Unit 14 · Ecosystems and Heredity

Picture a pond in a Chicago park in early summer. Frogs call from the edges. If you counted every bullfrog in that pond, you would have measured a population: all the individuals of one species living in one place at one time. The pond also has a population of bluegill, a population of cattails and a population of mosquitoes. Together, all of them and the water, mud and sunlight make an ecosystem.

No population can grow forever. Each frog needs food, water, space and a place to lay eggs. These are resources. When resources are plentiful, a population grows fast. A pair of frogs can produce thousands of eggs. When the pond gets crowded, food runs short and growth slows. Some frogs starve, and fewer eggs hatch.

Scientists call the largest population a place can support over time its carrying capacity. The resource that runs out first sets that limit. Ecologists call it a limiting factor. For pond frogs it might be insects to eat. For prairie plants it might be water in a dry August. For nesting birds it might be tree holes. Find the limiting factor, and you can often predict how a population will change.

Two oak seedlings sprout side by side in a forest preserve. Both need light, water and soil minerals. There is not enough for both to grow tall. This is competition: two or more living things trying to use the same limited resource. The seedling that grows a little faster shades the other. The slower one dies. Competition happens within a species and between species.

Now watch a red-tailed hawk drop onto a field mouse. The hawk is a predator, an animal that hunts and eats other animals. The mouse is its prey. Predation is not cruelty; it is how the hawk gets energy. It also shapes the mouse population. When mice are plentiful, hawks raise more chicks. When hawks are plentiful, mice become scarce, and then some hawks go hungry.

Ecologists have tracked predators and prey for decades. The numbers often rise and fall in linked waves. Prey numbers climb first. Predator numbers climb a little later. Then prey numbers crash, and predators follow. The pattern is evidence that the two populations control each other. Remove the predator, and prey can boom until they eat their food supply bare.

A bumblebee lands on a purple coneflower in an Illinois prairie. The bee drinks sugary nectar. Pollen sticks to its fuzzy body and rides to the next flower, letting the plant make seeds. Both partners gain. Ecologists call this mutualism. Clownfish and sea anemones, and the bacteria in your own gut that help you digest food, are also mutualists.

Not every close relationship is fair. A tick clings to a deer and drinks its blood. The tick gains; the deer loses blood and may get sick. This is parasitism. A parasite lives on or in another organism, called the host, and harms it, usually without killing it right away. Tapeworms, fleas and the fungus that causes athlete’s foot are parasites.

Sometimes one partner gains and the other is not affected much. A barnacle riding on a whale gets a free trip to food-rich water; the whale barely notices. Scientists call that commensalism. Together, mutualism, parasitism, competition and predation are the threads that tie an ecosystem together. Pull one thread, and others move.

Put a leaf under the site’s microscope and you will see tiny green dots packed inside the cells. These are chloroplasts. Inside them, photosynthesis happens. The plant takes in carbon dioxide from the air through tiny pores and water from the soil through its roots. Using the energy of sunlight, it links those simple molecules into sugar. Oxygen is released as a leftover.

That sugar is stored chemical energy. The plant uses some of it to grow. The rest is stored in leaves, stems, roots and seeds. When a rabbit eats clover, it takes in that stored energy. When a fox eats the rabbit, the energy moves again. Nearly all the energy in an ecosystem entered it as sunlight caught by a producer, an organism that makes its own food.

You can test this. Put a water plant like elodea in a jar of water in bright light. Bubbles rise from the leaves. In the dark, the bubbling stops. The bubbles are oxygen, released only when light drives photosynthesis. In the 1770s, Jan Ingenhousz did a version of this experiment and showed that green plants give off oxygen only in light.

Photosynthesis also explains the air you breathe. About 21 percent of the air is oxygen, almost all of it made by producers over billions of years. Carbon dioxide is far rarer, about 0.04 percent, yet every gram of sugar in every plant was built from it.

A food chain is a simple line: grass to grasshopper to sparrow to hawk. Real ecosystems are messier. The sparrow also eats seeds. The hawk also eats snakes. A food web is a diagram of many linked chains that shows who eats whom in a whole community. Arrows point in the direction the energy moves, from the eaten to the eater.

Every organism in a web sits at a level. Producers are the first level. Animals that eat producers are herbivores, the second level. Animals that eat herbivores are the third, and so on. An organism that eats other organisms is a consumer. Some consumers, like raccoons and people, eat at several levels.

