Where does biodiversity come from? A simple answer would be mutation, which creates the heritable variation that fuels natural selection and other evolutionary forces. However, mutations and their impacts are, in turn, affected by the size and structure of an organism’s genome. For example, organisms with large genomes are more likely to encounter mutations during each generation—copying more DNA simply presents more opportunities for errors to occur.
So, how do genomes change in size and structure? One major cause is whole-genome duplication, which produces polyploid organisms. Polyploids possess three or more copies of each chromosome. In contrast, diploid organisms (including humans) possess just two copies of each chromosome. There are multiple mechanisms of whole-genome duplication, but most polyploids originate from abnormalities during sexual reproduction1.
Normally, diploids reproduce by generating haploid (n) sex cells, or gametes, through meiosis. These gametes then fuse to produce a diploid (2n) zygote, which completes the life cycle of the organism. Rarely, a phase of meiosis will fail, resulting in the production of a diploid, or unreduced, gamete. Unlike normal gametes, unreduced gametes contain the same amount of genetic material (2n) as the organism that produced them. When an unreduced gamete fuses with another gamete, it will form a polyploid zygote—an unreduced gamete that fuses with a normal, haploid gamete will produce a triploid (3n) zygote, whereas two unreduced gametes that fuse will produce a tetraploid (4n) zygote. Unreduced gamete production is often correlated with stressful conditions (e.g. extreme heat or cold). Hybrid organisms also tend to produce unreduced gametes, as incompatibilities between different species’ genomes often effect irregular meiosis1.
Successful polyploids are rare. The sudden doubling of genetic material in every cell of an organism upsets many biological processes. In mammals, whole-genome duplication imposes severe developmental challenges that cause nearly all polyploid zygotes to perish before birth2. In contrast, plants have overcome these challenges so frequently that polyploidy has profoundly shaped their evolutionary history. Ancient genome duplications are found throughout the plant tree of life3, and an estimated 35% of all vascular plant species are recent polyploids4. Whole-genome duplication actually causes speciation because new polyploids are reproductively isolated from the diploids that produced them.
Polyploidy has significantly enhanced the physical and biochemical diversity of plants. The increased size of many polyploids relative to their diploid parents has been particularly useful in breeding ornamental plants with larger, showier flowers. Immediate physiological changes in polyploids have also fueled adaptation to challenging conditions, such as drought or saline soil5.
Finally, the large size and highly redundant nature of polyploid genomes fundamentally changes the way they experience mutation. The possession of more copies of each gene mitigates the effects of harmful mutations6, while simultaneously increasing the odds of encountering beneficial mutations7. Furthermore, duplicated genes may evolve independently to develop different or even completely novel functions. In the mustard family, duplicated genes diversified to create the chemical pathways that produce glucosinolates8, which give plants like arugula, wasabi, and horseradish their distinctive piquancy.
Biologists are still uncovering the relationships between polyploidy and plant diversity. One fundamental question that remains is: how many polyploid species exist? Current estimates are likely robust, but basic data like chromosome number and genome size are lacking for many species, especially those found in tropical climates. Gathering these data will increase our understanding of plant genomic diversity and illuminate the tangled evolutionary relationships between plant species.
- Comai, L. (2005). The advantages and disadvantages of being polyploid. Nature reviews genetics 6: 836-846.
- Otto, S. P., & Whitton, J. (2000). Polyploid incidence and evolution. Annual review of genetics, 34: 401-437.
- Jiao, Y., Wickett, N. J., Ayyampalayam, S., Chanderbali, A. S., Landherr, L., Ralph, P. E., … & Soltis, D. E. (2011). Ancestral polyploidy in seed plants and angiosperms. Nature, 473: 97-100.
- Wood, T. E., Takebayashi, N., Barker, M. S., Mayrose, I., Greenspoon, P. B., & Rieseberg, L. H. (2009). The frequency of polyploid speciation in vascular plants. Proceedings of the national Academy of sciences, 106: 13875-13879.
- del Pozo JC, Ramirez-Parra E. 2014. Deciphering the molecular bases for drought tolerance in Arabidopsis autotetraploids. Plant, Cell & Environment 37: 2722–2737.
- Tsai, H., Missirian, V., Ngo, K. J., Tran, R. K., Chan, S. R., Sundaresan, V., & Comai, L. (2013). Production of a high-efficiency TILLING population through polyploidization. Plant physiology 161: 1604-1614.
- Selmecki, A. M., Maruvka, Y. E., Richmond, P. A., Guillet, M., Shoresh, N., Sorenson, A. L., … & Pellman, D. (2015). Polyploidy can drive rapid adaptation in yeast. Nature 519: 349-352.
- Hofberger, J. A., Lyons, E., Edger, P. P., Chris Pires, J., & Eric Schranz, M. (2013). Whole genome and tandem duplicate retention facilitated glucosinolate pathway diversification in the mustard family. Genome biology and evolution 5: 2155-2173.