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The evolutionary transition from single-celled to multicellular individuality requires organismal fitness to shift from the cell level to a cell group. This reorganization of fitness occurs by re-allocating the two components of fitness, survival and reproduction, between two specialized cell types in the multicellular group: soma and germ, respectively. How does the genetic basis for such fitness reorganization evolve? One possible mechanism is the co-option of life history genes present in the unicellular ancestors of a multicellular lineage. For instance, single-celled organisms must regulate their investment in survival and reproduction in response to environmental changes, particularly decreasing reproduction to ensure survival under stress. Such stress response life history genes can provide the genetic basis for the evolution of cellular differentiation in multicellular lineages. The regA-like gene family in the volvocine green algal lineage provides an excellent model system to study how this co-option can occur. We discuss the origin and evolution of the volvocine regA-like gene family, including regA—the gene that controls somatic cell development in the model organism Volvox carteri. We hypothesize that the co-option of life history trade-off genes is a general mechanism involved in the transition to multicellular individuality, making volvocine algae and the regA-like family a useful template for similar investigations in other lineages.
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The Evolution of Genetic Robustness for Cellular Cooperation in Early Multicellular Organisms
The major evolutionary transition to multicellularity shifted the unit of selection from individual cells to multicellular organisms. Constituent cells must regulate their growth and cooperate to benefit the whole organism, even when such behaviors would have been maladaptive were they free living. Mutations that disrupt cellular cooperation can lead to various ailments, including physical deformities and cancer. Organisms therefore employ mechanisms to enforce cooperation, such as error correction, policing, and genetic robustness. We built a simulation to study this last mechanism under a range of evolutionary conditions. Specifically, we asked: How does genetic robustness against cellular cheating evolve in multicellular organisms? We focused on early multicellular organisms (with only one cell type) where cells must control their growth to avoid overwriting each other. In our model, unrestrained cells will outcompete restrained cells within an organism, but restrained cells alone will result in faster reproduction for the organism. Ultimately, we demonstrate a clear selective pressure for genetic robustness in multicellular organisms and show that this pressure increases with the total number of cells in the organism.
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- Award ID(s):
- 1655715
- PAR ID:
- 10394101
- Editor(s):
- Holler, Silvia; Löffler, Richard; Bartlett, Stuart
- Date Published:
- Journal Name:
- Proceedings of the 2022 Conference on Artificial Life
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Conference Paper:
- https://doi.org/10.1162/isal_a_00536
