Did fungi help mammals dominate Earth?


From SMBC-Comics


Posted by Kasra


The Cretaceous mass extinction is one of the most exciting topics in evolutionary biology. There are always discussions on what caused the mass extinction, what happened during the extinction, what happened to all the dinosaurs, why did the mammals and birds survive, and so on. A recent article in PLoS Pathogens by Arturo Casadevall brings forward an interesting hypothesis: Fungi might have given mammals an evolutionary advantage during this period of time.

Casadevall mentions that humans and other mammals are generally resistant to fungal infections and most pathogenic fungi are in fact only opportunistic pathogens. He suggests that this is due to the mammalian control of body temperature – higher than optimal growth temperature of fungi – and evolution of powerful adaptive immunity. On the other hand, he brings forward examples of amphibians, being ectothermic, and primitive mammals, having lower body temperature, are more susceptible to fungal infections.

He next states that the Cretaceous-Tertiary (K-T) boundary included a cooling period with plenty of dust in the atmosphere and lack of sufficient sunlight. This led to a fungal bloom on the Earth and possible growth of pathogenic fungi. The hypothesis states that this higher than normal presence of fungi selected against surviving ectothermic reptiles and in favour of endothermic mammals. Thus, fungi might have indirectly helped mammals and possibly warm-blooded birds by killing off their competitors for the limited food resources.

Like any other scientific hypothesis, this one also needs to be tested. Unfortunately fossil records cannot tell us much of how common fungal infections were at the time. However, one can first look more closely if warm-bloodedness or higher body temperature does indeed aid in protection from fungal infection, given similar immune systems. Comparing today’s amphibians, reptiles and mammals can be tricky as the host-pathogen interactions may greatly differ among the groups. This could lead to conclusions that are confounded by differences in pathogenicity of fungi or power of the host immune system. Pooling data together from larger numbers host-pathogen pairs can lead to more robust conclusions. Application of heat-resistant fungi can also be beneficial for performing more controlled experiments rather than comparing natural histories. Casadevall himself suggests that climate change can promote evolution of fungi that can better survive in elevated temperatures and be threats as emerging pathogens. In this case, we would be a step in advance knowing what to expect, should these new pathogens emerge.

Casadevall A (2012). Fungi and the rise of mammals. PLoS pathogens, 8 (8) PMID: 22916007


Science answers WHY questions: programmed cell death in unicellular parasites

Posted by Kasra

Famous geneticist Josh Haldane once famously said “I would lay down my life for two brothers or eight cousins”.

Programmed cell death, otherwise known as apoptosis is a well justified procedure in multicellular organisms. All cells within a multicellular organism are originated from a single zygote and are genetically identical (except for some sets of immune cells that go through somatic mutation and genomic rearrangements, but that is different story). The purpose of the organism is to pass on the genetic material to the next generation and to maximize this genetic transfer. Therefore, if programmed death of some cells within the organism would help this purpose (i.e. increase the organism’s fitness), its evolution is logical. After all, often only a handful of cells (the gametes) get to pass their genetic material to the next generation and rest die eventually anyway.

This said, occurrence programmed cell death in unicellular organisms brings up an evolutionary dilemma. Scientists have found markers of apoptosis in unicellular organisms as wide as Plasmodium, Trypanosoma, Giardia and Saccharomyceses. Unicellular organisms within an ecosystem are usually competing with one another for resources, the same way animals and plants do in a larger scale. Therefore, evolution of a trait as strong and costly as altruistic death is worth a closer look, both mechanistically and rationally.

Reece et al. have discussed this matter in a recent review article published in PLoS Pathogens. Mainly focusing on Plasmodium, this review addresses hard questions such as why would altruism evolve in unicellular organisms? What could be the benefits of it? What are the factors that control its occurrence?

Discussing the ideas and hypotheses presented in the review here would be spoilers for those who are eager to read it. In that case you may stop right now and download the open access article right here. If not, you can continue reading as I bring up a few highlights of the paper that I found most interesting.

Hamilton’s rule in evolutionary biology states that cooperation can evolve under these circumstances:

rb – c > 0

Where <r> is relatedness, (for instance the ratio of relatedness between siblings is 0.5 because they share 50% of their genome), <b> is the benefit the receiver gets, and <c> is the cost of the giver. So if benefit x relatedness is larger than cost, then cooperation or sacrifice can be actually be worth it. It is with reference to this rule that Josh Haldane was willing to give away his life for two brothers or eight cousins.

Within multicellular organisms, r = 1 because all cells have been deriven from a single clone. Therefore, wherever, b > c, cell death can evolve. But in unicellular organisms, the story is different. For instance, the population of Plasmodium or Leishmania parasites in the mosquito can be genetically very close or very diverse. Now the evolutionary theory would predict that if occurrence of apoptosis is for altruism and cooperation, it is favourable if the parasites within the population are genetically close to one another. This is a theory that can be tested in a lab: both genetic diversity of different parasite populations and occurence of apoptosis within those populations are measurable with today’s techniques.

Going further from the evolutionary strategy behind evolution of programmed cell death in unicellular organisms, we should also think about what could be possibly the benefits of the receivers that would favor death of the others. One of the theories is that overgrowth of parasites can result in limitation of resources and/or harm to the vector (in this case the Phlebotomine mosquito). If the vector gets overwhelmed by the parasites, it cannot transfer them to the next stage in the life cycle. Thus as Reece et al. suggest, death can be density dependent to control the parasite popultion, another hypothesis which is also readily testable.

And finally, we get to (in my opinion) the difficult part, which is to discover the mechanism underneath these strategies. How can parasites detect relatedness or density? It is possible that sophisticated strategies and mechanisms simply do not exist in certain populations because infecting populations have always been clonal and measurement of relatedness has not been needed. But it cannot always be case. Reece et al. point out to some studies which show evidence of detection of genetic diversity by parasites and existence of mechanisms similar to bacterial quorum sensing.

There is still a lot more to learn and be amazed with.

Reece SE, Pollitt LC, Colegrave N, & Gardner A (2011). The meaning of death: evolution and ecology of apoptosis in protozoan parasites. PLoS pathogens, 7 (12) PMID: 22174671


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