are freshwater cnidarians widely used as a biological model to study different questions such as senescence or phenotypic plasticity but also tumoral development. The spontaneous tumors found in these organisms have been so far described in two female lab strains domesticated years ago (Hydra oligactis and Pelmatohydra robusta) and the extent to which these tumors can be representative of tumors within the diversity of wild hydras is completely unknown.

In this study, we examined individuals isolated from recently sampled wild strains of different sex and geographical origin, which have developed outgrowths looking like tumors. These tumefactions have common features with the tumors previously described in lab strains: are composed of an accumulation of abnormal cells, resulting in a similar enlargement of the tissue layers. However, we also found diversity within these new types of tumors. Indeed, not only females, but also males seem prone to form these tumors. Finally, the microbiota associated to these tumors is different from the one involved in the previous lineages exhibiting tumors. We found that tumorous individuals hosted yet undescribed Chlamydiales vacuoles.

This study brings new insights into the understanding of tumor susceptibility and diversity in brown hydras from different origins.

Authors: Jean-Pascal Capp, Frédéric Thomas, Andriy Marusyk, Antoine M. Dujon, Sophie Tissot, Robert Gatenby, Benjamin Roche, Beata Ujvari, James DeGregori, Joel S. Brown, Aurora M. Nedelcu

Source: Evolutionary Applications (Jul 2023)

Abstract

It is traditionally assumed that during cancer development, tumor cells abort their initially cooperative behavior (i.e., cheat) in favor of evolutionary strategies designed solely to enhance their own fitness (i.e., a “selfish” life style) at the expense of that of the multicellular organism. However, the growth and progress of solid tumors can also involve cooperation among these presumed selfish cells (which, by definition, should be noncooperative) and with stromal cells.

The ultimate and proximate reasons behind this paradox are not fully understood. Here, in the light of current theories on the evolution of cooperation, we discuss the possible evolutionary mechanisms that could explain the apparent cooperative behaviors among selfish malignant cells.

In addition to the most classical explanations for cooperation in cancer and in general (by-product mutualism, kin selection, direct reciprocity, indirect reciprocity, network reciprocity, group selection), we propose the idea that “greenbeard” effects are relevant to explaining some cooperative behaviors in cancer.

Also, we discuss the possibility that malignant cooperative cells express or co-opt cooperative traits normally expressed by healthy cells. We provide examples where considerations of these processes could help understand tumorigenesis and metastasis and argue that this framework provides novel insights into cancer biology and potential strategies for cancer prevention and treatment.

The Burrunan dolphins that live in Victoria’s waterways are a unique species. Find out more about this critically endangered mammal in the latest blog post from the Ecological Society of Australia, hosting Grace Day (PhD candidate, The Wild Genes Group, Deakin University).

Listen to Prof Thomas Madsen (Deakin University) explaining how a long-term study of an adder population has provided evidence that polyandry and non-random fertilisation can have positive effects on genetic diversity. Thomas argues that factoring in mating dynamics could help to improve conservation genetic analyses.

Authors: Antoine M. Dujon, Orsolya Vincze, Jean-François Lemaitre, Catherine Alix-Panabières, Pascal Pujol, Mathieu Giraudeau, Beata Ujvari and Frédéric Thomas

Source: Proceedings of the Royal Society B: Biological Sciences (Jun 2023)

Abstract

Reproduction is a central activity for all living organisms but is also associated with a diversity of costs that are detrimental for survival. Until recently, the cost of cancer as a selective force has been poorly considered.

Considering 191 mammal species, we found cancer mortality was more likely to be detected in species having large, rather than low, litter sizes and long lactation lengths regardless of the placentation types. However, increasing litter size and gestation length are not per se associated with an enhanced cancer mortality risk. Contrary to basic theoretical expectations, the species with the highest cancer mortality were not those with the most invasive (i.e. haemochorial) placentation, but those with a moderately invasive (i.e. endotheliochorial) one.

