A team of scientists led by Kate Evans, a Washington State University horticulture professor who leads WSU’s pome fruit (apples and pears) breeding program, found that public plant breeding programs are seeing decreases in funding and personnel.

The study was published in the journal Crop Science.

Evans and her colleagues conducted a survey of 278 plant breeding programs around the country. Public programs are chiefly federal programs, like those run by the U.S. Department of Agriculture, or based at public research universities.

In the surveys, respondents estimated a 21.4% decline in full time employee (FTE) time for program leaders over the past five years and an estimated 17.7% decline in FTE time for technical support personnel.

The researchers also found that retirement looms for a significant number of plant breeding program leaders. Over a third of the responding programs reported having leaders over the age of 60 and 62% are led by people over 50.

This decline is concerning because plant breeding has a direct impact on food security, Evans said.

“Plant breeding plays a fundamental part of the long-term food security of this country,” Evans said. “The tremendous increases in food production over the past century are largely due to plant breeding, and the world’s population is only increasing.”

The focus on food security has received more attention in the last few months, as the COVID-19 pandemic has moved around the world, she said.

“Plant breeding is a long-term, sustainable way to address concerns over having enough food and keeping our food sources secure,” said Evans, who is based at WSU’s Tree Fruit Research & Extension Center in Wenatchee.

Plant breeding takes on many forms, from breeding disease tolerance, increasing production, introducing new delicious varieties, or improving drought tolerance.

“It could be a disease, a pest, climate change, any number of things,” Evans said. “We do not live in a stable environment, and there are many different ways to deal with that.”

Plant pathogens, like bacteria, and pests are always adapting, so varieties of crops that were bred to naturally fight off a disease start to lose their defenses. Plant breeding programs help growers stay ahead of those potentially harmful adaptations.

Another impact of declining breeding programs is losing those with a local focus.

“In Washington, for example, our cereal breeding programs are very focused on local production,” Evans said. “They breed wheat that grows very well for eastern Washington.”

Another example is the citrus industry. Citrus greening disease has been devastating to growers, particularly in Florida, when trees produce bitter, green, and misshapen fruit. Plant breeding programs are working hard to develop varieties that naturally repel the pest that causes the problems.

One reason that plant breeding programs are declining is expense. It takes many years to develop a new variety of a crop, Evans said. And funding a program for that long requires significant investment.

“We can’t rely on grants because those are often only for a few years,” she said. “You can’t do anything in plant breeding in three years, it requires long-term sustained funding to get a program going.”

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Materials provided by Washington State University. Original written by Scott Weybright. Note: Content may be edited for style and length.

Researchers at the University of California, Berkeley, and Ruhr-Universität Bochum (RUB) have taken a step towards this vision. They showed that atom probe tomography can be used to read a complex spatial arrangement of metal ions in multivariate metal-organic frameworks.

Metal-organic frameworks (MOFs) are crystalline porous networks of multi-metal nodes linked together by organic units to form a well-defined structure. To encode information using a sequence of metals, it is essential to be first able to read the metal arrangement. However, reading the arrangement was extremely challenging. Recently, the interest in characterizing metal sequences is growing because of the extensive information such multivariate structures would be able to offer.

Fundamentally, there was no method to read the metal sequence in MOFs. In the current study, the research team has successfully done so by using atom probe tomography (APT), in which the Bochum-based materials scientist Tong Li is an expert. The researchers chose MOF-74, made by the Yaghi group in 2005, as an object of interest. They designed the MOFs with mixed combinations of cobalt, cadmium, lead, and manganese, and then decrypted their spatial structure using APT.

Li, professor and head of the Atomic-Scale Characterisation research group at the Institute for Materials at RUB, describes the method together with Dr. Zhe Ji and Professor Omar Yaghi from UC Berkeley in the journal Science, published online on August 7, 2020.

Just as sophisticated as biology

In the future, MOFs could form the basis of programmable chemical molecules: for instance, an MOF could be programmed to introduce an active pharmaceutical ingredient into the body to target infected cells and then break down the active ingredient into harmless substances once it is no longer needed. Or MOFs could be programmed to release different drugs at different times.

“This is very powerful, because you are basically coding the behavior of molecules leaving the pores,” Yaghi said.

They could also be used to capture CO₂ and, at the same time, convert the CO₂ into a useful raw material for the chemical industry.

“In the long term, such structures with programmed atomic sequences can completely change our way of thinking about material synthesis,” write the authors. “The synthetic world could reach a whole new level of precision and sophistication that has previously been reserved for biology.”

The work was supported by the Center of Excellence for Nanomaterials and Clean Energy Applications at King Abdulaziz City for Science and Technology.

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Materials provided by University of California – Berkeley. Original written by Robert Sanders. Note: Content may be edited for style and length.

The team’s results could help biologists to better understand the origins of many ordered structures in nature, from spots and stripes on animal coats, to clusters of vegetation in arid environments. In Turing’s original model, he introduced two diffusing chemical species to different points on a closed ring of cells. As they diffused across adjacent cells, these species ‘competed’ with each other as they interacted; eventually organising to form patterns. This pattern formation depended on the fact that the symmetry during this process could be broken to different degrees, depending on the ratio between the diffusion speeds of each species; a mechanism now named the ‘Turing instability.’ However, a significant drawback of Turing’s mechanism was that it relied on the unrealistic assumption that many chemicals diffuse at different paces.

Through their calculations, Asllani’s team showed that in sufficiently large rings of cells, where diffusion asymmetry causes both species to travel in the same direction, the instabilities which generate ordered patterns will always arise — even when competing chemicals diffuse at the same rate. Once formed, the patterns will either remain stationary, or propagate steadily around the ring as waves. The team’s result addresses one of Turing’s key concerns about his own theory, and is an important step forward in our understanding of the innate drive for living systems to organise themselves.

