Mon, 02 Sep 2019
In a Duke University lab, a couple of scientists photographed some larvae of gall midges that can leap 30 times their body length — without legs! The Duke team filmed them in slow-motion at 20,000 frames per second; you can watch the results here:
Electron micrographs show that certain patches on the ends of these larvae are covered with adhesive protrusions just one micron in size. Here’s how their “hydrostatic legless propulsion” works:
Attaching its head to its tail to form a ring, a 3-millimeter larva of the goldenrod gall midge squeezes some internal fluids into its tail section, swelling it and raising the pressure like an inner tube.
When the adhesive bond between the head and tail can no longer hold, the tension is sprung, launching the worm into a high, tumbling flight that will carry it 20 to 30 body-lengths away in a tenth of a second at speeds comparable to a jumping insect with actual legs. [Emphasis added.]
This mode of travel is “28 times more energy efficient (and a heck of a lot faster) than crawling like a regular old caterpillar.” Obviously there is not much control on the direction of take-off, and the landing is bouncy, but “it’s apparently none the worse for wear.” In addition, the scientists found that the larva’s body is hinged to improve thrust, and the micron-sized protrusions on the adhesive patches may create Van der Waal’s forces at the atomic level, like in gecko toes. The larvae don’t appear to need this ability to survive. With all this evident design, one biologist nevertheless contributes this groaner:
Perhaps it’s a leftover skill from some earlier evolution of the worm, [Michael] Wise suggests. Or perhaps it’s to avoid predators and curious biologists.
There wasn’t much time for such speculation in the lab. After opening the petri dish with a dozen galls and dissecting some, Wise found only two left: “They were jumping all over the office!” He called his colleague with the high-speed camera to film them for fun. Then he thought, “this might actually be an interesting new field.” Design, once again, stimulated new discoveries. And now, with support from the U.S. Army and the National Science Foundation, research into this lowly maggot’s unique method of propulsion may find its way into artificial muscles in soft robots.
Plant Cells by Design
Biologists at McGill University are finding there are reasons for the shapes of plant cells and leaves. In this quote, we see Darwin exit stage left rapidly, and an engineer enter stage right.
“The photosynthetic tissue on the inside of a leaf has a sponge-like architecture formed from star-shaped cells that promotes the passage of oxygen and carbon dioxide. The leaf’s ‘skin’ tissue, the epidermis, on the other hand, is a flat layer of tightly connected, flat cells that doesn’t let anything pass through except at designated openings. But we really didn’t know how these strikingly different cell shapes come to be,” said Anja Geitmann, professor and dean of McGill’s Faculty of Agricultural and Environmental Sciences.
Working from the premise that biological organisms must abide by physical laws, Geitmann and her colleagues used engineering principles to run computer simulations of the pressures and forces required to give a plant cell a given shape.
Darwin from stage left begs not to be forgotten, so the biologists offer him a line:
“We think plants evolved this way so that the leaves can better resist destructive mechanical stress and we are performing both modelling and experimental tests to show this. Science is slowly unraveling the puzzle of life, one piece at a time,” she said.
The whole article, though, deals with engineering principles in plant shapes. They are not random shapes from chance mutations; they have a purpose. Cellulose and pectin come into play so that the physical characteristics actually work, like car tires.
“The typical pressure in a plant cell is higher than that in a car tire,” Geitmann explained. “A growing plant cell can, therefore, be compared with a rubber balloon being inflated. If pressure drives plant cell growth, we wondered how it could be possible to generate a balloon (or cell) that is not simply spherical but has a characteristic jigsaw puzzle-like shape, like that of the cells forming the leaf epidermal cells.”
The predictions obtained from their computer simulations served as the starting point to find the biological structures that determine a cell’s shape.
Protective Joint Cushions
Macrophages are usually thought of as immune-system cells that “eat” stray invaders. A “News and Views” article for Nature relates the surprise of biologists who found them playing another role.
Immune cells called macrophages commonly function as scavenger-like (phagocytic) cells that ingest and remove damaged cells. Writing in Nature, Culemann et al. report that the macrophages present in joints also fulfil an unexpectedly different role.
It makes sense that these well-equipped defense cells are present in joints, where they can offer both a structural and protective barrier to inflammation.
