Twilight zone at risk from climate change

Photo Credit: PublicDomainPictures

Life in the ocean’s “twilight zone” could decline dramatically due to climate change, new research suggests.

The twilight zone (200m to 1,000m deep) gets very little light but is home to a wide variety of organisms and billions of tons of organic matter.

The new study warns that climate change could cause a 20-40% reduction in twilight zone life by the end of the century.

And in a high-emissions future, life in the twilight zone could be severely depleted within 150 years, with no recovery for thousands of years.

“We still know relatively little about the ocean twilight zone, but using evidence from the past we can understand what may happen in the future,” said Dr Katherine Crichton, from the University of Exeter, and lead author of the study.

The research team, made up of paleontologists and ocean modelers, looked at how abundant life was in the twilight zone in past warm climates, using records from preserved microscopic shells in ocean sediments.

How wiggly spaghetti guard the genome

The image shows an artistic impression of the rocky scaffold structure of the nuclear pore complex filled with intrinsically disordered nucleoporins in the central channel depicted as seaweeds. In this work, the viewer dives into the dark hole of the nuclear pore complex to shine light on the disordered nucleoporins.
Illustration Credit: ©: Sara Mingu

Tiny pores in the cell nucleus play an essential role for healthy aging by protecting and preserving the genetic material. A team from the Department of Theoretical Biophysics at the Max Planck Institute of Biophysics in Frankfurt am Main and the Synthetic Biophysics of Protein Disorder group at Johannes Gutenberg University Mainz (JGU) has literally filled a hole in the understanding of the structure and function of these nuclear pores. The scientists found out how intrinsically disordered proteins in the center of the pore can form a spaghetti-like mobile barrier that is permeable for important cellular factors but blocks viruses or other pathogens.

Human cells shield their genetic material inside the cell nucleus, protected by the nuclear membrane. As the control center of the cell, the nucleus must be able to exchange important messenger molecules, metabolites or proteins with the rest of the cell. About 2,000 pores are therefore built into the nuclear membrane, each consisting of about 1,000 proteins.

Drug for rare form of ALS approved by FDA

A new drug has been approved by the Food and Drug Administration (FDA) for a rare, inherited form of amyotrophic lateral sclerosis (ALS). Called tofersen, the drug — developed by Biogen Inc. and based in part on research conducted at Washington University School of Medicine in St. Louis — slows the progression of the deadly, paralyzing disease. 

Video Credit: Huy Mach and Tamara Bhandari

A new drug has been approved by the Food and Drug Administration (FDA) for a rare, inherited form of amyotrophic lateral sclerosis (ALS), a paralyzing neurological disease. Known as tofersen, the drug has been shown to slow progression of the deadly disease. International clinical trials of tofersen, developed by the global biotechnology company Biogen Inc., were led by a neurologist at Washington University School of Medicine in St. Louis.

Tofersen, also known by the brand name Qalsody, is designed for ALS patients whose disease is caused by mutations in the gene SOD1. In the phase 3 clinical trial, the drug reduced molecular signs of disease and curbed neurodegeneration in the first six months of use. Over longer time frames, some participants experienced a stabilization of muscle strength and control.

The drug is approved under the accelerated approval pathway, under which FDA may approve drugs for serious conditions where there is an unmet medical need and a drug is shown to have an effect on a surrogate endpoint that is reasonably likely to predict a clinical benefit to patients.

Membrane proteins of cyanobacteria and higher organisms are structurally highly similar

SynDLP, the dynamin-like protein of the cyanobacterium Synechocystis, forms highly ordered oligomeric structures that bind to membranes.
Illustration Credit: ©: Lucas Gewehr, Dirk Schneider

The cells of living organisms are equipped with proteins that are involved in the shaping and remodeling of cellular membranes, thereby performing important tasks. The cell membrane encloses the cell interior, but is constantly remodeled, for example, due to membrane budding, invagination, or fusion processes. This also involves various proteins that were long assumed to be present exclusively or predominantly in higher organisms. In the past 10 to 20 years, however, proteins have been identified or predicted to be present also in simple organisms that do not possess a nucleus. In a research collaboration, a protein involved in membrane remodeling in cyanobacteria has now been described for the first time. The existence of such a bacterial protein was suspected, but proof was still pending. The studied protein is likely a bacterial representative of a similar protein found in higher organisms such as animals and plants.

