PhD candidate Emily Massingham from UQ’s Faculty of Science managed a team of researchers which visited 79 villages across the Bornean orangutan range in Kalimantan, conducting face to face interviews with 431 people.

“Our study builds on previous research which indicated killing was one of the key reasons for orangutan population decline, alongside habitat loss,” Ms Massingham said.

“The aim of our project was to understand whether orangutans have been killed in recent times, to look at whether conservation projects are effectively preventing killing, and to gain insights into community perceptions and the motivations behind it.

“It has been almost 15 years since the previous study, and we did not find a clear decrease in killings despite Indonesia’s commendable efforts to reduce habitat loss.

“Thirty per cent of villages reported orangutans had been killed in the last 5 -10 years, despite the practice being both illegal and taboo — which also makes it hard to get an accurate picture of the true scale.”

Ms Massingham said Borneo’s orangutan population had decreased by 100,000 in recent decades, with current estimates suggesting fewer than 100,000 animals remain.

“Our findings did not indicate that conservation projects are reducing killing, highlighting an urgent need to improve the collective approach to orangutan conservation,” she said.

“Killing by humans needs to be addressed, as our findings suggest it may still be occurring and poses a real threat to the species.”

Ms Massingham said orangutans have long lifespans and breed slowly, so are particularly vulnerable to population declines driven by the death of adult apes.

“Our interviews revealed some of the situations which lead to the killing or displacement of individual orangutans,” she said.

“They include protecting crops and taking infant apes to keep as pets.”

The researchers outlined recommendations that could improve future conservation efforts.

“Working with communities and collaborating across disciplines and projects will be key,” Ms Massingham said.

“Conservationists need to work closely with individual villages to understand their needs and perspectives, identify the social drivers of killing of orangutans and implement solutions that reduce human-orangutan conflict.”

The research was conducted under a RISTEK permit, with the engagement of a local social development organisation to facilitate fieldwork.

A new study published today in the journal Neuron by researchers at the University of Wisconsin-Madison showed that FMRP, a protein deficient in individuals with fragile X syndrome, has a role in the function of mitochondria, part of a cell that produces energy, during prenatal development. Their results fundamentally change how scientists understand the developmental origins of fragile X syndrome and suggest a potential treatment for brain cells damaged by the dysfunction.

The study, led by four postdoctoral fellows — Minjie Shen, Carissa Sirois, Yu (Kristy) Guo and Meng Li — working in the lab of the lab of Xinyu Zhao, neuroscience professor and neurodevelopmental diseases researcher a UW-Madison’s Waisman Center, found FMRP regulating a gene called RACK1 to promote mitochondrial function. Using a drug to enhance mitochondrial function, they were able to rescue brain cells damaged by lack of FMRP.

Individuals with FXS may present developmental delays — not sitting, walking or talking at expected ages — as well as mild to severe intellectual disability, learning disabilities and social and behavioral problems. About half are also diagnosed with autism spectrum disorder.

In previous research, Zhao found that mitochondria in mice with an FMRP deficiency that imitates FXS were smaller and unhealthy. Diving deeper, they also discovered that FMRP regulates genes involved in mitochondria fission-fusion, a process into which mitochondria fuse into a bigger shape in order to produce more energy for the cell.

For the study, researchers grew brain cells called neurons grown from induced pluripotent stem cells. Because the stem cells came from people with FXS, the researchers could study the development of the disorder at a cellular level, determining whether mitochondria in human cells experienced issues similar to those in mice.

“And indeed, we found that human neurons also have fragmented (smaller) mitochondria,” Zhao says. They also found fewer mitochondria in neurons derived from FXS patients, which they did not see in the neurons of the mice modeling FXS.

“In human neurons, it’s a deficit in twofold. Not just fission-fusion, but also likely in the production of mitochondria,” Zhao says.

Although it has been long known that FMRP is deeply involved in FXS, the new discovery pinpoints a role for the protein in early development of the condition.

Symptoms of FXS present long after the baby is born. Many babies appear to be developing typically before showing slower development, autistic features or developmental deficits. Children with FXS are typically diagnosed at three years of age or older.

“Which means many scientists have been thinking that FMRP is more important for the postnatal maturation state,” Zhao says.