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Journal Reference:

1. Malbor Asllani, Timoteo Carletti, Duccio Fanelli, Philip K. Maini. A universal route to pattern formation in multicellular systems. The European Physical Journal B, 2020; 93 (7) DOI: 10.1140/epjb/e2020-10206-3

When fast-moving ions cross paths with large biomolecules, the resulting collisions produce many low-energy electrons which can go on to ionise the molecules even further. To fully understand how biological structures are affected by this radiation, it is important for physicists to measure how electrons are scattered during collisions. So far, however, researchers’ understanding of the process has remained limited. In new research published in EPJ D, researchers in India and Argentina, led by Lokesh Tribedi at the Tata Institute of Fundamental Research, have successfully determined the characteristics of electron emission when high-velocity ions collide with adenine — one of the four key nucleobases of DNA.

Since high-energy ions can break strands of DNA as they collide with them, the team’s findings could improve our understanding of how radiation damage increases the risk of cancer developing within cells. In their experiment, they considered the ‘double differential cross section’ (DDCS) of adenine ionisation. This value defines the probability that electrons with specific energies and scattering angles will be produced when ions and molecules collide head-on, and is critical for understanding the extent to which biomolecules will be ionised by the electrons they emit.

To measure the value, Tribedi and colleagues carefully prepared a jet of adenine molecule vapour, which they crossed with a beam of high-energy carbon ions. They then measured the resulting ionisation through the technique of electron spectroscopy, which allowed them to determine the adenine’s electron emissions over a wide range of energies and scattering angles. Subsequently, the team could characterise the DDCS of adenine-ion collision; producing a result which largely agreed with predictions made by computer models based on previous theories. Their findings could now lead to important advances in our knowledge of how biomolecules are affected by high-velocity ion radiation; potentially leading to a better understanding of how cancer in cells can arise following radiation damage.

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“This is a really important technical resource for advancing the study of circadian rhythms,” says study leader Joseph Takahashi, Ph.D., chair of the department of neuroscience at UT Southwestern Medical Center, a member of UT Southwestern’s Peter O’Donnell Jr. Brain Institute, and an investigator with the Howard Hughes Medical Institute (HHMI). “You can use these mice for many different applications.”

Nearly every cell in humans — and mice — has an internal circadian clock that fluctuates on a roughly 24-hour cycle. These cells help dictate not only hunger and sleep cycles, but biological functions such as immunity and metabolism. Defects in the circadian clock have been linked to diseases including cancer, diabetes, and Alzheimer’s, as well as sleep disorders. Scientists have long known that a small part of the brain — called the suprachiasmatic nucleus (SCN) — integrates information from the eyes about environmental light and dark cycles with the body’s master clock. In turn, the SCN helps keep the rest of the cells in the body in sync with each other.

“What makes the SCN a very special kind of clock is that it’s both robust and flexible,” says Takahashi. “It’s a very strong pacemaker that doesn’t lose track of time, but at the same time can shift to adapt to seasons, changing day lengths, or travel between time zones.”

To study the circadian clock in both the SCN and the rest of the body, Takahashi’s research group previously developed a mouse that had a bioluminescent version of PER2 — one of the key circadian proteins whose levels fluctuate over the course of a day. By watching the bioluminescence levels wax and wane, the researchers could see how PER2 cycled throughout the animals’ bodies during the day. But the protein is present in nearly every part of the body, sometimes making it difficult to distinguish the difference in circadian cycles between different cell types mixed together in the same tissue.

“If you observe a brain slice, for instance, almost every single cell has a PER2 signal, so you can’t really distinguish where any particular PER2 signal is coming from,” says Takahashi.

In the new work, the scientists overcame this problem by turning to a new bioluminescence system that changed color — from red to green — only in cells that expressed a particular gene known as Cre. Then, the researchers could engineer mice so that Cre, which is not naturally found in mouse cells, was only present in one cell type at a time.

To test the utility of the approach, Takahashi and his colleagues studied two types of cells that make up the brain’s SCN — arginine vasopressin (AVP) and vasoactive intestinal polypeptide (VIP) cells. In the past, scientists have hypothesized that VIP neurons hold the key to keeping the rest of the SCN synchronized.

When the research team looked at VIP neurons — expressing Cre in just those cells, so that PER2 luminesced green in VIP cells, while red elsewhere — they found that removing circadian genes from the neurons had little overall effect on the circadian rhythms of the VIP neurons, or the rest of the SCN. “Even when VIP neurons no longer had a functioning clock, the rest of the SCN behaved essentially the same,” explains Yongli Shan, Ph.D., a UTSW research scientist and lead author of the study. Nearby cells were able to signal to the VIP neurons to keep them in sync with the rest of the SCN, he says.

When they repeated the same experiment on AVP neurons, however — removing key clock genes — not only did AVP neurons themselves show disrupted rhythms, but the entire SCN stopped synchronously cycling on its usual 24-hour rhythm.

“What this showed us was that the clock in AVP neurons is really essential for the synchrony of the whole SCN network,” says Shan. “That’s a surprising result and somewhat counterintuitive, so we hope it leads to more work on AVP neurons going forward.”

Takahashi says other researchers who study circadian rhythms have already requested the mouse line from his lab to study the daily cycles of other cells. The mice might allow scientists to hone in on the differences in circadian rhythms between cell types within a single organ, or how tumor cells cycle differently than healthy cells, he says.

“In all sorts of complex or diseased tissues, this can let you see which cells have rhythms and how they might be similar or different from the rhythms of other cell types.”

This research was supported by funds from the HHMI, the National Institutes of Health (R01 NS106657, R01 GM114424, T32-HLO9701, F32-AG064886), and The Welch Foundation (AU-1971-20180324).