More Than 60 Years to Achieve Gender Equity? (Psychology / Astronomy)


It will take until at least 2080 before women make up just one-third of Australia’s professional astronomers, an analysis published today in the journal Nature Astronomy reveals.

“Astronomers have been leaders in gender equity initiatives, but our programs are not working fast enough,” says Professor Lisa Kewley, director of the ARC Centre of Excellence for All-Sky Astrophysics in 3 Dimensions (ASTRO 3D).

Kewley is also an ARC Laureate Fellow at the Australian National University’s Research School for Astronomy and Astrophysics. She developed workforce forward modelling that can predict the fraction of women at all levels in astronomy from 2021 to 2060, given different initiatives in hiring or retention. The models show that Australia’s university leadership need to adopt 50:50 or affirmative action hiring and introduce exit surveys and retention initiatives.

“With these initiatives we can reach one-third women in 11 years, growing to 50 per cent in 25,” she said.

“The gender gap in astronomy is not unique to Australia. This is a worldwide issue, particularly at senior levels.

“The fraction of women in senior astronomy positions in the US, Germany, Canada, Australia, China and the UK has sat at 20 per cent or less for decades – even though women earn about 40 per cent of the PhDs in the field.”

She said that female astronomers leave the industry two to three times more frequently than their male counterparts. Those who remain find advancement challenging due to a lack of senior role models at universities, and because they are often overlooked for invited seminars, grants, awards, and all-important telescope time.

In 2014, the Astronomical Society of Australia took steps to improve the ratio of women to men being hired and retained by introducing a gender equality rating system called the Pleiades Awards. The scheme triggered widespread change in many universities and other astronomy-centred research institutions.

These have made a difference, said Dr Anshu Gupta, an ASTRO 3D Fellow at Curtin University in Western Australia.

“I think the barriers to women in the field are lower than they used to be, but there are still serious reforms needed to retain and promote talented junior female academics into senior positions,” she said.

Some institutions have also introduced hiring practices designed to attract and retain women. ASTRO 3D and the ARC Centre of Excellence for Gravitational Wave Discovery (OzGrav) have hiring ratios of 50:50. The University of Sydney School of Physics recently hit a target of 78 per cent women appointed to permanent positions.

But hiring is not enough, Professor Kewley’s research shows. Retention initiatives are also needed to stem the flow of women out of the sector.

She said that successful retention policies include exit surveys, improving work-life balance for department members, clear action against sexism, insults, microaggression, exclusionary behaviour, and the removal of structural barriers by creating more permanent and fewer fixed-term positions.

“If this sort of program becomes widespread, the discipline can reach the 30 per cent target in a decade or so,” said Professor Kewley.

ANU Vice Chancellor and Nobel Laureate Brian Schmidt commented:

“We as university leaders need to step up in areas like astronomy, but also across all the academic areas in our institutions where the male-female imbalance is large.

“Professor Kewley’s research shows that workforce forward modelling is highly effective way to assess the potential impact and utility of new diversity policies and initiatives. I encourage my peers across the research sector to take a close look and use the tools to drive positive change.”

Featured image: Professor Lisa Kewley.
Credit: ASTRO 3D

Reference: Kewley, L.J. Closing the gender gap in the Australian astronomy workforce. Nat Astron (2021).

Provided by Astro3D

How Reef-building Corals Got Their Bones? (Biology)

Coral ancestors had the genetic toolkit to make skeletal structures and only took simple evolutionary steps to begin building reefs.

Coral reefs provide shelter, sustenance and stability to a range of organisms, but these vital ecosystems would not exist if not for the skeletal structure created by stony corals. Now, KAUST scientists together with an international team have revealed the underlying genetic story of how corals evolved from soft-bodied organisms to build the myriad calcified structures we see today.

“While the processes involved in coral calcification are well understood, it is less clear how corals’ ability to grow calcium carbonate skeletons actually evolved,” says Xin Wang, a former KAUST Ph.D. student who worked on the project under the supervision of Manual Aranda.

“How did a squishy anemone-like organism begin to build reefs?” asks Aranda. “Did the ‘tools’ already exist in their genetic code?”