Energy is lost at every step. A grasshopper uses most of the energy from the grass it eats just to move, breathe and stay alive. That energy leaves as heat. Only about 10 percent gets stored in the grasshopper’s body where a sparrow can get it. The same thing happens at each level. This is why a prairie can feed millions of insects, thousands of birds and only a few dozen hawks.

The pattern is called an energy pyramid. It explains something you can see everywhere: big predators are rare. It also explains why a food web rarely has more than four or five levels. By the fifth level there is almost no energy left to pass along.

Turn over a rotting log in a forest preserve. The wood is soft and crumbling. Threads of white fungus run through it. Beetles, worms and millions of bacteria are at work. These are decomposers: organisms that break dead material into simple substances. Without them, every fallen leaf and dead animal would pile up forever, and the minerals locked inside would never get back to the soil.

This points to a big difference between energy and matter. Energy moves one way. It enters as sunlight, passes up the food web, and leaves as heat. It is not recycled. Matter is different. The carbon atom in a leaf becomes part of a caterpillar, then a bird, then a decomposer, then carbon dioxide in the air, then a new leaf. Atoms are used over and over. This is cycling of matter.

The carbon cycle is the easiest to see. Plants pull carbon dioxide from the air. Animals eat plants and breathe out carbon dioxide. Decomposers release it as they rot dead things. Nitrogen and water cycle too. Rain falls, plants drink it, animals drink it, and it evaporates back to the sky. The same water has been through countless living things.

Illinois farmers rely on these cycles. Rich prairie soil formed over thousands of years as decomposers broke down dead grasses and roots. That dark soil holds nutrients that corn and soybeans now use. Take away the decomposers, and the soil would stop being renewed.

Walk a restored prairie at the Midewin National Tallgrass Prairie southwest of Chicago. In one square meter you may find a dozen kinds of grass and flower. Beneath them are insects, spiders, fungi and bacteria by the thousands. This variety is biodiversity: the number of different species in a place and the variety within each species.

Why care about variety? Think of a bank with many kinds of savings. If one loses value, others still hold. A prairie with thirty plant species can survive a dry summer better than a field of one crop. Some species will do poorly, but others will thrive and hold the soil. A monoculture, a field of just one kind, has no backup plan.

Ecosystems also do work for people for free. Wetlands soak up floodwater. Forests filter drinking water and hold hillsides in place. Bees and other insects pollinate the apple and pumpkin crops of Illinois. Decomposers build soil. Scientists call these ecosystem services. When biodiversity falls, these services get weaker, and replacing them with machines is costly or impossible.

Silver carp are not native to the Illinois River. Back home in Asia, their eggs and young are eaten by many predators, and diseases keep their numbers down. In the Mississippi basin, few of those checks exist. A single female can release hundreds of thousands of eggs. With little to stop them, the carp population exploded. A species that spreads in a new place and causes harm is an invasive species.

The carp cause harm in a quiet way. They filter plankton, the tiny floating organisms at the base of the river’s food web. Nearly every native fish eats plankton when it is young. When carp take that food, fewer young bass, crappie and bluegill survive. This is competition on a huge scale. In some stretches of the Illinois River, biologists have found that carp make up a large share of all the fish by weight.

Illinois is not alone. Zebra mussels arrived in the Great Lakes in ship ballast water in the 1980s and now coat pipes and rocks. Emerald ash borer beetles have killed millions of ash trees across the state. Garlic mustard shades out spring wildflowers in forest preserves. In each case the invader lacked the predators, parasites and competitors that limited it at home.

Fighting invaders takes many tools. For the carp, crews use nets, electric barriers in the canal, and a push to turn the fish into food. None of these will remove every carp. The goal is to keep the population low enough that native fish can recover and to keep the carp out of Lake Michigan.

In the summer of 2012, much of Illinois went weeks without real rain. Corn leaves curled. Ponds shrank to mud. Fish died in shallow water that got too warm and held too little oxygen. A disturbance is any event that changes an ecosystem quickly. Drought, flood, fire, storms and the arrival of an invader are all disturbances.

Fire sounds like pure destruction, but on a prairie it is an old friend. Before farms, lightning and Native American land managers set fires that swept the tallgrass every few years. Prairie plants grow from deep roots and buds below the soil, so they survive. Fire clears dead stems and kills young trees that would shade out the grass. Today, land managers at forest preserves set careful controlled burns for the same reason.

