Precise measurements of Cassini’s final trajectory have now allowed scientists to make the first accurate estimate of the amount of material in the planet’s rings, weighing them based on the strength of their gravitational pull.

That estimate — about 40 percent of the mass of Saturn’s moon Mimas, which itself is 2,000 times smaller than Earth’s moon — tells them that the rings are relatively recent, having originated less than 100 million years ago and perhaps as recently as 10 million years ago.

Their young age puts to rest a long-running argument among planetary scientists. Some thought that the rings formed along with the planet 4.5 billion years ago from icy debris remaining in orbit after the formation of the solar system. Others thought the rings were very young and that Saturn had, at some point, captured an object from the Kuiper belt or a comet and gradually reduced it to orbiting rubble.

The new mass estimate is based on a measurement of how much the flight path of Cassini was deflected by the gravity of the rings when the spacecraft flew between the planet and the rings on its final set of orbits in September 2017. Initially, however, the deflection did not match predictions based on models of the planet and rings. Only when the team accounted for very deep flowing winds in atmosphere on Saturn — something impossible to observe from space — did the measurements make sense, allowing them to calculate the mass of the rings.

“The first time I looked at the data I didn’t believe it, because I trusted our models and it took a while to sink in that there was some effect that changed the gravity field that we had not considered,” said Burkhard Militzer, a professor of earth and planetary science at the University of California, Berkeley, who models planetary interiors. “That turned out to be massive flows in the atmosphere at least 9,000 kilometers deep around the equatorial region. We thought preliminarily that these clouds were like clouds on Earth, which are confined to a thin layer and contain almost no mass. But on Saturn they are really massive.”

They also calculated that the surface clouds at Saturn’s equator rotate 4 percent faster than the layer 9,000 kilometers (about 6,000 miles) deep. That deeper layer takes 9 minutes longer to rotate than do the cloud tops at the equator, which go around the planet once every 10 hours, 33 minutes.

“The discovery of deeply rotating layers is a surprising revelation about the internal structure of the planet,” said Cassini project scientist Linda Spilker of NASA’s Jet Propulsion Laboratory in Pasadena, California. “The question is what causes the more rapidly rotating part of the atmosphere to go so deep and what does that tell us about Saturn’s interior.”

Militzer also was able to calculate that the rocky core of the planet must be between 15 and 18 times the mass of Earth, which is similar to earlier estimates.

The team, led by Luciano Iess at the Sapienza University of Rome, Italy, reported their results today in the journal Science.

Did rings come from icy comet?

Earlier estimates of the mass of Saturn’s rings — between one-half and one-third the mass of Mimas — came from studying the density waves that travel around the rocky, icy rings. These waves are caused by the planet’s 62 satellites, including Mimas, which creates the so-called Cassini division between the two largest rings, A and B. Mimas is smooth and round, 246 kilometers in diameter. It has a big impact crater that makes it resemble the Death Star from the Star Wars movies.

“People didn’t trust the wave measurements because there might be particles in the rings that are massive but are not participating in the waves,” Militzer said. “We always suspected there was some hidden mass that we could not see in the waves.”

Luckily, as Cassini approached the end of its life, NASA programmed it to perform 22 dives between the planet and the rings to probe Saturn’s gravity field. Earth-based radio telescopes measured the spacecraft’s velocity to within a fraction of a millimeter per second.

The new ring mass value is in the range of earlier estimates and allows the researchers to determine their age.

These age calculations, led by Philip Nicholson of Cornell University and Iess, built on a connection that scientists had previously made between the mass of the rings and their age. Lower mass points to a younger age, because the rings are initially made of ice and are bright but over time become contaminated and darkened by interplanetary debris.

“These measurements were only possible because Cassini flew so close to the surface in its final hours,” Militzer said. “It was a classic, spectacular way to end the mission.”

Scientists around the world are working on creating artificial, cell-like systems that mimic the behavior of living organisms. Friedrich Simmel and Aurore Dupin have now for the first time created such artificial cell assemblies in a fixed spatial arrangement. The highlight is that the cells are able to communicate with each other.

“Our system is a first step towards tissue-like, synthetic biological materials that exhibit complex spatial and temporal behavior in which individual cells specialize and differentiate themselves, not unlike biological organisms,” explains Friedrich Simmel, Professor of Physics of Synthetic Biosystems (E14) at TU Munich.

Gene expression in a fixed structure

Gels or emulsion droplets encapsulated in thin fat or polymer membranes serve as the basic building blocks for the artificial cells. Inside these 10 to 100 micron sized units, chemical and biochemical reactions can proceed uninhibited.

The research team used droplets enclosed by lipid membranes and assembled them into artificial multicellular structures called “micro-tissues.” The biochemical reaction solutions used in the droplets can produce RNA and proteins, giving the cells a of a kind of gene expression ability.