There is a debate surrounding when calcified corals first began to emerge; the earliest fossils found to date are around 265 million years old, but their evolution began far earlier.

The complex genomic analysis took two years to complete on KAUST's Shaheen-II Supercomputer.
The complex genomic analysis took two years to complete on KAUST’s Shaheen-II Supercomputer. © 2021 Morgan Bennett Smith

“We conducted a genomic search for conserved genes that might be involved in calcification,” says Wang. “Our findings suggest that corals evolved to calcify somewhere between 308 and 265 million years ago.”

The team compared the genomes of six different related species — two evolutionary divergent reef-building corals, two of their closest noncalcifying relatives and two sea anemones. The complex analysis took two years using the KAUST supercomputer.

“We found that the necessary proteins to make coral skeletons were already present in the soft-bodied ancestor and that various existing proteins were recruited to boost the calcifying process. Essentially, we believe we’ve found the genetic toolkit for coral skeleton creation,” says Wang.

To calcify, corals must draw in positively charged calcium ions from seawater. To make this process as efficient as possible, the coral proteins that help the calcium precipitate should be negatively charged and the pH balance of the calcifying fluid must be just right.

The team pinpointed the genes responsible for transporting calcium and removing protons in the soft-bodied organisms, and they showed that two of the three gene copies found in corals have been recruited to the calcifying tissue. The researchers then identified a gene encoding an acid-rich protein that was duplicated in corals twice and then recruited to precipitate and stabilize calcium carbonate in the initial stage of skeleton building. They also highlighted transmembrane proteins involved in bone matrix adhesion.

“This is a great example of how latent traits can evolve to become dominant given certain environmental pressures,” says Aranda. “Next we hope to verify which of these components is critical to calcification and investigate how coral reefs might be influenced by the changing pH of future oceans.”

Featured image: The genetic toolkit to produce skeletal structures that corals developed from their soft-bodied ancestors has been identified by KAUST researchers. © 2021 Morgan Bennett Smith


  1. Wang, X., Zoccola, D., Liew, Y.J., Tambutte, E., Cui, G., Allemand, D., Tambutte, S. & Aranda, M. The evolution of calcification in reef-building corals. Molecular Biology and Evolution advance online publication, 19 April2021.| article

Provided by KAUST

She’s Not Interested in Sex But He Thinks She Is (Psychology)

Women and men misunderstand each other’s signals of friendliness and sexual interest. But these misinterpretations are no surprise to evolutionary psychologists.

Imagine the following scenario: a woman and a man are having a conversation. She is interested in the conversation, and is friendly, smiling and warm. He interprets her behaviour as sexual interest.

Or maybe: a man is sexually attracted to a woman he has just met, and signals this in various ways. She thinks that he is just being friendly.

Recognize these situations? If so, you’re not alone.

We misunderstand each other

In a recent study at the Department of Psychology at NTNU, women reported that men often misinterpret their signals of friendliness as sexual interest. Conversely, the men in the study reported that women often misinterpret their signals of sexual interest as friendliness.

“The results are no surprise, seen from an evolutionary perspective,” researcher Mons Bendixen explains. “The fascinating thing is that our results are identical to a study done in the USA, even though Norway is one of the most gender-equal, sexually liberal countries in the world.”

In most areas of psychology, there is little to no difference between genders: mental capacity, intellectual achievements, food preferences — men and women are all more or less the same. But when it comes to reproduction and challenges related to finding a sexual partner, there are suddenly differences to be found.

Evolutionary psychology is the study of how the human mind has evolved, developed and adapted over time. One thing that evolutionary psychologists are specifically interested in is gendered sexual psychology between cultures and social groups. Seen through the lens of evolutionary psychology, we can better understand why men often wrongly assume that women who smile and laugh during conversation may want to sleep with them.

Men can’t be picky

A man’s ability to reproduce is all about seizing every opportunity. He has to spend both money and time on courtship, which still may not lead to sex. But it costs even more to not try, because then he won’t be able to reproduce.

“A man’s reproductive fitness, meaning the amount offspring he produces, is dependent on how many women he is able to make pregnant. But that’s not how it works for women,” Bendixen explains.

