In every parent’s life there comes a singular moment, a knife edge when the world bisects neatly into two parts. There’s life before, and life after. Mine split irreversibly on a frigid December morning, just past 4 a.m., as my son took his first breath and sent me reeling over the threshold of fatherhood, ecstatic and teary-eyed.

Witnessing the birth of my first child opened up whole new avenues of developmental biology for me, as a science writer, to ponder. How could our little miracle, with his wriggling legs, searching gaze, tiny, grasping hands, emerge from a minuscule ball of cells? The basic concept has been drilled into our brains since we were kids: From the union of sperm and egg comes an embryo. But as that egg divides and grows, how does the structure of a body come to be?

It’s a doozy of a question. For more than half a century, the go-to answer has been DNA and biochemistry: Nearly every aspect of development, researchers thought, could be brought on by triggering the right genes at the right times or adding the right chemical signal, creating a cascade of precise transformations. Over the past few decades, though, a growing body of work has cast a spotlight on another starring role in this show. Physical and mechanical forces — things that pull and stretch and twist and squish cells — act alongside genes, and play a major role in everything from the formation of organs to the structure of our limbs to the onset of disease. Serious conditions like certain types of muscular dystrophy and cancer, which seem entirely disparate on the surface, may result from a breakdown of force-sensing mechanisms in cells.

The idea isn’t exactly new. “If you get books on science from the 1890s to the 1910s, everything’s explained mechanically,” says bioengineer and cell biologist Don Ingber, the founding director of Harvard’s Wyss Institute and coauthor of a 2013 overview of the role of mechanics in cell development in the Annual Review of Cell and Developmental Biology. “Then chemistry came in, genetics came in, and the baby was thrown out with the bathwater.”

Armed with technology that can probe and measure forces at a cellular level, more scientists are starting to return to these century-old concepts — and according to Ingber, it’s becoming increasingly clear that physical forces and mechanics are a crucial part of developmental biology.

A key 2006 study in the journal Cell showed just how dramatically force can change cell function. When adult stem cells grew on a soft surface, the paper reported, they started to form something that looked like developing neurons — but when they grew on a hard substrate, they instead took on the shape of osteoblasts, the precursor cells to bone.

“If the cell is round and floppy, or spread out wide and pulled taut, you get totally different functions,” Ingber says. In other words, the forces that a stem cell “feels” on its surface may determine what sort of tissue it will ultimately become.

It’s still not obvious how those minute forces help to shape the formation of all of a body’s requisite parts, however. What signals do they provide that drive the development of limbs? Of organs? Of a brain that harbors thoughts and feelings and fears?

“Those are the mysteries still being uncovered,” says Celeste Nelson, a developmental bioengineer at Princeton University who studies developmental mechanics and coauthored an article on aspects of the topic in the Annual Review of Biomedical Engineering. “The best guess is that yes, mechanical force is important and mechanical stresses are essential. But what exact signals are being sent, and how those are being translated into alterations in cells at these early stages, is still a bit unclear. This is what half of my lab is working on right now.”

Sensing force

The clues to how this all works, Nelson says, might be revealed by studying how cells sense force in the first place — and there are a few different ways a cell can pull this off.

It can use stretch-sensitive ion channels, tiny valves in the cell membrane that let charged atoms like calcium flow in and out, triggering a variety of biochemical signals. Or it can exploit cell-cell junctions, points where certain types of cells are “spot-welded” to their neighbors by globs of proteins.

It could also be leaning on well-studied structures that sense forces during development: clusters of proteins called focal adhesions.

These adhesions anchor cells to the extracellular matrix, the fibrous scaffold that surrounds them. And as that scaffold pulls or stretches a focal adhesion, two things happen: First, proteins inside the adhesion trigger a flood of biochemical signals that alter structural functions inside the cell. Second, and more profoundly, the focal adhesion tugs on a vast structural web inside of cells, called the cytoskeleton.