Signal exchange and spatial differentiation of cells

But that’s not all: Small “signal molecules” can be exchanged between cells via their membranes or protein channels built into the membranes. This allows them to temporally and spatially couple with each other. The systems thus become dynamic — as in real life.

Chemical pulses thus propagate through the cell structures and pass on information. The signals can also act as triggers, allowing initially identical cells to develop differently. “Our system is the first example of a multicellular system in which artificial cells with gene expression have a fixed arrangement and are coupled via chemical signals. In this way, we achieved a form of spatial differentiation, “says Simmel.

Models, mini factories and microsensors

Developing these kinds of synthetic systems is important since they allow scientists to investigate fundamental questions about the origins of life in a model. Complex organisms became possible only after cells began specializing and distributing work between cooperating cells. How this came about is among the most fascinating questions in basic research.

Using a modular construction kit of tailor-made cell systems, the researchers hope to simulate various properties of biological systems in the future. The idea is that cells react to their environment and learn to act independently.

The first applications are already on the horizon: In the long term, artificial cell assemblies can be deployed as mini-factories to produce specific biomolecules, or as tiny micro-robot sensors that process information and adapt to their environments.

Cells from a 3-D printer

Friedrich Simmel and Aurore Dupin still assemble their cell systems manually using micromanipulators. In the future, however, they plan to cooperate with the Munich University of Applied Sciences, for example, to systematically build larger and more lifelike systems using 3-D printing technology.

This work was funded by the European Research Council and the DFG Cluster of Excellence Nanosystems Initiative Munich (NIM). Aurore Dupin was supported by the DFG Research Training Group “Chemical Foundations of Synthetic Biology.”

Now, scientists have developed a gene therapy that blocks this process, preventing axon destruction in mice and suggesting a therapeutic strategy that could help prevent the loss of peripheral nerves in multiple conditions.

The study, from Washington University School of Medicine in St. Louis, appears in the Journal of Experimental Medicine.

The strategy could help prevent peripheral neuropathy, a disease that currently affects about 20 million people in the United States. Peripheral neuropathy can result from chemotherapy for cancer treatment or poorly controlled diabetes, and it causes persistent pain, numbness, burning, itching and muscle weakness.

“Peripheral neuropathies are the most common neurodegenerative diseases in the world,” said first author Stefanie Geisler, MD, an assistant professor of neurology. “Many peripheral neuropathies are caused by breakdown of nerve fibers, but we currently don’t have therapies that can directly block this process. For many neuropathies, we can’t halt progression of the disease and are limited to trying to treat the symptoms. We are somewhat successful decreasing neuropathic pain, but it is very difficult to alleviate numbness.

“I see many patients with chemotherapy-induced neuropathy, and it can severely impact their quality of life,” she said. “To benefit patients, we will need to test this treatment in human clinical trials, but our current finding is significant because we have shown for the first time that we can effectively block nerve fiber breakdown in mice with a standard viral gene therapy.”

When an axon is injured, whether cut or crushed by injury or damaged by drugs, a protein called SARM1 becomes active. In healthy nerves, this protein is switched off. Past studies by this research team have shown that activated SARM1 triggers axons to self-destruct, kicking off a chain of events that quickly consumes all of a nerve cell’s energy supply. The axons of such cells break into pieces.

In this study, scientists used a virus — one that can’t cause disease — to deliver into cells a mutated version of the SARM1 protein that blocks axon destruction.

This mutated SARM1 prevents the characteristic rapid energy loss and subsequent destruction of axons, even in the most extreme form of injury — a complete severing of the axon.

“With our viral gene therapy, we delivered a mutated form of SARM1 that is not only inactive itself but also blocks normal SARM1 proteins that have become activated in mice with nerve injuries,” said senior author Jeffrey D. Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics. “For a long time, viral gene therapy was a pipe dream, but there are now a number of ongoing clinical trials in other disorders that suggest we are on a promising track.”

For example, a similar viral gene therapy is now in clinical trials for a genetic disorder called Duchenne muscular dystrophy. In that case, a different protein is delivered to address muscle loss, but the virus is the same.

In theory, it could be possible to change the viral packaging to direct the viruses to deliver their gene payload to different types of cells — sensory neurons for peripheral neuropathy or motor neurons for ALS, for example.

“This has the potential to be transformative because it cuts across so many diseases,” said co-senior author Aaron DiAntonio, MD, PhD, the Alan A. and Edith L. Wolff Professor of Developmental Biology. “Rather than addressing a single disease, it is potentially a treatment for a disease process that is shared among many different neurodegenerative disorders.”

In addition to this viral gene therapy, the researchers are studying other possible ways to block SARM1, including small molecules for drug development.

This work was supported by the National Institutes of Health (NIH), grant numbers K08NS091448, R01CA219866, R01NS087632 and R01CA218263; the Muscular Dystrophy Association, grant number MDA344513; the Thompson Family Foundation Initiative; and the Hope Center Viral Vector Core at Washington University School of Medicine in St. Louis.