FMRP is protein that regulates the use of messenger RNA, sort of a of working copy of DNA used to produce the proteins that make things happen in cells. The researchers found that many of the mRNA strands that interact with FMRP are implicated in autism, providing a molecular link between FXS and autism spectrum disorder. Unexpectedly, many FMRP-bound mRNAs are expressed by genes classified as essential — genes that are very busy during prenatal development but less active after birth.

“This means that FMRP has a function in prenatal development that we have not really thought about before,” Zhao says. “The fact that we found that FMRP also regulates prenatal development is really interesting and is actually indicating that what we see in fragile X syndrome, some of the effects already happened within the prenatal development.”

One of those essential genes is RACK1, identified for the first time as playing a role in FXS.

“When RACK1 is lower in fragile X neurons, the mitochondria are suffering and the neurons exhibit mitochondrial deficit and hyperexcitability, like immature neurons. But when we reintroduce RACK1, we can rescue this,” Zhao says.

Using cultured neurons derived from individuals with FXS to screen for drugs, the researchers found a drug called leflunomide that corrected mitochondrial deficits. The treatment improved mitochondrial function and reduced the neurons’ hyperexcitability.

Next, Zhao wants to do a detailed biochemical analysis of mitochondrial dysfunction and figure out which key proteins are less present in FXS-affected neurons. She is also working on better understanding how RACK1 and leflunomide work to rescue mitochondrial function.

Other collaborators on the study include Waisman Center investigators Qiang Chang, Anita Bhattacharyya, Andre Sousa, Daifeng Wang, Donna Werling and UW-Madison neuroscience professor Jon Levine.

This research was supported by grants from the National Institutes of Health (R01MH118827, R01NS105200, R01MH116582, R01MH118827, R01HD064743, R01NS064025, R01AG067025, U01MH116492, P51 OD011106, U54HD090256, P50HD105353, R24HD000836 and T32 GM141013) and the Department of Defense (W81XWH-22-1-0621).

Though scientists have long known through observational data that the Milky Way is warped and its edges are flared like a skirt, no one could explain why.

Now, Harvard astronomers at the Center for Astrophysics | Harvard and Smithsonian (CfA) have performed the first calculations that fully explain this phenomenon, with compelling evidence pointing to the Milky Way’s envelopment in an off-kilter halo of dark matter. The work also bolsters current thinking about how the galaxy evolved and may offer clues into some of the mysteries of dark matter.

The new calculations were led by Jiwon Jesse Han, a Griffin Graduate School of Arts and Sciences student affiliated with the CfA. Published in Nature Astronomy, the work includes co-authors Charlie Conroy and Lars Hernquist, both faculty members at the CfA and in the Department of Astronomy.

Our galaxy is located inside a diffuse cloud called the stellar halo, which extends much farther out into the universe. In groundbreaking work published last year, the Harvard team deduced that the stellar halo is tilted and elliptical in shape, like a zeppelin or football.

Building on that, the team assumed the same shape for the dark matter halo, the larger entity that encompasses everything in and around the Milky Way. Dark matter makes up 80 percent of the galaxy’s mass but is invisible because it doesn’t interact with light, so the shape of that halo must be inferred. Using models to calculate the orbits of stars within a tilted, oblong dark matter halo, the team found a near-perfect match to existing observations of a warped, flared galaxy.

“A tilted dark halo is actually fairly common in simulations, but no one had explored its effect on the Milky Way,” Conroy said. “It turns out that the tilt is an elegant way to explain both the magnitude and direction of our galaxy’s wobbly disk.”

Scientists had long surmised that the Milky Way formed due to a galactic collision; the astronomers’ work further underscores that hypothesis.

“If the galaxy was just evolving on its own, it would have had this nice, spherical halo, this nice, flat disk,” Han said. “So the fact that the halo is tilted and has a football-like shape suggests that our galaxy experienced a merger event, where two galaxies collide.”

Their calculation of the dark matter halo’s probable shape may also provide clues as to the properties and particle nature of dark matter itself, which remain unsolved mysteries in physics. “The fact that the galaxy is not spherical in our data implies that there is some limit to which dark matter can interact with itself,” Han explained.

Confidence in these findings might lead to better ways to cleverly study the unobservable dark matter that makes up most of the universe. This includes new ways to pick up on kinematic signatures of dark sub-halos, which are miniature dark matter halos zipping around the galaxy.