In this incredible experiment, the team was trying to figure out exactly what drove single-celled organisms to become multicellular all those years ago. One hypothesis is that it was predation that put selective pressure on single-celled organisms, causing them to become more complex. So to test the validity of this in the lab, the team led by evolutionary biologist William Ratcliff, took populations of single-celled green alga Chlamydomonas reinhardtii.
They then put a single-celled filter-feeding predator in the mix, Paramecium tetraurelia and watched what happened. Today, many millions of years later, most plants, animals, fungi, and algae are composed of multiple cells that work collaboratively as a single being. Despite the various ways these organisms achieved multicellularity, their conglomeration of cells operate cooperatively to consume energy, survive, and reproduce. But how did multicellularity evolve?
Did it evolve once or multiple times? How did cells make the transition from life as a solo cell to associating and cooperating with other cells such that they work as a single, cohesive unit?
Karl Niklas Cornell University, Ithaca, NY , a plant evolutionary biologist, is interested in how plants have changed over the past few million years, in particular their size, shape, structure, and reproduction. As the first article in a series of Centennial Review papers celebrating years of the American Journal of Botany , Niklas reviews the history of multicellularity and the changes that cells must have had to go through—such as aspects of their shape, function, structure, and development—in order to be able to functionally combine with other cells.
He also explores the underlying driving forces and constraints from natural selection to genetics and physical laws that influence the evolution of multicellularity. As a student, Niklas started out being interested in mathematics, but then turned to studying plants because of their "mathematical-like structure. Indeed, no matter how it is defined, scientists agree that multicellularity has occurred multiple times across many clades.
Here it is important to point out that the cell wall surrounding Chlamydomonas has two parts: an inner layer and an outer one. Volvox has versions of both, but the inner layer is greatly expanded compared to the Chlamydomonas inner layer. It makes up the bulk of the ECM that is not present in Chlamydomonas , and it helps cement the Volvox cells together. Researchers believe that the explosion in cell wall genes, and the morphing of some of those genes into different kinds of cell wall genes, is what drove the creation of ECM in Volvox.
Clearly, pure comparative genomic approaches have their limitations; they cannot tell us everything there is to know about how developmental processes and multicellularity evolve. But genetic screens are possible for Volvox and Chlamydomonas. What insights have these screens provided into how multicellularity evolved in the volvocine lineage? All four genes have easily recognizable orthologs in Chlamydomonas that are very similar to their Volvox counterparts.
Researchers have cloned Chlamydomonas orthologs corresponding to two of the Volvox developmental genes. One set of investigators showed that the GAR1 gene of Chlamydomonas , which is orthologous to glsA , is able to function just like glsA : When transformed into glsA mutants, it repaired, or rescued, their asymmetric division defect Cheng et al.
Likewise, another set of researchers found that IAR1 orthologous to invA can rescue the inversion defect of invA mutants Nishii et al. Figure 3: Gene and pathway co-option and the origins of asymmetric cell division and cellular differentiation in Volvox A The function of glsA appears to have been co-opted without change from an unknown function in the unicellular ancestor of Volvox, so that it is now part of a pathway shaded green that is required for asymmetric cell division.
This may have happened because some not yet identified gene X that acted in the same pathway shaded gray as the ancestor of glsA proto-glsA changed to take on a new function, generating the new asymmetric division pathway. The dashed arrow indicates that the ancestral pathway may or may not exist in Volvox.
B The evolution of the somatic cell fate appears to have involved gene duplication and then change divergence of one of the gene copies, regA. Scientists hypothesize that the ancestor of regA, proto-regA, acted in a stress-activated pathway shaded gray that led to the repression of growth and cell division. Thus, regA could have gained its cell fate function because it changed in a way that permitted it to co-opt an existing pathway that repressed growth and cell division.
A beige oval at the top of panel A shows the gls-A pathway in a unicellular ancestor. A bold arrow aimed downward points to the altered pathway in Volvox. The original pathway is still present in Volvox and is shown in a beige oval. In addition to this ancestral pathway, Volvox has a new pathway, which is shown in a green oval that overlaps with the beige oval and slopes downward to the right.
Panel B shows how duplication of an ancestral regA could lead to a new pathway in Volvox. A beige oval at the top of panel B shows the ancestral regA pathway. A stress stimulus acts on proto-regA, which inhibits growth and cell division. A bold arrow leads to an intermediate pathway in which regA is duplicated. This intermediate pathway is also shown in a beige oval.
A second bold arrow points downward to the Volvox pathway. Volvox has the unicellular ancestral pathway, which is shown in a beige oval. A second pathway, which is shown in green below the first pathway and points upward to the right where it intersects with the first pathway, partially overlaps the end of the original pathway.
In this second pathway, a developmental cue acts on regA, which inhibits growth and cell division. Thus, the duplication of regA has allowed two different stimuli stress and a developmental cue to lead to the inhibition of growth and cell division. One way to think about how existing genes like glsA and invA might be incorporated or co-opted without change into a new developmental pathway is to consider the analogy of the gas-electric hybrid car.
