With clones like these, who needs anemones?

Finding Nemo makes marine biologists of us all

I once lived a block away from a beach in Northern California, and when my sons and I wandered the sands at low tide, we often saw sea anemones attached to the rocks, closed up and looking much like rocks themselves, waiting for the water to return. My sons, fans of Finding Nemo, still find these animals intriguing because of their association with a cartoon clownfish, but as it turns out, these brainless organisms have a few lessons to teach the grownups about the art of war.

Attack of the clones

Anemones, which look like plants that open and close with the rise and fall of the tides, are really animals from the phylum Cnidaria, which makes them close relatives of corals and jellyfish. Although they do provide a home for clownfish in a mutualistic relationship, where both the clownfish and the anemone benefit from the association, anemones are predators. They consist primarily of their stinging tentacles and a central mouth that allows them to eat fish, mussels, plankton, and marine worms.

Although anemones seem to be adhered permanently to rocks, they can, in fact, move around. Anemones have a “foot” that they use to attach to objects, but they also can be free-swimming, which comes in handy in the art of sea anemone warfare. (To see them in action, click on video, above.)

Sea anemone warfare could well be characterized as an attack of the clones. These animals reproduce by a process called lateral fission, in which new anemones grow by mitosis from an existing anemone, although they can engage in sexual reproduction when necessary. But when a colony of anemones is engaged in a battle, it consists entirely of genetically identical clones.

Yet even though they are identical, these clones, like the genetically identical cells in your liver and your heart, have different jobs to do in anemone warfare. Scientists have known that anemones can be aggressive with one another, tossing around stinging cells as their weapons of choice in battle. But observing groups of anemones in their natural environment is almost impossible because the creatures only fight at high tide, masked by the waves.

To solve this problem, a group of California researchers took a rock with two clone tribes of anemones on it into the lab and created their own, controlled high and low tides. What they saw astonished them. The clones, although identical, appeared to have different jobs and assorted themselves in different positions depending on their role in the colony.

Battle arms, or “acrorhagi”

The warring groups had a clearly marked demilitarized zone on the rock, a border region that researchers say can be maintained for long periods in the wild. When the tide is high, though, one group of clones will send out scouts, anemones that venture into the border area in an apparent bid to expand the territory for the colony. When the opposition colony senses the presence of the scouts, its warriors go into action, puffing up large specialized battle arms called acrorhagi, tripling their body length, and firing off salvos of stinging cells at the adventuresome scouts. Even warriors as far as four rows back get into the action, rearing up the toss cells and defend their territory.

In the midst of this battle, the reproductive clones hunker down in the center of the colony, protected and able to produce more clones. Clones differentiate into warriors or scouts or reproducers based on environmental signals interacting with their genes; every clonal group has a different response to these signals and arranges its armies in different permutations.

Poor Stumpy

Warriors very rarely win a battle, and typically, the anemones maintained their territories rather than achieving any major expansions. The scouts appear to run the greatest risk; one hapless scout from the lab studies, whom the researchers nicknamed Stumpy, was so aggressive in its explorations that when it returned to its home colony, it was attacked by its own clones. Researchers speculated that it bore far too many foreign stinging cells sustained in the attacks, thus resulting in a case of mistaken identity for poor Stumpy.

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Identical twins grow less identical

DNA sequence is just a starting point

Identical twins are identical only in that their DNA is the same. In what might be an argument against cloning yourself or a pet hoping to get an identical reproduction, scientists have found that having an identical genetic code does not translate into being exactly alike. We have long known that identical twins do not always share the same health fate, for example. One twin can have schizophrenia while another twin may never develop it. Or one twin might develop cancer or diabetes, while the other remains disease-free, even though there can be a strong genetic component to all of these disorders.

So a burning question in the field of genetics and disease has been identifying the difference between a twin who gets a disease and one who does not. A strong candidate mechanism has been the process of genomic modification in which molecules attached to the DNA can silence a gene or turn it on. Typically, methyl groups attached to DNA will make the code unavailable, and acetyl groups attached to the histone proteins that support DNA will ensure that the code is used.

Chemical tags modify DNA sequences

This process of genomic regulation is involved in some interesting aspects of biology. For example, methylation is the hallmark of genomic imprinting, in which each set of genes we inherit from our parents comes with its own special pattern of methylation. The way some genetic disorders manifest can be traced to genomic imprinting. In Prader-Willi syndrome, a person inherits a paternal mutant allele and manifests characteristic symptoms of the disorder, which include obesity and intellectual disability. But people who inherit the same mutant allele from the mothers will instead have Angelman’s syndrome, in which they are small and gracile, have a characteristic elfin face, and also have intellectual disability. Modification from methyl or acetyl groups, also called epigenetic modification, plays a role in dosage compensation for the X chromosome. Women, who have two X chromosomes, shut most of one down through methylation to produce an X chromosome gene dosage like that of men, who have a single X.

Twinning: Nature’s clones

Identical twins have identical DNA because they arise from a single fertilized egg. The egg divides mitotically into two identical cells, and then each cell, for reasons we don’t understand well, resets the developmental process to the beginning and develops as a new individual. The process of twinning carries interesting implications for bioethics, cloning discussions, and questions about when life begins, but it also has helped us tease apart the influences of genetics and environment. A recent study examining life history differences and differences in epigenetic modification in 80 pairs of twins ranging in age from 3 to 74 has revealed some fascinating results that have implications for our understanding of nature vs. nurture and our investigations into the role of epigenesis in development of disease.

You are what you do to yourself

The older the twins were, the more differences researchers found in methylation or acetylation of their DNA and histones. For twins raised apart, these differences were even more extreme. Researchers also concluded that environmental influences, such as smoking, diet, and lifestyle, may have contributed to the differences in the twins’ epigenetic modifications. The three-year-old twins were almost identical in their methylation patterns, but for twins older than 28 years, the patterns were significantly different for 60 percent of the pairs.

These results have major implications for our understanding of disease. For example, we can use this knowledge to identify genes that are differently methylated in people with and without a disorder and use that as a lead in identifying the genes involved in that disease state. We also may be able to pinpoint which environmental triggers result in differential methylation and find ways to avoid this mechanism of disease.

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