Cells adapt to changes in their environment by regulating the expression of multiple genes. Adaptation to changing conditions involves a global reorganization of the gene expression process. ~ molecular biologists Guilhem Chalancon, Kai Kruse, & Madan Babu
The material artifacts of inheritance and adaptation manifest at the cellular level in a constant process of integrating information. Micromanagers to the hilt, cells adjust their functioning based upon instant needs, immediate conditions, and current supplies.
There doesn’t seem to be any end in sight. ~ American evolutionary biologist Richard Lenski on the perpetuation of evolution
Evolution is a restless dynamic, even in an unchanging environment. There always seems to be opportunity for creative adaptation.
American evolutionary biologist Richard Lenski stored E. coli bacteria in 4,000 vials of various sugary solutions. After 25 years and 58,000 generations (6.6 per day), still stuck in the simplest habitat, Lenski’s bacteria were still evolving.
The bacteria’s fitness improved rapidly early on; later slowing, but still going. Different colonies took distinct evolutionary paths.
In a single flask 2 different colony types evolved: one with small populations and relatively small cells, while another went for large cells in large populations. Domination of one type was expected. Instead, interactions between the different colony types created an ecosystem which allowed both to be viable: a win for pluck in negotiation.
Lenski put the bacteria on different media. One colony was running out of glucose, so it evolved to getting its energy from the citrate in the medium, allowing a much greater population density. Citrate is a citric acid derivative.
The citrate-consuming bacteria adapted by employing numerous genetic transformations. In the process, they speciated, as one of E. coli’s defining characteristics is not being able to use citrate as an energy source in the presence of oxygen.
The generic operations that living cells have been shown to carry out on their genomic molecules indicate that any rearrangement is possible as long as the product is compatible with the basic rules of DNA structure. ~ American molecular biologist James Shapiro
Practically every cell is equipped with the biochemical tools to edit genes. Cell division presents a ripe opportunity for natural genetic engineering: adaptive genomic restructuring to transform cell functioning to a new normal.
Paramecia are typical ciliate protozoa. These single-celled eukaryotes are widespread in freshwater, and fond of forming scums. Brackish and saltwater paramecia also exist.
Many ciliates stay grounded by living in soil. Others toil as symbionts in the guts of their host, from termites to ungulates, digesting cellulose.
Cilia are tiny hair-like protuberances on the external membrane that cells use to move or sense their environment. Paramecia propel themselves by waving their cilia in coordinated unison.
Ciliates can be as large as 2 mm. They are among the most complex protozoans.
Ciliates are conspicuous for their odd genome arrangement. Each cell of a ciliate protozoan has 2 nuclei: a micronucleus and a macronucleus. The small micronucleus carries the germline chromosomes but is transcriptionally silent. (Germline is the gene set employed for reproducing offspring.) The larger macronucleus is the working genome. Transcriptionally active, the macronucleus produces the functional RNAs for cell growth and living.
When stressed (e.g., starved), ciliates can respond by constructing a germline genome for their offspring with a radically different organization. This creative construction is an adaptive response to changed conditions.
It’s one of Nature’s early attempts to become more complex despite staying small in the sense of being unicellular. ~ American evolutionary biologist Laura Landweber
Oxytricha trifallax is a pond-dwelling ciliate: a single cell roughly 10 times the size of a typical human cell. Extensively studied, O. trifallax is typical of its genus.
Oxytricha has mastery of its genome: employing some of the same biological mechanisms that normally protect chromosomes from falling apart to construct the contents of the germline nucleus that it bequeaths its offspring. Oxytricha does this by intelligently sorting through ~225,000 DNA sequences.
Oxytricha’s working macronucleus is also unusually complex. Whereas humans have only 46 chromosomes, Oxytricha have 16,000.
Oxytricha has sex solely to exchange DNA, not to reproduce. Oxytricha spawn daughters asexually.
Oxytricha don’t bother mating if well fed. But if stressed and feeling the need for genetic diversity, Oxytricha seek sex.
2 Oxytricha fuse and share genetic information while mating. The object is for each cell to replace aging genes with lively DNA from its partner. This sexual encounter takes about 2 days.
It really is like it’s running an algorithm, and it’s a cellular computer. ~ Laura Landweber
Together, mating Oxytricha construct new working nuclei with a selectively fresh set of chromosomes. This both diversifies their genetic material and rejuvenates them.