Resilience is an ecosystem’s ability to recover after a disturbance. A prairie with many species and deep roots is resilient to fire and drought. A lawn of one grass type is not. Resilience has limits. If fires come too often, or a drought lasts years, or an invader never leaves, an ecosystem can tip into a different state and stay there. A shallow lake choked with algae may not turn clear again on its own.

Scientists measure resilience by tracking a place over time. They count species before and after a disturbance and record how long recovery takes. That evidence helps decide where to protect land, where to burn, and when to step in.

Suppose your class is asked to help a small creek in your town. Fish have disappeared. Where do you start? Engineers begin by defining the problem. What exactly went wrong? Perhaps a new parking lot sends muddy water into the creek after every storm. Mud buries the gravel where fish lay eggs. Now the problem is clear: too much sediment reaching the creek.

Next come the criteria: what a good solution must do. It must cut the mud reaching the creek. It must not flood the parking lot. Then come the constraints: the limits. There is a budget. The lot must stay open. The fix must be built by spring. A solution that fails a constraint is not a real option, no matter how clever.

Finally, decide how you will know it worked. Ecologists set a measurable goal, like the amount of mud in a water sample or the number of fish counted next summer. Without a measurement, you can only guess. Defining the problem well is often half the job.

With the muddy creek problem defined, the class brainstorms. One group wants a strip of native plants between the lot and the creek. Roots slow the water and trap mud. Another group wants a small basin that catches storm water. A third wants to replace part of the lot with pavement that lets rain soak through. None of these is obviously best. Each must be scored against the criteria and constraints.

Engineers then test on a small scale. The class builds three tray models with a sloped surface, sprinkles water from a can, and measures how much soil washes into a cup at the bottom. The plant strip cuts the mud by about half. The basin catches nearly all of it but overflows in a heavy pour. The porous pavement works but costs the most.

Every choice has a trade-off: something you give up to get something else. The basin takes space. The plant strip needs years to grow. Porous pavement needs cleaning. Sometimes the best answer combines ideas. The class might pick a plant strip plus a small basin and plan to measure creek clarity every month to see if fish come back.

This is how real projects go. When Illinois planned electric barriers against the carp, engineers compared a barrier with dams, locks and nets, weighed cost and shipping traffic, and then monitored the results for years. Protecting an ecosystem is not one decision. It is a cycle of trying, measuring and improving.

Look at a dividing onion root cell under the site’s microscope at high power. Inside the nucleus, dark threads appear, line up and pull apart. These threads are chromosomes. Each one is a tightly coiled strand of DNA, a long molecule shaped like a twisted ladder. The rungs of the ladder are pairs of four chemical bases, usually written A, T, C and G. The order of those letters is the instruction.

Your body cells each hold 46 chromosomes, in 23 pairs. One chromosome of each pair came from your mother and one from your father. Dogs have 78. Fruit flies have 8. The pea plants Mendel grew have 14. The number does not measure how complex an organism is; it is just how that species packages its DNA.

The instructions are astonishingly long. All the DNA in one human cell holds about 3 billion base pairs. Stretched out, it would be about 2 meters long, yet it fits inside a nucleus far too small to see without a microscope. When a cell divides, it copies every chromosome first, so each new cell gets a full set.

A chromosome is like a long book. A gene is one recipe in that book: a stretch of DNA that carries the instructions for building one protein. Proteins are the working molecules of a cell. Some are building blocks, like the collagen in your skin and the keratin in your hair. Some are tools, like the enzymes that break down your lunch. Some carry signals, like insulin.

Here is how the recipe becomes a trait. A cell reads a gene and links together a chain of small units called amino acids in the order the gene spells out. The chain folds into a protein with a specific shape. That shape decides what the protein can do. A pea plant with a working gene for a starch-building enzyme makes round seeds. If that enzyme does not form correctly, the seed dries out wrinkled. Mendel’s round and wrinkled traits come down to one protein.

Humans have roughly 20,000 protein-coding genes. Your eye color, your blood type, whether you can digest milk as an adult, and how your body handles some medicines all trace back to which versions of certain genes you carry and which proteins they build. Many traits, like height, depend on hundreds of genes working together plus food and environment.

Mendel’s peas carried a secret he could not see. Each plant has two copies of the gene for seed shape, one on each chromosome of a pair. Different versions of a gene are called alleles. Call the round allele R and the wrinkled allele r. A plant with two R alleles, RR, makes round seeds. A plant with rr makes wrinkled seeds. A plant with Rr makes round seeds too, because one working enzyme gene is enough.