Overall, these results suggest that (i) high reproductive efforts favour oncogenic processes’ dynamics, presumably because of trade-offs between allocation in reproduction effort and anti-cancer defences, (ii) cancer defence mechanisms in animals are most often adjusted to align reproductive lifespan, and (iii) malignant cells co-opt existing molecular and physiological pathways for placentation, but species with the most invasive placentation have also selected for potent barriers against lethal cancers.

This work suggests that the logic of Peto’s paradox seems to be applicable to other traits that promote tumorigenesis.

Authors: Rodrigo Hamede, Nicholas M. Fountain-Jones, Fernando Arce, Menna Jones, Andrew Storfer, Paul A. Hohenlohe, Hamish McCallum, Benjamin Roche, Beata Ujvari, Frédéric Thomas

Source: Evolutionary Applications (Jun 2023)

Abstract

Infectious diseases are a major threat for biodiversity conservation and can exert strong influence on wildlife population dynamics. Understanding the mechanisms driving infection rates and epidemic outcomes requires empirical data on the evolutionary trajectory of pathogens and host selective processes. Phylodynamics is a robust framework to understand the interaction of pathogen evolutionary processes with epidemiological dynamics, providing a powerful tool to evaluate disease control strategies.

Tasmanian devils have been threatened by a fatal transmissible cancer, devil facial tumour disease (DFTD), for more than two decades. Here we employ a phylodynamic approach using tumour mitochondrial genomes to assess the role of tumour genetic diversity in epidemiological and population dynamics in a devil population subject to 12 years of intensive monitoring, since the beginning of the epidemic outbreak. DFTD molecular clock estimates of disease introduction mirrored observed estimates in the field, and DFTD genetic diversity was positively correlated with estimates of devil population size.

However, prevalence and force of infection were the lowest when devil population size and tumour genetic diversity was the highest. This could be due to either differential virulence or transmissibility in tumour lineages or the development of host defence strategies against infection.

Our results support the view that evolutionary processes and epidemiological trade-offs can drive host-pathogen coexistence, even when disease-induced mortality is extremely high. We highlight the importance of integrating pathogen and population evolutionary interactions to better understand long-term epidemic dynamics and evaluating disease control strategies.

Further reading about this research is available here:

• Tasmanian devil facial tumours reveal secrets of cancer evolution – News and stories by University of Tasmania
• Facial tumours evolve to coexist with Tasmanian devil populations – SCIMEX: Breaking science news for Australia & New zealand

Authors: Margaux Bieuville, Dominique Faugère, Virginie Galibert, Morgane Henard, Antoine M. Dujon, Beata Ujvari, Pascal Pujol, Benjamin Roche and Frédéric Thomas

Source: Frontiers in Ecology and Evolution (Feb 2023)

Abstract

It is increasingly thought that part of human susceptibility to cancer is the result of evolutionary mismatches: our ancestors evolved cancer suppression mechanisms in a world largely different from our modern environments. In that context, it has been shown in cohorts from general Western populations that reproductive traits modulate breast cancer risk.

Overall, the more menses women experience, the more at risk they are to develop postmenopausal breast cancer. This points towards an evolutionary mismatch but brings the question whether the reproductive pattern also modulates the breast cancer risk in menopausal women at high familial risk.

We thus studied the influence of menses on breast cancer risk in a case–control study of 90 postmenopausal women (including BRCA1/2 and non BRCA1/2) nested within a cohort at high familial risk. We tested the association of the lifetime number of menses and the number of menses before first full-term pregnancy with postmenopausal breast cancer risk using Cox survival models.

We showed that the total lifetime number of menses was significantly associated with postmenopausal breast cancer risk and associated with a quicker onset of breast cancer after menopause. Those results align with similar studies lead in general cohorts and suggest that the reproductive pattern modulates the familial risk of developing breast cancer after menopause.

Altogether, those results impact how we envision breast cancer prevention and call for more research on how ecological and genetic factors shape breast cancer risk.