The authors carried out RNA sequencing, including single-cell sequencing, to profile the barrier macrophages. These cells express genes typically associated with barrier formation in a type of non-immune cell called an epithelial cell. For example, the macrophage profile included genes that encode proteins associated with the formation of a structure called a tight junction that connects epithelial cells by forming a ‘seal’ between adjacent epithelial cells. This is surprising, because macrophages are usually thought of as having a signalling or scavenging role, rather than having a structural, barrier-like function.
The finding could have implications for how doctors treat arthritis. In fact, people with active rheumatoid arthritis lack these barrier macrophages. Be thankful for the versatile engineering in these important cells!
Culemann and colleagues’ work adds to studies showing that macrophages are exquisitely adapted to the functions they perform in the tissues in which they reside. Barrier macrophages join a growing list of types of macrophage that shield tissues from damage caused by infection, inflammation or cancer. Tissue-resident macrophages can prevent neutrophil-mediated inflammatory damage by physically shielding damaged tissue from neutrophils. Furthermore, in large body cavities, such as those surrounding the gut, heart and lungs, specialized macrophages have been described that are thought to repair mechanical damage.
Nature Had Control Theory First
This is a great article, if we can first get past the obligatory homage to Darwin. Ignore him, and enjoy the main design thrust of the opening paragraph:
In the last 150 years, engineers have developed and mastered ways to stabilize dynamic systems, without lag or overshoot, using what’s known as control theory. Now, a team of University of Arizona researchers has shown that cells and organisms evolved complex biochemical circuits that follow the principles of control theory, millions of years before the first engineer put pencil to paper.
Think of the astounding import of that statement: control theory, which we know required human intelligence to invent, was already at work in living things!
Control theory can be seen in a thermostat, the article continues. You set a desired temperature, and control systems aim for it in a “feedforward” manner, slowing down and stopping when the target is reached. But then the system’s work is not over. It has to maintain that target temperature with small bursts in order to keep it on the target. The controller gets feedback from the sensor — two systems working in concert — for the control system to work.
A UA team discovered that the coupling of two interconnected biochemical circuits within a cell — the TOR and PKA pathways — work like a thermostat to control the growth of cells in response to the availability of nutrients. For decades, it has been known that mutations in both PKA and TOR cause disease; The new research found that each pathway has its own distinct role and teased out exactly how and why the two pathways work together.
Researchers wondered why cells needed both pathways to control growth, when one system was apparently sufficient. They found that having two provided rapid response to changing nutrient supplies.
“If you just have the TOR pathway, you’d always replicate at a good pace. The problem would be that when the conditions change, it would take a cell hours to adjust its growth rate. So nature added PKA,” Capaldi said. When you run out of nutrient, PKA can also quickly shut things down to let TOR take over again. “What’s happening is you have two controls — one whose job it is to speed up the response, and the other to keep it exactly right.”
Chemical engineers use this strategy to tightly control temperature,. And like all engineers, they use their brains, not mutations and natural selection. In order to keep the temperature of their solutions exactly right, chemical engineers imbed their intelligence into computer systems. Understanding control theory, they program two controls which are able to adjust deviations quickly, even when they are not present to watch. These tightly connected controls are known as hubs. Computer control systems use hubs. Cells and organisms use hubs. When the TOR-PKA control hub fails in the body, diseases from epilepsy to clinical depression to cancer can result.
Now, for the “wow” factor:
Because cells must be incredibly precise, cellular pathways are numerous and complex.
“Our cells have 30,000 proteins, and biologists have shown that if there’s anything wrong in one of a few thousand that control growth, then you can get a disease,” Capaldi said. “That is because these pathways do not work as simple on-and-off switches. As we have shown in our new study, they act like complex circuits, even computers.”
Indeed, we have a virtual internet of complex circuits, the article continues. Does anyone doubt that design-based research is good for science? Hear what they say with passion:
“The most important take-home message is to think about all the different pathways in a cell in this way — that is, think about how pathways work together to provide precise control. We won’t be able to design truly effective drugs until we do,” he said.
“I want our research to continue along the same theme,” Capaldi added. “We’ll keep trying to figure out how different pieces of the growth-control network work together. There are hundreds and hundreds of signaling pathways that are interconnected, but we still don’t know how or why they talk to each other. There is just so much we still have to learn.”
Except for the very few and irrelevant references to evolution in the above articles, that was fun!