The allele that shows even when only one copy is present is dominant. The one that hides is recessive. When Mendel crossed RR with rr, every offspring got one R and one r. All were Rr, and all were round. The wrinkled allele had not vanished. It was riding along, hidden.

When Rr plants fertilized themselves, each parent passed on either R or r, at random. The offspring could be RR, Rr, rR or rr, each equally likely. Three of those four combinations contain at least one R and look round. One is rr and looks wrinkled. Three to one. Mendel’s ratio was not magic. It was two alleles per plant, one passed on by each parent, sorted by chance.

Snap a stem off a spider plant, put it in water, and roots grow. The new plant is a copy of the old one, with identical DNA. This is asexual reproduction: one parent, no mixing, offspring that are clones. Bacteria split in two this way. So do hydras, some lizards and many plants. It is fast, and it works well when conditions are stable.

Most animals and plants also reproduce sexually. In sexual reproduction, each parent makes special cells, egg or sperm in animals, that carry only one chromosome from each pair. In humans that is 23. When egg and sperm join, the offspring gets 46: half from each parent. Which chromosome of each pair ends up in a given egg or sperm is random, so every child of the same parents gets a different mix.

That mixing creates variation, differences among individuals. Two siblings share parents but not the same combination of alleles. Variation is why a family’s children look alike but never identical, unless they are identical twins from one fertilized egg. It also matters for survival. If a new disease strikes, a population with variation is more likely to include some individuals that resist it.

Around 1905, an English geneticist named Reginald Punnett drew a simple grid to keep track of Mendel’s crosses. It is still used today. Write one parent’s two alleles across the top and the other parent’s two alleles down the side. Fill each box with one allele from the top and one from the side. The four boxes show every possible offspring.

Try a cross of two Rr plants. Across the top: R, r. Down the side: R, r. The boxes read RR, Rr, Rr, rr. Three boxes hold at least one R, so three quarters of the offspring are expected to be round. One box is rr, so one quarter are expected to be wrinkled. That is Mendel’s three-to-one ratio drawn as a picture.

Now try Rr crossed with rr. The boxes read Rr, Rr, rr, rr. Half round, half wrinkled. The Punnett square does not tell you what any single seed will be. It tells you the chances. An organism with two identical alleles, like RR or rr, is homozygous. One with two different alleles, like Rr, is heterozygous. A heterozygous plant looks like a homozygous dominant one, but it carries the hidden allele.

Flip a coin four times. You expect two heads, but you might get four, or none. Each flip is separate. Alleles work the same way. A Punnett square for Rr times Rr predicts one wrinkled seed in four. A single pod with six seeds might hold zero wrinkled seeds, or three. Only when you count thousands, as Mendel did, does the count settle close to the prediction.

This is why Mendel’s numbers were 5,474 to 1,850, not exactly 5,475 to 1,825. Probability tells you the chance of each outcome, not the result of any one event. A couple who each carry one allele for a recessive condition has a one-in-four chance with each child. Having one child with the condition does not lower the chance for the next. Each fertilization is a new coin flip.

Understanding chance protects you from a common mistake. People sometimes say a trait "skipped a generation." It did not skip anything. A recessive allele was carried, hidden, by heterozygous parents. When two carriers happened to pass it on together, the trait appeared. Chance decided when, not any plan.

Every time a cell divides, it copies about 3 billion base pairs. The copying machinery is remarkably accurate, and repair enzymes fix most slips, but a few errors get through. A single base may be swapped for another, dropped or added. Any change in the DNA sequence is a mutation. Ultraviolet light from the sun, some chemicals in tobacco smoke, and radiation can also damage DNA and cause mutations.

Where a mutation happens matters. A mutation in a skin cell affects only that cell and the cells that grow from it. It cannot be passed to children. A mutation in an egg or sperm cell can be passed on, and then every cell of the offspring will carry it. Mendel’s wrinkled allele began, long ago, as a mutation in one pea plant that got passed down.

Most mutations change one letter among billions. Many land in stretches of DNA that do not code for any protein, so nothing happens. Others change one amino acid in a protein. Sometimes that makes no difference to the protein’s shape. Sometimes it ruins it. Sometimes, rarely, it makes the protein work better in a new way. Mutations are the ultimate source of every new allele.