This mesh acts like a series of I beams and guy wires, supporting the cell membrane and lending the cell its overall shape and form. Crucially, it also connects the focal adhesions to the cell’s nucleus, where its DNA is stored. And that, says Jan Lammerding, a biomedical engineer at Cornell University, could be one of the keys to how physical force influences a cell’s fate.

Any force on the cell’s surface, he says, may be transmitted through the cytoskeleton and passed on to the nucleus, which itself will be stretched or twisted. As the nucleus is squished around, some genes inside it will be newly exposed, and become more active. Others will be suddenly hidden, making them less active. In effect, it may be possible to modify the genetic function of a cell just by yanking on its nucleus.

Those changes go both ways. When the nucleus senses force, proteins inside it called Lamin A pile together en masse, making the organelle stiffer. As the nucleus hardens, it can alter the activity of genes inside it, and some of these changes can set off a chain of events that makes the extracellular matrix stiffer. The matrix, in turn, exerts even stronger forces back into the cell.

This constant push and pull between a cell and its matrix creates a powerful feedback loop. Any changes in the cell will trigger changes in the matrix; any changes in the matrix will trigger even more changes in the cell, and with each iteration, the cell is steered further and further toward its final incarnation, be it a muscle cell, nerve cell, liver cell or any other cell in the body. Sheets or clusters of those differentiated cells expand and fold and, steered by mechanical forces and other inputs, come to sculpt whole organs.

Matters of the heart

In truly poetic fashion, the first organ to emerge in a human embryo is the heart. It starts as a loosely organized tube, explains Dennis Discher, a bioengineer at the University of Pennsylvania, and as it grows, the cells within it harden gradually more each day. That’s a fact cynics everywhere will relish. But according to a 2016 study by Discher and his lab, this hardening may be responsible for the fact that the heart beats at all.

Inside the nascent organ, molecules of Lamin A collect inside the nucleus of cells called cardiac myocytes, causing them to stiffen and elongate. At the same time, the cells exude an increasing amount of collagen, a tough, stringy protein that hardens the extracellular matrix around them. The forces each exerts on the other progressively increase, like a game of cellular tug-of-war, until they reach a critical threshold, Discher says.

As the forces hit that breaking point, a cell somewhere in the mix will spontaneously contract, yank on its neighbors and cause them to contract as well. The resulting chain reaction ripples out among the cardiac cells, triggering an initial heartbeat. “As soon as you get one contracting a certain amount, if it’s connected to all the other cells around it mechanically, then it’s going to set off a reaction called a peristaltic wave that goes on down the line,” Discher says.

Thanks to the constant feedback between forces inside and outside the cells, every pulse of that wave will increase the stiffness of the cardiac cells and the scaffold they sit in, progressively steering the cells’ development. Gradually, that and other inputs will lead them to morph into the specialized, four-chambered muscle that sustains us throughout our lives.

A similar process may happen as lungs and other organs develop. As cells there mature and tissues stiffen, ones that formerly grew in flat sheets (epithelial cells) change their arrangement. This shuffling exerts new forces that can cause the sheets to buckle and fold, like a pair of hands pushing on a tablecloth. Those folds start to rise out from the sheet, creating bud-like shapes that lend organs their initial three-dimensional structures.

“The way you get the patterns of almost all your tissues is through progressive budding or branching in fractal-like ways. All of these patterns are dependent on branches on top of branches, or buds on top of buds,” Ingber says.

Squeezing out a tooth

Given the number of buds that grow on top of each other in a lung or a pancreas or a liver, breaking down how mechanical forces shape such complex structures is no easy task. “In the pancreas or in blood vessels, there are millions of branches and buds, in all three dimensions,” Ingber says. Instead, the best way to get a sense of how the process occurs is to distill it down to the formation of a single bud.

With that in mind, in an elegant 2011 study, he and his colleagues focused on one of the only organs that emerges naturally from a lone bud — a tooth. Rather than needing millions of branches to form its structure, it requires only one. That branch grows in two sections: a part that bows out to form the exterior, and another that pops inward to form roots. By investigating how and when those sections grew, Ingber’s team hoped to unravel the role of physical force in the process.