A woman can have sex with multiple men over a short period of time without producing any more children. So for men, it is a low-risk, potentially high-reward situation for men to have sex with women whenever the opportunity presents itself.

On the other hand, the cost is potentially great for a woman if she thinks that a man is more sexually interested than she is. A woman risks pregnancy, birth, nursing and raising the child, as well as lost oppotunities to reproduce with others. Across thousands of generations, women’s psychology has evolved to set the bar higher, which means they need much clearer signals than men before they consider sex.

“Even though these processes aren’t conscious, we can still empirically measure the results,” Bendixen says.

Similar to an American study

The recent study at NTNU included 308 heterosexual participants between the ages of 18 and 30. Fifty-nine per cent of participants were women.

The participants were all heterosexual because sexual intercourse between men and women is necessary for reproduction. Half of the women and 40 per cent of the men were in relationships. The questions were identical to questions asked in a similar American study from 2003. Here are a few examples:

Have you ever been friendly to a person of the opposite gender, and had your actions interpreted as sexual interest? If yes, how many times has this happened?

Have you ever been sexually attracted to someone and shown interest, and had the other person misinterpret your signals as friendliness? If yes, how many times has this happened?

Men misinterpret most often

The results show that both men and women find that their social signals are misinterpreted by the opposite sex. Women in the study answered that they had acted friendly towards a man about 3.5 times over the past year on average, and had this misinterpreted as sexual interest. The men in the study also reported having been misinterpreted by the opposite sex in this way, but far less often.

The results also show that men rarely misinterpret women who actually do signal sexual interest. The study also shows that this is independent of whether or not the person is in a steady relationship or not.

Bedixen points out that Norway is considered to be one of the most gender-equal countries in the world. The USA, on the other hand, where a similar study was done in 2003, is ranked as 20th on the World Economic Forum’s list for equality around the world.

“The fact that the hypothesis in evolutionary psychology is supported even when the study is in a society where gender equality is strong, weakens alternative claims that the social roles of men and women in different cultures determine their psychology in these situations,” he says.

Does not excuse sexual harassment

Researchers at the Department of Psychology are now going to use data collected from high school students to see if the results of this study are also valid for people aged 16-19, and if these miscommunications might lead to sexual harassment.

“Even though evolutionary psychology and our findings can help account for some sexually inappropriate behaviour in men, it doesn’t mean that evolutionary psychologists defend this happening. Measures can be taken to prevent sexual harassment. It will help if we just teach men that a woman who laughs at your jokes, stands close, or touches your arm at a party doesn’t mean that she’s sexually interested, even if you think she is,” Bendixen says.

Featured image: Women and men misunderstand each other all around the world, even in Norway, one of the most gender-equal, sexually liberal countries in the world. © Norwegian Science and Technology

Mons Bendixen (2014) Evidence of Systematic Bias in Sexual Over- and Underperception of Naturally Occurring Events: A Direct Replication of Haselton (2003) in a More Gender-Equal Culture. Evolutionary Psychology, 12(5), 1004-1021.

Provided by Norwegian Science and Technology

When Does the Green Monster of Jealousy Awake in People? (Psychology)

Women and men are often jealous for completely different reasons. This gender difference occurs so early that it surprised the researchers.

Adult heterosexual women and men are often jealous about completely different threats to their relationship. These differences in jealousy seem to establish themselves far sooner than people need them. The finding surprised a research group at NTNU that has studied the topic.

“You don’t really need this jealousy until you need to protect yourself from being deceived,” says Professor Leif Edward Ottesen Kennair at NTNU’s Department of Psychology.

Romantic jealousy can be experienced as horrible at its worst. But jealousy associated with a partner’s infidelity has clearly been an evolutionary advantage.

“Jealousy is activated when a relationship we care about is threatened. The function is probably to minimize threats to this relationship. These threats have historically been somewhat different for men and women,” says Per Helge H. Larsen, a master’s student in the Department of Psychology at NTNU.

Evolutionary psychology can help explain the gender differences having to do with this jealousy.