All cars have brakes. Hybrids are engineered to convert the potential energy generated during braking into electricity. The brakes on hybrids still function as brakes, but they have also been co-opted into a new "pathway" that generates electricity.
Take away the brakes from a hybrid car and it no longer produces electricity. Think of glsA and invA as the brakes in this analogy; they likely have the same function they had in the unicellular ancestor of Volvox , but take them away and Volvox can no longer do asymmetric division or inversion Figure 3A.
Additional insights of a different sort have come from analysis of the somatic regenerator, or regA , gene. This gene is required for maintenance of the somatic cell fate in Volvox ; regA mutant somatic cells develop normally at first, but instead of remaining somatic cells their entire lives and then eventually dying, as somatic cells usually do, they enlarge and regenerate as gonidia that eventually divide to produce new spheroids Kirk Therefore regA somehow prevents somatic cells from growing and dividing, and keeps them from having the stem cell-like potential that gonidia possess.
Think of regA as a tumor suppressor gene that prevents the sort of uncontrolled growth that cancer cells exhibit. On analyzing the Volvox and Chlamydomonas genomes to determine how many regA -like genes they have, investigators discovered that both algae have a large family of paralogous genes that encode proteins resembling the regA product. But using phylogenetic analyses and other methods, they also found that Chlamydomonas does not have a regA gene Duncan et al.
Why not? In addition, where did regA come from in the first place, and how did it come to take on its role as a master regulator of the somatic cell fate? Researchers found answers to some of these questions through further archaeological analysis of the Chlamydomonas and Volvox genomes.
Their analyses revealed that regA likely was generated when a progenitor gene in the ancestor of Chlamydomonas and Volvox was inadvertently copied to produce two paralogous genes: one that eventually gave rise to regA , and one that gave rise to a related gene.
While Volvox retained both regA and the other gene a paralog , Chlamydomonas lost regA. In terms of how the regA function evolved, the modern-day versions of that other gene offer the best place to look for clues. Investigators studying this question found that the Chlamydomonas version of that regA -like gene, named RLS1 , is turned on when Chlamydomonas is deprived of light or certain nutrients Nedelcu This correlation suggests that perhaps RLS1 functions when cells are deprived of energy or nutrients.
Since regA represses reproduction, it seems logical that RLS1 probably does too. This could have happened when the gene that controls that pathway was copied and then used to co-opt the entire pathway to repress growth and division in a developmental context Figure 3B.
Think of the hybrid car analogy again, except in this case the entire stress response pathway is the brake system. Something like this — the co-option of an existing genetic pathway so that it causes a cell to do something it would ordinarily do only under different circumstances — might explain, in general, how organisms evolve new cell types. What Volvox and Chlamydomonas have taught us so far is that multicellularity, at least certain aspects of it, can evolve through relatively minor modifications of the unicellular blueprint see Figure 3.
Presumably not just any unicellular blueprint will do; no doubt the unicellular ancestor of Volvox already had many of the requisite genetic and cell biological raw materials for multicellularity: a multiple fission cell division program, a cell wall that could be modified into ECM, and possibly a stress response pathway that could be adapted to repress growth and division of a subset of cells, causing them to lose the ability to reproduce.
But there is still much to learn. What new gene functions evolved to permit the evolution of asymmetric division and inversion? How did the other novel developmental traits of Volvox evolve? And are there similarities between the way multicellularity evolved in the volvocine algae and the way it evolved in other kinds of organisms?
With the rate of recent progress in this field, answers to these questions, and more, should be on their way soon. Cheng, Q. The role of GlsA in the evolution of asymmetric cell division in the green alga Volvox carteri. Development Genes and Evolution , — Duncan, L. Journal of Molecular Evolution 65 , 1—11 Herron, M. Triassic origin and early radiation of multicellular volvocine algae. PNAS , — Evolution of complexity in the volvocine algae: Transitions in individuality through Darwin's eye.
Evolution 62 , — King, N. The unicellular ancestry of animal development. Developmental Cell 7 , — Kirk, D. Researchers detailed these findings in the October 24, issue of the journal Science.
The first known single-celled organisms appeared on Earth about 3. More complex forms of life took longer to evolve, with the first multicellular animals not appearing until about million years ago.
However, one mystery about multicellular organisms is why cells did not return back to single-celled life. The answer to this question is usually cooperation, as cells benefitted more from working together than they would from living alone. Well, obviously the ant worker cannot reproduce, so it cannot start its own colony. But if it got a mutation that enabled it to do that, then this would be a real problem for the colony.
This kind of struggle is prevalent in the evolution of multicellularity because the first multicellular organisms were only a mutation away from being strictly unicellular. Experiments have shown that a group of microbes that secretes useful molecules that all members of the group can benefit from can grow faster than groups that do not.
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