Researchers had known for years that proteins called motility factors play a role in this process. Usually, they beckon cells to grow toward them like diehard fans flocking toward a celebrity, which squeezes them together into a dense, taut mass. But what if the growth factors were just a means to an end? What if the key to tooth development wasn’t those proteins themselves, but the physical squeezing that they cause as cells crowd together?

To test this idea, Ingber and his colleagues first removed growth factors from the equation, and found that tooth development ground to a halt. Then they tried growing the developing buds between two sheets of a rubbery polymer. Shockingly, as they squeezed those sheets together, the tooth’s normal formation started once again. The scientists later showed that cells started to mineralize and lay down what looked like dentin, a key toothy building block. The force exerted on the cells by the polymer sheets alone was enough to kick off the entire cascade of development.

When force goes awry

The physical forces in and around early cells may spark the formation of organs — but they can also cause the body to fail in spectacular ways. An entire laundry list of seemingly unrelated diseases can be linked to errors in how cells sense force during and after development.

Spina bifida, a condition where an embryonic structure called the neural tube (which eventually forms the brain and spinal cord) fails to close, is connected to a breakdown in cellular forces, new research suggests. Likewise, cleft palate, which occurs when two sides of a person’s palate are deformed, could be caused by force-sensing gone awry at specific points during embryonic development.

Sometimes, the effects of these force-sensing glitches can lead to problems later in life, notes Lammerding. Some types of muscular dystrophy, a disease that results in muscle atrophy over time, may be linked to a breakdown in force-sensing mechanisms within muscle cells.

“Normally if you go to the gym to exercise, the muscles will adapt to the higher mechanical load,” Lammerding says. When muscle tissue feels the physical force of weight pulling on it, the cells inside it lay down more fibers of proteins called actin and myosin in their cytoskeletons. The more of those fibers the muscle cells contain, the stronger they get.

But in one form of the disease called Emery-Dreifuss muscular dystrophy, the cells have trouble sensing the forces stretching them, so they can’t create more muscle fiber in response to the load. As a result, they don’t grow stronger with exercise, and instead atrophy slowly on the bone. Although the symptoms of the disease set in several years after birth, their root cause is a breakdown in cellular force sensing, Lammerding says.

New treatments

For many of these diseases, there’s currently no way to prevent them before they emerge. But bioengineers are searching for new ways to harness the physical forces that shape cell development, and might one day be able to apply them in treatments.

The dream goal, Nelson says, would be to use mechanical force, along with other inputs, to grow tissues and organs on demand in the lab — a development that could do away with long waiting lists for transplants in patients with life-threatening diseases. “Ultimately, what I want to do is know this well enough that we can take a population of maybe a hundred cells, put them in a dish and provide them with two or three initiating stimuli, and have them build themselves into a lung,” she says. Granted, the idea is far-fetched, but based on how quickly research is progressing, she thinks we may see success in a decade or less.

In the meantime, other researchers are working on more immediate applications. Ingber, for one, is taking what he’s learning about the way cellular scaffolds and mechanical forces affect development to create lifelike organ tissues in the lab.

To accomplish that feat, he’s artificially steering the development of cells by growing them on surfaces that mimic the physical and chemical environment of specific organs. With the right mechanical stimulation, he says, cells placed there will develop into a fully formed layer of organ tissue. The result, called an organ-on-a-chip, provides a thin cross section of working kidney, liver or other organ, complete with its own three-dimensional structure.

Devices like these, he adds, could provide accurate models of full-sized organs within tiny pieces of translucent material, letting scientists and drug companies test new treatments for disease more rapidly and effectively than ever before.

Other researchers want to manipulate cellular forces to treat severe wounds. Treena Arinzeh, a biomedical engineer at the New Jersey Institute of Technology, is working to develop new types of materials that could help regrow large sections of missing bone, doing away with the need for metal implants or grafts from cadavers. By putting stem cells on a specially engineered scaffold — a sort of spongy structure made in the lab — she provides them with a bed that has just the right amount of stiffness to coax them into becoming bone and cartilage cells.