The function of jealousy is probably to minimize threats to the relationship. These threats have historically been somewhat different for men and women. Thus the jealousy too. Illustration photo: Shutterstock, NTB

Gender differences around jealousy

The differences in sexual jealousy between the sexes, simply put, revolve around the possibilities for their own children. Previous research has already established that:

  • Men more often react more negatively when their partner has had sex with others than if she falls in love or spends time with someone without having sex. It’s easy to explain: if the woman is sexually unfaithful, it ultimately means that her partner might need to use his own resources to raise another man’s children.
  • Women, on the other hand, are always sure that the child is theirs. They tend to react more negatively to their partner having feelings for another woman than that he’s had sex with her. This response can also be explained. Historically, she could suffer a loss of resources and status for herself and their child if he left her for someone else.

We should note that these differences have been with us since long before birth control pills and the possibility for women to feed and raise their children alone. A few generations aren’t enough to change either biology or culture very much.

Jealousy not risk free

The gender differences that lead to jealousy are easy to explain. They are evolutionary adaptations that get passed on to the next generation – but why does this gender difference arise so early?

Precisely this question presents theoretical challenges for the researchers, because jealousy has historically not been risk-free, either.

“Jealousy is potentially a costly reaction, perhaps especially for the man before he is physically strong enough to defend himself and his partner against rivals, and before he would normally have had the opportunity to have a steady partner through marriage,” says Kennair.

Throughout history, jealous boys and men have run a great risk by expressing their jealousy. Being ostracized, injured or killed in competing for women is all too well known.

“Throughout evolutionary history, the usefulness of man’s form of jealousy would probably have been reserved for men of high status who had a great ability to defend themselves,” says Kennair.

So why be jealous before you’re able to take care of your partner?

Why be jealous before you are able to take care of your partner? Photo: Shutterstock, NTB

Present in adolescence

“We knew that this difference becomes established in the early 20s, but through our study we’ve shown that it appears even earlier,” says Larsen.

The research group at NTNU wanted to find out when these gender differences around jealousy, sex and emotions begin. To this end they studied 1266 pupils aged 16 to 19 years in upper secondary school. However, it turns out the participants weren’t young enough for the researchers to answer this question as to when gender differences develop.

“The gender difference was stable and clear throughout the age range of the study. This is pretty startling,” says Professor Mons Bendixen in the Department of Psychology.

“The gender difference wasn’t affected by whether the teens currently had a boyfriend or girlfriend, or whether they had made their sexual debut. The difference thus doesn’t seem to have anything to do with experience,” Bendixen adds.

We can imagine, and perhaps assume, that the gender differences in jealousy responses arise even earlier than age 16. But we don’t know that for sure yet. To confirm it, we need to study even younger boys and girls.

“It’s also unclear how young study participants can be to research this in a meaningful way,” says Kennair.

Distinguishing between sexual jealousy and other types of jealousy can quickly become meaningless for the very youngest among us.

Does jealousy prepare us for adulthood?

In one way or another, the benefits of this early, gender-specific sexual jealousy must have outweighed its dangers.

“It could be that the early development of sexual jealousy is simply preparing us for adulthood, and that it has no other function at a younger age.” But Kennair emphasized that jealousy is a dangerous feeling. Young men could put themselves in danger by experiencing this feeling before it was appropriate and they were physically strong enough to defend the relationship.

But the researchers are clear that this idea is still speculation.

“We need further research and theory development on the basis of these findings,” Kennair said.

The results from the youth group study were recently published in the Nature journal Scientific Reports.

Featured image: We don’t need sexual jealousy until we need to protect ourselves from being deceived. But researchers still found gender differences in jealousy early on. Illustration photo: Shutterstock, NTB

Source: Per Helge H. Larsen, Mons Bendixen, Trond Viggo Grøntvedt, Andrea M. Kessler, Leif Edward Ottesen Kennair. Investigating the emergence of sex differences in jealousy responses in a large community sample from an evolutionary perspective. Scientific Reports:

Provided by Norwegian Science and Technology

How SARS-CoV-2 Hijacks Human Cells to Evade Immune System? (Medicine)

Researchers at University of California San Diego School of Medicine have discovered one way in which SARS-CoV-2, the coronavirus that causes COVID-19, hijacks human cell machinery to blunt the immune response, allowing it to establish infection, replicate and cause disease.