Consider one famous mutation. A single base change in the gene for hemoglobin, the protein that carries oxygen in red blood cells, swaps one amino acid. With two copies of this allele, a person’s red blood cells can bend into a stiff sickle shape, block small blood vessels and cause pain and organ damage. This is sickle cell disease. In that form, the mutation is clearly harmful.

Yet the same allele is common in parts of Africa, India and the Mediterranean where malaria is widespread. People with one sickle allele and one normal allele are mostly healthy, and they are much less likely to die of severe malaria. In a place with malaria, carrying one copy is helpful. In a place without it, the allele gives no benefit. Helpful and harmful are not fixed labels. They depend on the environment.

Another example is closer to lunch. Most mammals stop making lactase, the enzyme that digests milk sugar, after infancy. Thousands of years ago, mutations arose in some human populations that keep the lactase gene switched on into adulthood. Where people herded cattle and drank milk, this allele spread. Where they did not, it stayed rare.

Most mutations are neutral: they change nothing you can measure. Your DNA differs from a classmate’s at millions of positions, and nearly all of those differences have no effect at all. Neutral changes still matter to scientists. They pile up at a steady pace and can be used, like a clock, to estimate how long ago two populations or two species separated.

Drive through Illinois in August and you see corn to the horizon. Its ancestor was a wild grass from Mexico called teosinte, with tiny ears of a few hard kernels. Over thousands of years, farmers saved seed from the plants with the biggest, softest kernels and planted those. Generation by generation, the ears grew. This is selective breeding: humans choosing which individuals reproduce based on the traits they want.

Selective breeding does not create new alleles. It works on the variation that mutation and sexual reproduction already provide. A farmer cannot choose a trait that no plant in the field shows. But by breeding only the plants that lean the right way, the farmer makes the wanted alleles more common. Every dog breed, from Chihuahua to Great Dane, came from wolves this way. Cabbage, broccoli, kale and Brussels sprouts were all bred from one wild mustard plant.

There are trade-offs. Breeding for one trait can drag others along. Some dog breeds bred for a flat face struggle to breathe. Crop varieties bred for yield can lose disease resistance, which is why seed banks store older varieties. Illinois is home to a long-running corn experiment at the University of Illinois that has selected corn for high and low oil content every year since 1896, and the two lines still keep moving apart.

Before the 1980s, people with diabetes relied on insulin taken from the pancreases of pigs and cattle. Then scientists cut the human insulin gene out of human DNA and pasted it into bacteria. The bacteria read the gene and built human insulin. It was approved for patients in 1982, and most insulin is made this way today. This is genetic engineering: changing an organism’s DNA directly, often by adding a gene from another species.

Farmers use it too. Much of the corn grown in Illinois carries a gene from a soil bacterium that makes a protein toxic to certain caterpillars but not to people. Other crops carry genes that let them survive a weed killer. Newer tools such as CRISPR let scientists edit a gene in place, changing a few letters rather than adding a whole gene from elsewhere.

Genetic engineering is far faster than breeding and can move genes between species that could never breed. That power brings questions. Could an engineered gene spread to wild relatives? Are edited foods safe to eat? Who should own a gene? Scientists test engineered crops for years before approval, and the evidence so far shows approved foods are as safe as conventional ones, but debate about rules, labels and uses continues.

Compare the two methods with a pea plant. A breeder wanting a disease-resistant pea searches thousands of plants for one that resists, then crosses for years. An engineer finds the resistance gene, perhaps in a wild pea, and inserts it in one season. Both rely on the same fact: a gene is a recipe, and a cell will follow a recipe it is given.

In 1990 scientists in the United States and several other countries set out to read every base of human DNA, all 3 billion letters. The effort, called the Human Genome Project, took thirteen years and thousands of researchers. In 2003 they announced the sequence was essentially complete. A genome is an organism’s entire set of DNA. Reading it is like getting the whole cookbook instead of one recipe.

The map surprised people. Humans have roughly 20,000 protein-coding genes, far fewer than many had guessed, and about the same number as a mouse. Only a small fraction of the genome codes for proteins. Much of the rest controls when and where genes are switched on. Two unrelated people share about 99.9 percent of their sequence.

Since then, the cost of reading a genome has dropped from billions of dollars to a few hundred, and reading takes days instead of years. Doctors can now find the exact mutation behind some rare diseases in a child. Researchers compare genomes across species to trace how genes changed over time. The same map also raises questions about privacy and who may see your genetic information, questions that laws are still catching up with.