This, she hopes, can one day help treat injuries from trauma, weakened bones from osteoporosis, and potentially a whole host of other conditions. “Even though the fundamental science is still developing, we are trying to at least take some of that knowledge and develop therapies out of it,” she says. “We’re probably only right at the tip of the iceberg in terms of what we can do.”

As with any cutting-edge science, the knowledge that emerges from research like this will inform the next questions scientists ask to understand how the body takes shape. Eventually, cellular force-sensing might even become the basis for a radical new interpretation of developmental biology. The research is still in its early stages, and there are still many open mysteries about the ways mechanical forces steer the fate of cells. But the answers to those puzzles — and the new medical treatments that they enable — may surface within our lifetime.

Until then, I won’t need to look very far to revel in the unlikely miracle of the human form. Like all new parents, I’m struck each day by the profound wonder of a tiny person developing before my eyes. The growing confidence of little feet plodding across a bare wood floor; the wailing cries that arrive as new teeth sprout from sensitive gums; the tiniest milestones, new abilities and revelatory moments of a new body coming into its own — all of those made possible by the complex ballet of cells and tissue unfolding to create a small, sweet, curious little boy.

There’s a place in West Virginia where trees grow upside-down. Branches sprout from their trunks in the ordinary fashion, but then they do an about-face, curving toward the soil. On a chilly December day, the confused trees’ bare branches bob and weave in the breeze like slender snakes straining to touch the ground.

I’m visiting an orchard at the Appalachian Fruit Research Station, an outpost of the US Department of Agriculture nestled in the sleepy Shenandoah Valley. Here, at Dardick’s workplace, the disoriented plums are but one in an orchard of oddities, their outlines, seasonally stripped of leaves, standing out in stark relief.

There are trees with branches that shoot straight up, standing to attention in disciplined rows, with nary a sideways branch. There are trees with branches that elegantly arch, like woody umbrellas; others with appendages that lazily wander this way and that.

Dwarf trees crouch, sporting ball-like crowns akin to Truffula trees. Compact “trees” poke from the ground in clumps of scraggly, knee-high sticks. Apple trees with some hidden predicaments grow in a greenhouse nearby: Their roots reach sideways rather than down. The topsy-turvy growth of all of these trees comes from genetic variations that cause the dialing up, dialing down or elimination altogether of the activity of key genes controlling plant architecture.

Understanding these misfits has real-world applications: It could help grow the next generation of orchards that, densely packed with trees, produce more fruit while using less land and labor than today. But Dardick is also trying to answer a fundamental question: How do different trees get their distinctive shapes? From the towering spires of spruce and fir, the massive spreading limbs of an oak to the stately arching canopies of an elm, the skeletal shapes of trees offer signature silhouettes.

Dardick’s work and that of other researchers also could help to explain how the shapes of individual trees are far from fixed. Trees, much more than we can, will morph in response to their literal neck of the woods. Limbs in the shade reach toward spots of sunlight. Trees on windswept hills bend trunk and branches into gnarled architectures.

Work by breeders, biologists and botanists have revealed sizable pockets of knowledge about the hormones, genes and processes that yield the diverse shapes of trees and other plants, between species and within species. It has not been easy: Two of trees’ most appealing attributes — their long lives and large sizes — make them intractable research subjects.

But as scientists pursue these questions, commonalities are emerging between vastly different species. The puzzle of shape diversity and adaptability turns out to be tied to the fundamentals of being a plant: grappling with gravity, fighting for sunlight, all while anchored in one place for a lifetime.

“Plants are stuck. The best they can do is grow toward something,” says Courtney Hollender, a former postdoc of Dardick’s who now runs her own lab in the Department of Horticulture at Michigan State University in East Lansing. “That’s all they’ve got; they can’t run, they have to adapt to their environment. And they’ve developed brilliant ways to do it.”

Available at all branches

Scientists have a word for the ability to adapt so readily: plasticity. In plants, this feature is both obvious and astounding. Most animals are born in specific shapes then just grow larger, but plants are modular — they grow in various iterations of two building blocks: shoots and roots.