They stop aging by trading in their old parts. ~ Laura Landweber
Bacterial genomes are highly dynamic in both size and composition. The extensive variation in gene repertoires that characterizes prokaryotic genomes can be caused by genome expansion via horizontal gene transfer and gene duplication or, alternatively, contraction due to gene loss. ~ German microbiologists Glen D’Souza & Christian Kost
Bacteria can be genic packrats: soaking up genetic material from the environment, including long-dead organisms. DNA bits are only added if they may be of potential use.
Bacteria shed genetic material they feel they no longer need. For example, in the instance of living in an environment rich in a certain nutrient previously biosynthesized, a bacterium may discard the ability to fabricate the essential metabolite. Such economic gene shedding is how bacteria become dependent upon their situation.
Nutrient-containing environments drive the loss of biosynthetic genes from bacterial genomes and facilitate the establishment of metabolic cross-feeding interactions among bacteria. ~ Glen D’Souza & Christian Kost
Besides genic scavenging, bacteria swap genes among themselves. Many bacteria shed and uptake plasmids, which are independent DNA molecules. These transfers enable bacteria to quickly evolve so as evade destruction by antibiotics and toxic compounds, sometimes by alchemic genes that can transform mercury or other heavy metals into less noxious forms.
Prokaryotes come by 88% to 98% of new DNA through pickup, particularly horizontal gene transfer (HGT), which lets microbes acquire preexisting adaptations from other microbes: ready-made evolution. This is one reason bacteria can acquire antibiotic resistance so quickly. Another is that highly resistant bacteria try to shelter less resilient members of the population to preserve their society.
Self-evaluative genetic modification is the dominant force in microbial evolution. Bacteria populations intelligently adapt via HGT.
Microbial gene pickup played a key role in the evolution of more complex life forms. It continues.
Horizontal gene transfer is rampant, and occurs among distantly related organisms: viruses, bacteria, fungi, plants, and animals. The microbiome within complex eukaryotes is a largely invisible driver of host adaptation by way of selective genic exchange.
Over evolutionary time many infectious bacteria have decided to join rather than keep on fighting. Via genetic pickup and adaptation, they learned new skills that allowed them to contribute to a host rather than harm it. In the process, bacteria inactivate and then eliminate genes that no longer serve them.
Obligate host-associated bacteria often have reduced genome sizes in comparison to related bacteria that are known to engage in free-living or opportunistic lifestyles. ~ American biologist Adam Clayton et al
For energetic efficiency emergent endosymbionts streamline their gene inventory to one compatible with their new lifestyle. Their pathogenic past is shed, but their knowledge of how to evade host immune system destruction is retained until a truce is obtained. How this perceptive shift is achieved is not known.
For their hosts, commensal microbes provide adaptation opportunities, though mutually beneficial relationships take time to develop. Plants have been most successful in cultivating partnerships with other organisms, both microbial and macrobial.
Many herbivorous insects harbor microbial symbionts that provide essential nutrients and that help protect against parasites and predators by priming the immune system.
Gut bacteria may allow a host to expand its range of edible vegetation: detoxifying plant metabolites and manipulating plant defense responses to render them ineffective.
Western corn rootworms’ gut flora suppress defensive gene expression in maize roots, allowing their host to feast. Colorado potato beetle larvae chew potato and tomato plant leaves thanks to bacterial symbionts that defuse plant defenses.
The microbiome can affect speciation. Microbes reduce the viability of animal hybrids, even of those otherwise closely related. This arises from self-interest. The microbiome seeks an accommodating environment for itself. It rejects an uncomfortable habitat.
Hybrids can create irregularities that microbes find intolerable. This is especially true for gut bacteria, which are very community oriented. Gut flora incompatibility causes lethality in certain interspecific hybrids. Hence, the microbiome vectors host evolution by genetic contribution and by veto. Internal environmental pressures can be as significant as those in the external environment. The envirotype is both within and without.
The pathogenesis of infection is a continuously evolving battle between the host and the infecting microbe. ~ American physician Marcia Goldberg et al
Pathogens present a constant adaptive pressure (as well as facing it themselves). Germs have been a primary driver of human evolution, more so than diet or climate conditions, precisely because survival is instantly at stake; and the tools are found within, as pathogens leave genetic material that provides an investigative basis for intelligent adaptation.
Adaptation includes going about business at different paces. This involves distinct subpopulations of invading cells employing their own alleles to set their rate of development. How this is accomplished is not known, but pathogenic bacteria employ this approach to evade host defense systems.
Plants and animals have self-produced antibiotics and immune systems to fight off pathogens. Invading bacteria evolved a 2-pronged strategy to deal with these destructive powers. 1st, multiply fast. One bacterium can become millions within hours. Overwhelming numbers may prevail. The 2nd stratagem is a fail-safe: lay low.