Chest E-Tattoo Boasts Major Improvements in Heart Monitoring

A new flexible, wearable medical device could provide a major boost in the fight against heart disease, the leading cause of death in the United States.
Photo Credit: University of Texas at Austin / Cockrell School of Engineering

A team led by researchers at The University of Texas at Austin has developed an ultrathin, lightweight electronic tattoo, or e-tattoo, that attaches to the chest for continuous, mobile heart monitoring outside of a clinical setting. It includes two sensors that together provide a clear picture of heart health, giving clinicians a better chance to catch red flags for heart disease early.

“Most heart conditions are not very obvious. The damage is being done in the background and we don’t even know it,” said Nanshu Lu, a professor in the Department of Aerospace and Engineering Mechanics and a lead author of the study. “If we can have continuous, mobile monitoring at home, then we can do early diagnosis and treatment, and if that can be done, 80% of heart disease can be prevented.”

The study is published in Advanced Electronic Materials.

A 'cocktail' of human antibodies shows promise in fighting severe SARS-CoV-2 infections

Antibody 2A10 (yellow shades) and antibody 1H2 (blue shades) were isolated from a vaccinated research volunteer. The LJI team found these two antibodies can neutralize many SARS-CoV-2 variants.
Illustration Credit: Saphire Lab, La Jolla Institute for Immunology.

An anonymous San Diego resident has become a fascinating example of how the human immune system fights SARS-CoV-2. In a new investigation, scientists from La Jolla Institute for Immunology (LJI) have shown how antibodies, collected from this clinical study volunteer, bind to the SARS-CoV-2 “Spike” protein to neutralize the virus.

Although studies have shown antibodies bound to Spike before, this new research reveals how the original Moderna SARS-CoV-2 vaccine could prompt the body to produce antibodies against the later Omicron variants of SARS-CoV-2. The researchers also captured highly detailed, 3D structures of three promising neutralizing antibodies bound to Spike.

This important work shows exactly where Spike is vulnerable to human antibodies—and how future vaccines and antibody therapeutics might exploit these weaknesses. In fact, studies in mice suggest some of these antibodies may help prevent severe cases of COVID-19.

“To blunt the next pandemic and protect people from seasonal re-emergence of this one, we need antibodies of the broadest possible capacity—ones that are not escaped,” says LJI President and CEO Erica Ollmann Saphire, Ph.D., senior author of the new Cell Reports study. “We found those in a vaccinated San Diegan.”

Toward a Therapy for a Rare Genetic Disease

Researchers have designed a “mini gene” that could eventually be developed into a gene therapy for Usher Syndrome type 1F
Photo Credit: Subin

Usher Syndrome type 1F is a rare but severe genetic disease that causes deafness, lack of balance, and progressive blindness.

Now, a team led by researchers at Harvard Medical School, Massachusetts Eye and Ear, and The Ohio State University has made an important first step toward developing a gene therapy for the disease.

The research, conducted in mice, is described Apr. 26 in Nature Communications.

The scientists designed a “mini gene” — a shortened version of a gene — to replace the gene that is mutated in Usher 1F. The mutation renders hair cells inside the inner ear incapable of producing a key protein involved in sound transmission. In mice, the mini gene increased production of the missing protein, enabling the hair cells to sense sound and restoring hearing.

Because vision loss in Usher 1F involves a slightly different form of the same protein, the researchers say the same approach may be useful for preventing blindness.