It is the first of these — where and when a shoot grows or doesn’t grow — that governs the basic form a tree takes.

Some aspects are hardwired. Leaves emerge in a pattern that is usually fixed throughout the tree’s life, with structural arrangements that tend to be shared by members of a given plant family. And shoots emerge where leaves meet the stem. So, for example, plants in the maple family, which have leaves set opposite each other, have branches in the same format. Members of the beech family have leaves, and thus branches, that alternate up the stem.

But the interplay between physiology and external forces also plays a large part. Take your standard-issue plant with a main central stem that grows upward and has few side branches. Most plants, from basil to birch, start out this way, a growth habit that probably evolved because it enables them to quickly reach the light — more rapidly than the competition. Called apical dominance (the tip of the plant is the “apex”), this is largely under the purview of the plant hormone indole acetic acid, also known as auxin. Made in the tip, auxin diffuses downward and blocks the growth of side branches.

This is why pinching the tips off of basil or geranium makes them bushy — you are removing the source of that bossy auxin, freeing buds on the stem’s sides from the prohibition and allowing them to grow. (Though auxin is mighty, it’s not the only player here. Other plant hormones, along with light intensity and access to nutrients, also wield power.)

Another related and less-understood phenomenon occurs in some tree species. Called apical control, it also is imposed by the tip of a tree and probably also by auxin. But rather than operating at the scale of a branch, it commandeers the whole dang tree.

Think of a pine. At the top, there’s a pointy tip, then upper branches that tend to reach skyward. Moving down, the branches become more horizontal, growing out more than up. But unlike a basil plant, a pine tree does not become bushy when you lop off the top. Instead, a new bud near the top grows upward, becoming the new leader. Or an existing branch reorients to grow up and become the new dominant tip.

These two principles are always in the back of arborists’ minds as they work. “They have to consider, ‘If we cut a branch here, that bud below is going to break and we’ll just get a branch in basically the same spot,’” Dardick says. “All of their rules of what to prune and where are based on these physiological factors that contribute to tree shape.”

A natural reaction

Physiology also underpins the plastic responses trees have to more extreme situations they may face. A tree on a high mountain peak or windswept coast must contend with exposure to mechanical forces that could topple and kill it. To survive, such trees become short and stocky, their bent, asymmetric crowns reducing drag and presumably protecting a tree from violent gusts. The driver is the wind’s very touch — a response now called thigmomorphogenesis that has been observed for hundreds of years.

How it works is still unclear, but over the past decade researchers have made some headway. They’re actively studying force-sensing proteins and processes that may be involved. And recent work suggests an important role for hormones such as jasmonate, which accumulates in all kinds of plants in response to damage and mechanical stress. In experiments with a weedy mustard called Arabidopsis, plants became stunted when researchers bent their leaves back and forth twice a day. Mutants that couldn’t make jasmonate, though, grew normally.

Sometimes, wind does more than gust against a tree: It blows the whole tree over, and that tree, if still rooted, must reorient the growth of its branches and buds toward the sky. Avalanches, erosion and landslides deal similar fates. And trees in all sorts of circumstances must grow around obstacles, away from competitors and toward the light. To get these jobs done, trees make a special kind of wood called reaction wood.

Hardwoods such as maple, beech, oak and poplar form this tough stuff (in this case called tension wood) on the upper side of their stems. Incredibly, it creates a tensile force that pulls the stem upward. “If you walk around the woods, you can see that most species, if not all species, have this kind of reaction wood response,” says Andrew Groover, a research geneticist with the USDA Forest Service’s Pacific Southwest Research Station in Davis, California.

The hardwood tree first discerns that it is off-kilter using specialized gravity-sensing cells. Where these cells reside in trees — the woody stem? the tip of new shoots? — was unknown until Groover and colleagues detected them in woody and soft tissues of poplar, a few years back. The cells contain organelles called statoliths that sink down in the cell and indicate to the plant that it’s leaning one way or the other. This, in turn, causes that influential auxin to mobilize, triggering the growth of tension wood on the top. Cellulose with a peculiar gelatinous layer is thought to act as the “muscle” that generates the pulling-up force.