Antibiotics kill rapidly populating bacteria. Immune system macrophages gobble up marauders and apply microbiocidal remedy.
For pathogens to survive, the solution is to slow down. This confers antibiotic resistance simply by not taking the bait. If digested by a macrophage, a sluggish bacterium simply has to wait out its imprisonment before being pronounced dead and disgorged. Free at last, the little germ can go about its business of mayhem.
Salmonella take this 2-track approach to cause gastric distress and other ailments in vertebrates. While the majority go gangbusters, a few leisurely reproduce and bide their time.
The conflict between cellular and viral organisms has been the major engine of biological evolution. ~ French molecular biologist Patrick Forterre
A primary driver of evolution has been the eternal pestilence of cells everywhere: viruses. Virus success in surviving, replicating, and spreading depends upon productive interaction with many cell components. These host dependency factors are proteins that a cell requires for normal functioning but are hijacked by a virus to suit its needs.
Another class of cellular components which interact with viruses are restriction factors: cell proteins which play no obvious role in normal functioning, but seemingly exist solely to interfere with a virus’ life cycle. Many restriction factor proteins are encoded by genes whose expression is induced by interferons: proteins produced in response to the presence of abnormalities, including viruses, bacteria, and tumors.
All life must survive their corresponding viruses. Thus, antiviral systems are essential in all living organisms. ~ American virologist Luis Villarreal
Detecting a virus results in a cascade of genetically scripted responses. First comes interferon manufacture, followed by unleashing restriction factors.
All viruses recognize their cellular hosts by binding to specific molecules on the cell’s surface, typically a specific glycoprotein. This binding site is called a receptor by virologists; a term off-putting to biologists, as a cell plays no active role in inviting infection by sporting viral reception sites.
To a virus, the receptor provides an appropriate attachment point as well as telling the virus that it has come to the right place to invade the cell membrane and initiate its enterprise. The virus-binding region of a receptor is often unrelated to the receptor’s normal function. Generally, surface receptors act as an interface for cellular operations, including intercellular communication.
Virus evolves a mechanism to persist, cells evolve a way to defeat that mechanism, virus evolves a way to defeat what the cell just evolved. ~ American virologist Rob Kalejta
Cells evolve resistance to viral infection by altering amino acids in the binding site without disturbing the part of the receptor critical to proper functioning. This highly specific molecular tweaking comes via intelligent genetic adaptation: either epigenetically or by altering DNA coding sequences as necessary.
The genes that script the production of proteins involved in normal functions resist mutations by removing errors in DNA replication. In contrast, genes encoding restriction factors rapidly adapt. They must, as viruses are constantly evolving to evade restriction factors.
Viruses quickly adapt to changes in their binding sites. Some, such as HIV, figure out how to inactivate restriction factors. This creates an intense cycle of competitive coevolution at the molecular level between a virus and its host cell.
In contrast to the sometimes rapidly revolving adaptations in restriction factors, host dependency factors seldom change. That is because viruses and cells employ host dependency factors in the same way, for the same functionality.
A cell relies upon host dependency factors for its own operations. It cannot afford to alter these important proteins to thwart viruses. Hence, the genes of host dependency factors are conserved.
Spiraling virus and host cell coevolution adds to the virus’ knowledge base, yielding greater flexibility in recognizing receptors. This invaluable education can graduate a virus to the next level: learning how to hop from one species to another.
Evolvable organisms naturally separate themselves from less evolvable organisms simply by becoming increasingly diverse. Evolvable species accumulate over time. Evolvability is inevitable. ~ American computer scientist Kenneth Stanley
Evolution often involves augmenting the capacity to evolve by creating variation genes which may become useful later. Evolvability is especially critical to pathogens in their race to stay one step ahead of their hosts: by having a ready reserve of possibilities to apply depending upon what barrier to entry is encountered.
The bacterium Borrelia burgdorferi – using ticks as transport – causes Lyme disease in mammals. The Lyme bacterium has a single protein essential to establishing a long-term infection. B. burgdorferi keeps in its genome – left unexpressed unless needed – an assortment of genes to alter the expressed protein to overcome a host’s immune defenses.
Adaptive evolvability includes pre-adaptations: innovative by-products of adaptation that may later become employed as needed. Crystallin, which is the transparent light-refracting protein in the cornea and lens of vertebrate eyes, originated as an enzyme. Proto-feathers arose in dinosaurs for mating display, and perhaps insulation, long before birds took them under their wing to fly.
