How a long-lived fungus keeps mutations in check.

One of the oldest and largest living organisms is part of the mushroom-forming fungus Armillaria bulbosa.  This fungus can live and persist past 1500 years old and has found to weigh more than 10,000 kg.  However, with such a long life expectancy, one cannot help but wonder how they can keep the number of deleterious mutations in check during somatic growth.  Duur K. Aanen (2014) addressed that such anomaly could be the result of low genetic variation and mutation rate among the genus Armillaria.

Bulbous honey fungus—Armillaria gallica

Armillaria fungi are tree root pathogens and they develop through single mating between two haploid gametes to become a diploid.  In order for fungi to spread from one tree to another a rhizomorph structure is needed.  These are root-like structures that consist of bundles of hyphae, which mutations can localize in.  These somatic mutations were identified and mapped out by comparing the full genome of various samples of a fungus that covered an area about 200 m x 60 m.  According to Aanen (2014) the genotypes occurred in a spatially clear pattern, which meant that the mutation rate could be calculated per year.  For instance, two samples separated by 100 m varied at approximately 60 areas in their genomes meant the haploid mutation rate per site was about 6 x 10^-10 per year.

To further understand the low variations, Aanen (2014) discussed the work of two researchers­ Anderson and Catona.  Anderson and Catona hypothesized that the rhizomorphs of this fungus grow like plant shoots, where most cell divisions take place under the apex instead of the apical zone, therefore, preventing the population from accumulating new mutations.  It is also understood that in fungi, as well as plants, the mutated-free cells remained at the growth front.  This is accomplished because of asymmetric division of stem cells, which forms a new stem cell and a differentiated cell (Aanen, 2014). Therefore, because asymmetric cell division results into two specific cells, it reduces the number of stem cell and is indicative of a decrease in the number of stem cell mutations.

In comparison to animals, because somatic mutations can lead to cancer, the mutated-free cells of self-renewing tissues remain on the inside, which suggests an increase in the number of mutations.  With that in mind, I wonder if our cells were at the growth front and if we underwent asymmetric cell division, would we too have a lower risk of mutations.

Citation:

Duur K. Aanen. (2014). Science. 346 (6212), 922-923. doi:10.1126/science.1261401. Retrieved from: http://www.sciencemag.org/content/346/6212/922.full