When genes defy gravity

Much of the knowledge about the architecture of plants is rooted in millennia of human efforts to alter crop shapes to make them more suitable for cultivation, and modern science is now revealing the genetic changes that lie behind these creations. The lessons, it turns out, apply broadly across the plant kingdom, to herbaceous and woody species alike.

It is hard to overstate the importance to human history of some of these plant-shape changes, says plant molecular geneticist Jiayang Li, who details some of their genetic underpinnings in the Annual Review of Plant Biology. A classic example is the transformation of the ancestor of corn (maize) into a key staple crop for much of the world. It arose from a species of the Central American grasses called teosintes — bushy plants with many branches. Domestication, among other things, abolished that branching, yielding the single-stalked upright corn we plant today.

Similarly, explains Li, who works at the Chinese Academy of Sciences’ Institute of Genetics and Developmental Biology, the green revolution of the 20^th century ushered in compact, dwarf varieties of wheat and rice . By modifying the height and thickness of the stems of these grasses, breeders developed varieties that could carry more grain without toppling over in wind and rain.

Much of Li’s own research has focused on architectural variation in rice, although the work turns out to have implications for the architecture of plants in general, from lowly mosses to towering trees. Like other grasses, rice grows shoots called tillers — specialized, grain-bearing branches that emerge from the base. In cultivated rice, the angle at which these tillers grow varies widely: Some varieties are squat and wide-spreading, others have shoots that are more upright. Breeders are interested in altering tiller angle because upright plants can be grown more densely, giving farmers more bang for their acreage.

In a key advance, in 2007, a team including Li reported they’d discovered the genetic cause of the spread-out architecture trait. The scientists named the responsible gene TAC1, short for “tiller angle control.” A functional TAC1 gene increases rice’s tiller angle, leading to open, widely branching plants. Mutations in TAC1 lead to the opposite: plants with erect shoots that reach up, instead of out.

That same year, Li’s team and a group in Japan both reported another major achievement: finding a long-sought gene behind a curious trait in some rice varieties that gives plant branches a scruffy, lounging look. The trait, known as “lazy,” had intrigued plant breeders and geneticists since the 1930s, when researchers described its extreme manifestation in corn: “The lazy plants grow along the ground, following the unevenness of the surface.”

The cause, it turns out, was errors in a gene that normally makes branches shoot straight up. Li and his colleagues surveyed some 30,000 mutant rice plants to pin down that gene, now called LAZY (names of genes, confusingly, often refer to what happens when a gene is mutated and doesn’t work, rather than when it is functioning properly). And they provided convincing evidence for an idea batted around for decades — that lazy plants have muddled perceptions of gravity and that auxin is centrally involved.

A common test for whether a plant’s gravity-perception machinery is working is to lay the plant on its side. If it knows up from down, it won’t continue to grow sideways, but will start to grow up again, akin to the reaction-wood response of a toppled tree’s branches. An important step in this reorienting involves auxin pooling on the bottom side of the shoot. But in lazy mutants, proteins that help ferry auxin around the plant are malfunctioning, so instead of shoots growing in the correct direction, they’re prone to casually sprawl about.

Scientists now know that LAZY genes come in multiple versions. Some appear to operate in plant roots, telling them which way is down, probably using similar, auxin-related signals. If those genes are absent or inactive, confused roots grow upward. And though the genes were first found in monocots, a branch of the plant kingdom including rice and corn, researchers now know that LAZY genes exist in numerous plants, including the plums growing in the fruit research station in West Virginia.

Reaching upward and outwards

As our boots crunch along the uneven ground, Dardick points at an errant orchard cat watching our tree tour from a distance. One row of trees stands so upright that a fencepost at the end of it is enough to block the row from view. These regimented trees are “pillar” peaches, and they are favorites of landscapers (one reason: it’s easy to get around them with a lawnmower). They also were key to uncovering genes like LAZY and TAC1 at the Shenandoah Valley station.