Pre-adaptations exceed adaptations several-fold. ~ Austrian evolutionary biologist Andreas Wagner
A primary driver of adaptation is being able to take advantage of new energy sources. Metabolism exemplifies the need for evolvability.
Metabolism is one of the most complex biological tasks. The metabolic genotype of an organism encodes a reaction network with hundreds of enzyme-catalyzed chemical reactions needed to consume a food source, even one as simple as a sugar.
A fundamental task in metabolism is to synthesize biomass precursor molecules from a food source as a prelude to digestion. A metabolic network is considered viable if it can synthesize all the precursor molecules it needs from its food.
There are over 5,000 biochemical reactions related to breaking down molecules for food. Any one organism employs only a small fraction of these possibilities to eat. For macrobes, many necessary reactions are performed by gut microbes in concert with host catabolic activity.
Becoming viable on a new food source allows an organism to thrive in the instance that its previous diet becomes less available. This ability often originates as a pre-adaptation.
The forgoing examples illustrate how the genome acts as a toolkit that is intelligently and creatively employed. Evolvability is itself an integral aspect of adaptation. Pre-adaptation is a key mechanism for evolvability.
Adaptation in Disguise
A trait that’s maladaptive in one environment can be adaptive in another. ~ American marine molecular biologist William Detrich
Adaptation may be disguised in a broader context not readily recognized. Human resistance to malaria, prevalent in sub-Saharan Africa, has been a dual-track genetic adaptation: immune system modifications and alterations in human red blood cells (erythrocytes) that hinder the ability of the malaria parasite to invade and replicate there.
The altered erythrocytes may polymerize into a sickle shape when deoxygenated. The cell’s hemoglobin – the protein, iron-bound transport for oxygen and other gases – stops working properly.
The upshot of sickle-cell anemia is a shortened life span, to an average of 42 years in males and 48 in females. That is a better fate than succumbing to malaria in childhood.
Like blood type, eye color, and other traits, sickle-cell is passed down genetically. Out of context, it appears maladaptive. In context, it may be lifesaving.
The protein hemoglobin tells a tale of adaptive evolution. Hemoglobin and hemoglobin-like proteins are found in bacteria, fungi, plants, and invertebrates, as well as all vertebrates.
One reason is that hemoglobin is a model of flexibility. The protein can work in multiple conformations. Each shape offers slightly different functionality. Hemoglobin adapted to meet the needs of its many customers. A plant variant of the molecule, leghemoglobin, carries nitrogen and scavenges oxygen, which is a poison to anaerobic systems.
The ancestral globin gene duplicated itself and diverged in sequence some 450 MYA in fish. Such genome duplication yielded core conservation while affording adaptation. Legumes created a symbiotic relationship with nitrogen-fixing bacteria via the same trick.
For fetal use several animals independently evolved a 2nd hemoglobin type – a genetic variant of the 1st – with a modified amino acid sequence. Fetal hemoglobin can rob oxygen from maternal circulation, thus improving healthy growth prospects for the little one.
The bar-headed goose flies over the Himalayan mountains at 9,200 meters, an altitude with 29% of the oxygen available at sea level. A single amino acid alteration lets the goose make better use of available oxygen compared to its lowland relative.
Conceptually similar to the hemoglobin adaptation of bar-headed geese, octopi adapt to frigid water by a simple genetic expression tweak that speeds neuron processing which otherwise slows from the chill.
Organisms that sexually reproduce are granted the great advantage of genetic shuffle during meiosis. But even mitotic haploids manage to coherently adapt.
Transported and delivered by mosquitos, the protozoan parasite Plasmodium falcipanum causes malaria in humans.
Numerous antimalarial medications have been tried. Quinine was the first, beginning in the 17th century.
Invariably the parasite evolves resistance to these drugs. This is peculiar because Plasmodium are haploid. Lacking meiosis, each generation is ostensibly a clone of its parent. But adaptation still occurs.
One treatment tested against Plasmodium involved inhibiting the enzyme required for biosynthesis of nucleic acids and a precursor, pyrimidine. (The nucleobases for cytosine, thymine, and uracil are pyrimidine derivatives.) Plasmodium developed resistance, but not by point mutation, where a new base nucleotide is substituted for the old. Instead, multiple copies of the gene for making the specific enzyme appeared, allowing production of the requisite enzyme. This was a pre-adaptation aimed at contingency flexibility.
The genic copies were constructed during mitosis by rearranging scattered RNA segments. Further, the number of copies made go up or down depending on drug pressure. Adaptive resistance by Plasmodium is specific and based upon risk assessment.