“Patients with Usher 1F are born with profound hearing loss and progressive vision loss, and so far, we have been able to offer very few solutions to these families,” said co-senior author Artur Indzhykulian, HMS assistant professor of otolaryngology–head and neck surgery at Mass Eye and Ear.

Brain circuits for locomotion evolved long before appendages and skeletons

The sea slug, Pleurobranchea californica 
Photo Credit: Fred Zwicky

Hundreds of millions of years before the evolution of animals with segmented bodies, jointed skeletons or appendages, soft-bodied invertebrates like sea slugs ruled the seas. A new study finds parallels between the brain architecture that drives locomotion in sea slugs and that of more complex segmented creatures with jointed skeletons and appendages. 

Reported in the Journal of Neuroscience, the study suggests that, rather than developing an entirely new set of neural circuits to govern the movement of segmented body parts, the insects, crustaceans and even vertebrates like mammals adapted a network of neurons, a module, that guided locomotion and posture in much simpler organisms. 

“Sea slugs may still have that module, a smallish network of neurons called the ‘A-cluster,’ with 23 neurons identified so far,” said University of Illinois Urbana-Champaign molecular and integrative physiology professor Rhanor Gillette, who led the new research. 

“The question that we addressed in this study is whether the similarities we see between sea slugs and more complex creatures evolved independently or whether those with segmented body parts and appendages may have inherited their underlying neural circuitry from a soft-bodied, bilaterally symmetrical common ancestor,” he said. 

Predators decrease prey disease levels but also population size

Microscope image showing a phantom midge larva (genus Chaoborus), top left, preying on a Daphnia dentifera water flea, bottom right. Chaoborus is a fierce predator with a complex “catching basket” on its head for quickly trapping small crustaceans like water fleas.
Photo Credit: Meghan Duffy, University of Michigan.

Nature documentaries will tell you that lions, cheetahs, wolves and other top predators target the weakest or slowest animals and that this culling benefits prey herds, whether it’s antelope in Africa or elk in Wyoming.

This idea has been widely accepted by biologists for many years and was formalized in 2003 as the healthy herds hypothesis. It proposes that predators can help prey populations by picking off the sick and injured and leaving healthy, strong animals to reproduce.

The healthy herds hypothesis has even been used to suggest that manipulating predator numbers to protect prey might be a useful conservation strategy. Even so, hard evidence supporting the hypothesis is scarce, and in recent years many of its assumptions and predictions have been questioned.

In a study published online April 26 in the journal Ecology, a University of Michigan-led research team used a pint-sized predator-prey-parasite system inside 20-gallon water tanks to test the healthy herds hypothesis.

Woodpecker helps managers promote new life in burned forests

A male Black-backed Woodpecker at Silvio O. Conte National Wildlife Refuge, Brunswick, Vermont, USA.
Photo Credit: U.S. Fish and Wildlife Service Northeast Region
(CC BY 2.0)

Scientists have created a tool based on the habitat preferences of the black-backed woodpecker to help forest managers make decisions that promote regrowth and biodiversity following wildfires.

“Wildfire is like a 10,000-piece puzzle, and climate change is rearranging the pieces,” said Andrew Stillman, a postdoctoral researcher at the Cornell Atkinson Center for Sustainability and the Cornell Lab of Ornithology and first author of “Incorporating Pyrodiversity into Wildlife Habitat Assessments for RapidPost-Fire Management: A Woodpecker Case Study,” published April 25 in Ecological Applications.

“Gigantic, severe fires are becoming the new norm in California due to drought, longer burn seasons and dense forests. But birds do really well in landscapes that are ‘pyrodiverse’ – areas where fire results in uneven patches burned at high, medium, and low severity,” Stillman said.

Black-backed woodpeckers love pyrodiversity. They prefer to build their nest cavities in newly burned areas after high severity fires. But they also like to be adjacent to areas that burned at low intensity, where their young can hide from predators among living trees that still provide cover. Because of the species’ unique habitat associations, they are sensitive to the removal of trees after fire, and forest managers use information on the woodpecker to guide their post-fire planning.