By comparing ordinary peaches to pillar peaches, and drawing on decades of work by former lead scientist Ralph Scorza, a team of station scientists and others in the US and Germany discovered the cause of the pillar trait: mutations in the peach version of TAC1.

The team also found that LAZY was at work in many of their misfits. Just as with the corn plants described nearly 100 years ago, mutations in LAZY made plums grow topsy-turvy, their branches seeking the soil. Apple trees with LAZY mutations have similarly disoriented roots. And when multiple copies of LAZY genes malfunction in the weed Arabidopsis, its roots grow up, its shoots down.

In the last decade, researchers have found that TAC1 influences branch angle in plums, poplar trees, the grass Miscanthus and Arabidopsis, and it appears to affect leaf angle in corn. But LAZY genes have even deeper roots. They’re found in all manner of plants, including the evolutionarily older Loblolly pine and even more ancient mosses.

This finding suggests a very old role for LAZY: It may have allowed plants to grow up, literally, when they first colonized land. Plants got their start in water. There, rootless and leafless, they were buoyed, unconcerned with gravity. The transition to land spurred the development of proper roots and stems, and plants then had to figure out up from down. LAZY seems to have allowed plants to orient their above-ground growth away from gravity and up toward the sun.

Scientists think that TAC1 evolved somewhat later, providing a counterpoint to LAZY — ensuring that branches don’t only grow straight up, but also reach out. Together, these genes laid critical groundwork for the diversity of plant forms we see today, all seeking sustenance in their own ways.

“Once you start to grow up as a vascular plant, you need to maximize your resources, you need to capture as much sun as possible,” says Hollender, who has been working on yet another gene, called WEEP, that — when nonfunctional — lends plants a weeping, waterfall-like structure seen here and there in trees of ornamental gardens. (But it’s probably not responsible for the shape of weeping willow trees.) “Modifying your shoot angles is an important adaptive trait for plants that allows them to capture light. It’s essential for them to survive.”

This kind of research has broad economic implications. Fruit and nut trees bring $25 billion annually in the US alone and there are hefty costs associated with pruning, bending and tying branches; spraying hormones; and the manual labor of picking fruit from an unruly cacophony of limbs. Understanding the genetic controls behind tree architecture could help scientists breed trees that make the whole fruit-farming enterprise more efficient and environmentally friendly.

“Orchard systems are not the most sustainable in the world,” Dardick says. “The idea is, if we can modify tree architecture, if we could reduce their size and limit the amount of area they take up, then we could plant them at higher density and potentially increase their sustainability.”

And there may be odder outcomes than friendlier outdoor orchards: In collaboration with NASA, the USDA team is investigating genetic tweaks that might even help bring fruit to space. On that December day, Dardick takes me to a greenhouse tucked in a corner of the lab. In it are plum and apple trees whose shape is so transformed that they look more like the love children of shrubs and vines. This strange growth habit is a side-effect of efforts to breed plants that flower and make fruit sooner and then do so continuously, rather than flowering after growing for several years, and then only in the spring.

The genetic tweaks that sent the trees’ developmental program into overdrive have also transformed their architecture. In the greenhouse, these precocious “trees” sprawl, draping lazily along wire trellises, happily flowering and heavy with fruit. “They’re growing almost like tomatoes,” Dardick says. “So we’re broaching the concept of, can we bring an orchard indoors?”

Those ambitions aside, Dardick has his hands full trying to answer numerous basic-science questions about how trees do what they do. Researchers still don’t know how different tree species set the angles of their branches — going wide like an oak, or arching like an elm. They don’t know how trees alter those angles during the course of mature growth, as branches sprout from branches sprouted from branches, until some of them finally point down. Trees are both kindred and foreign to us, their various forms so familiar, but their architectural rules still in so many ways opaque.

“I find myself looking at trees all the time now in a new way; they fill space so beautifully and efficiently,” Dardick says. “They are the biggest organism we have that’s visible, that’s in our face all the time. But there’s so much we don’t know.”