Nynke Raven, we are so proud of you! Keep up the good work 🙂
Brief summary of the paper: Polyandry, a common reproductive strategy in various animal species, has potential female benefits, which include enhanced offspring fitness. Benefits can be direct, such as reduced risk of male infanticide of offspring, or indirect, such as increased genetic diversity of offspring and the acquisition of ‘good genes’. Multiple paternity of litters has been recorded in numerous marsupial species but has not been reported in Tasmanian devils, Sarcophilus harrisii (Boitard).
We investigated whether multiple paternity occurred in litters within a wild population of Tasmanian devils. Using major histocompatibility complex-linked and neutral microsatellite markers, the paternity of nine litters was analysed. We found multiple paternity in four out of nine litters and that yearling (> 1, < 2 years old) male devils were siring offspring. This is the first record of multiple paternity and of male precocial breeding in wild Tasmanian devils.
To date, there are no data relating to the subsequent survival of devils from single- vs. multiple-sired litters; therefore, we do not know whether multiple paternity increases offspring survival in the wild. These results have implications for the Tasmanian devil captive insurance programme, because group housing can lead to multiple-sired litters, making the maintenance of genetic diversity over time difficult to manage.
Brief summary of the paper: The origin and subsequent maintenance of sex and recombination are among the most elusive and controversial problems in evolutionary biology.
Here, we propose a novel hypothesis, suggesting that sexual reproduction not only evolved to reduce the negative effects of the accumulation of deleterious mutations and processes associated with pathogen and/or parasite resistance but also to prevent invasion by transmissible selfish neoplastic cheater cells, henceforth referred to as transmissible cancer cells.
Sexual reproduction permits systematic change of the multicellular organism’s genotype and hence an enhanced detection of transmissible cancer cells by immune system.
Given the omnipresence of oncogenic processes in multicellular organisms, together with the fact that transmissible cancer cells can have dramatic effects on their host fitness, our scenario suggests that the benefits of sex and concomitant recombination will be large and permanent, explaining why sexual reproduction is, despite its costs, the dominant mode of reproduction among eukaryotes.
Authors: Lynn B. Martin, BriAnne Addison, Andrew G.D. Bean, Katherine L. Buchanan, Ondi L. Crino, Justin R. Eastwood, Andrew S. Flies, Rodrigo Hamede, Geoffrey E. Hill, Marcel Klaassen, Rebecca E. Koch, Johanne M. Martens, Constanza Napolitano, Edward J. Narayan, Lee Peacock, Alison J. Peel, Anne Peters, Nynke Raven, Alice Risely, Michael J. Roast, Lee A. Rollins, Manuel Ruiz-Aravena, Dan Selechnik, Helena S. Stokes, Beata Ujvari, Laura F. Grogan
Brief summary of the paper: A few members of host populations, so-called superspreaders, have disproportionate impacts on the risk of infectious disease emergence and spread.
Several other forms of EC exist; some of which might be exceptionally protective.
To discover and understand forms of EC, it is imperative to describe the distribution of, and covariation among, traits of individual hosts that mediate the many stages of host–parasite interactions.
Here, we provide a framework to do so, emphasizing how interplay among host traits related to parasite exposure behavior, susceptibility, replicability of parasites on/in hosts, and transmissibility, comprise host competence.
We hope this framework helps reveal new forms of EC and informs and improves management of disease risk.
Individual hosts differ extensively in their competence for parasites, but traditional research has discounted this variation, partly because modeling such heterogeneity is difficult. This discounting has diminished as tools have improved and recognition has grown that some hosts, the extremely competent, can have exceptional impacts on disease dynamics. Most prominent among these hosts are the superspreaders, but other forms of extreme competence (EC) exist and others await discovery; each with potentially strong but distinct implications for disease emergence and spread. Here, we propose a framework for the study and discovery of EC, suitable for different host–parasite systems, which we hope enhances our understanding of how parasites circulate and evolve in host communities.
So far, six animal species are known to carry transmissible, “parasitic” forms of cancer, but researchers are still mystified as to how cancer can become infectious .
Read the full article at TheScientist.
What do you reckon will be the outcome if you mix one book about the ecology and evolution of cancer, lots of shared papers, one Dr Beata Ujvary, one Professor Fredric Thomas and a bit of funding from both the Australian Research Council and the French National Research Council ?
Well, the answer is simple – a very successful and productive international research collaboration that hopefully will allow us to better understand the mechanism of cancer. This collaboration success was recognized earlier this year as Beata Ujvary and the team received the 2018 Vice Chancellor’s Award for International Research Collaboration.
Below: Beata and Fredric shed some light on their collaboration
Authors: Cindy Gidoin, Beata Ujvari, Frédéric Thomas and Benjamin Roche
Brief summary of the paper:
A strong variability in cancer incidence is observed between human organs. Recently, it has been suggested that the relative contribution of organs to organism fitness (reproduction or survival) could explain at least a part of the observed variation.
The objective of this study is to investigate theoretically the main factors driving the evolution of tumour resistance mechanisms of organs when their relative contribution to organism fitness is considered. We use a population-scale model where individuals can develop a tumour in a key organ (i.e. in which even a small tumour can negatively impact organism fitness), an auxiliary organ (i.e. in which only a large tumour has a relatively significant impact) or both organs because of metastasis.
Our simulations show that natural selection acts in two different ways to prevent cancer in a key and an auxiliary organs. In the key organ, the strategy mostly selected is the highest resistance and only a high cost of resistance mitigates this behavior.
Inversely, we observe that a low resistance strategy can be selected in the auxiliary organ when the development of the tumour is slow and the effect of a large tumour on the mortality of the organism is relatively weak. Nevertheless, if the tumour can spread to a key organ, higher resistance strategies are selected in the auxiliary organ.
Finally, our study demonstrates that the relative contribution of organs to the organism fitness and the metastatic propensity of the tumour influence the evolution of tumour resistance at organ scale and should be considered by studies aiming to explain the variability in cancer incidence at organ-scale.
Authors: Tuul Sepp , Beata Ujvari , Paul W. Ewald , Frédéric Thomas and Mathieu Giraudeau
Brief summary of the paper: While it is generally known that the risk of several cancers in humans is higher in urban areas compared with rural areas, cancer is often deemed a problem of human societies with modern lifestyles.
At the same time, more and more wild animals are affected by urbanization processes and are faced with the need to adapt or acclimate to urban conditions. These include, among other things, increased exposure to an assortment of pollutants (e.g. chemicals, light and noise), novel types of food and new infections.
According to the abundant literature available for humans, all of these factors are associated with an increased probability of developing cancerous neoplasias; however, the link between the urban environment and cancer in wildlife has not been discussed in the scientific literature.
Here, we describe the available evidence linking environmental changes resulting from urbanization to cancer-related physiological changes in wild animals. We identify the knowledge gaps in this field and suggest future research avenues, with the ultimate aim of understanding how our modern lifestyle affects cancer prevalence in urbanizing wild populations.
In addition, we consider the possibilities of using urban wild animal populations as models to study the association between environmental factors and cancer epidemics in humans, as well as to understand the evolution of cancer and defence mechanisms against it.