In short, the virus’ genome gets tagged with a special marker by a human enzyme that tells the immune system to stand down, while at the same time ramping up production of the surface proteins that SARS-CoV-2 uses as a “doorknob” to enter cells.

The study, published April 22, 2021 in Cell Reports, helps lay the groundwork for new anti-viral immunotherapies — treatments that work by boosting a patient’s immune system, rather than directly killing the virus.

“It’s very smart of this virus to use host machinery to simultaneously go into stealth mode and get inside more cells,” said Tariq Rana, PhD, professor and chief of the Division of Genetics in the Department of Pediatrics at UC San Diego School of Medicine and Moores Cancer Center. “The more we know about how the virus establishes itself in the body, the better equipped we are to disrupt it.”

In human cells, genes (DNA) are transcribed into RNA, which is then translated into proteins, the molecules that make up the majority of cells. But it’s not always so straightforward. Cells can chemically modify RNA to influence protein production. One of these modifications is the addition of methyl groups to adenosine, one of the building blocks that make up RNA. Known as N6-methyladenosine (m6A), this modification is common in humans and other organisms, including viruses.

In contrast to humans, the entire genomes of some viruses, including SARS-CoV-2, are made up of RNA instead of DNA. And rather than carry around the machinery to translate that into proteins, the coronavirus gets human cells to do the work.

Rana and his team previously discovered that m6A plays an important role in HIV and Zika virus infections. In their latest study, the researchers discovered that the human enzyme METTL3 adds methyl groups to introduce m6A in SARS-CoV-2’s RNA. That modification prevents the virus’ RNA from triggering inflammatory molecules known as cytokines. To the team’s surprise, METTL3’s activity also led to increased expression of pro-viral genes — those that encode proteins needed for SARS-CoV-2 replication and survival, such as ACE2, the cell surface receptor that the virus uses to enter human cells.

“It remains to be seen why our cells help the virus out like this,” Rana said.

When the team removed METTL3 from cells in the laboratory, using gene silencing or other methods, they saw the reverse — a pro-inflammatory molecule known as RIG1 binds the viral RNA, more inflammatory cytokines were produced, and pro-viral genes were inhibited. Ultimately, inhibiting METTL3 suppressed viral replication.

To see how this mechanism plays out in the real world, the team compared post-mortem lung samples from COVID-19 patients and healthy lung biopsies. In patients who had died from severe COVID-19, the team found, METTL3 expression was lower and inflammatory genes were elevated. That makes sense in later stages of COVID-19, Rana said, because cytokine storm — the excessive activation of the patient’s own immune system — is known to worsen the disease.

“It’s like there are two phases of the infection — in the first, the virus needs METTL3 to help it evade the immune response,” he said, “but in the second phase, once the virus is replicating like crazy, it’s better to downregulate METTL3.”

Rana’s team is now validating their findings in animal models, and developing METTL3 inhibitors to test as potential experimental therapies for COVID-19.

“We hope that by manipulating m6A levels in the virus, we might be able to time the innate immune response in a way that benefits patients with COVID19, especially for the mild or moderate patients who haven’t developed cytokine storm,” Rana said. “The challenge is that cells have many other enzymes like METTL3, known as methyltransferases, so inhibiting it would need to be done very specifically, at a specific time.”

Co-authors of the study include: Na Li, Hui Hui, Bill Bray, Rob Knight, Davey Smith, Aaron F. Carlin, UC San Diego; Gwendolyn Michelle Gonzalez, Yinsheng Wang, UC Riverside; Mark Zeller, Kristian G. Anderson, Scripps Research.

Featured image: Human enzyme METTL3 adds methyl groups to introduce m6A in SARS-CoV-2’s RNA. That modification prevents the virus’ RNA from triggering inflammatory molecules known as cytokines. METTL3 also leads to increased expression of pro-viral genes — those that encode proteins needed for SARS-CoV-2 replication and survival. © UC San Diego Health Sciences

Reference: Na Li, Bill Bray, Hui Hui et al., “METTL3 regulates viral m6A RNA modification and host cell innate immune responses during SARS-CoV-2 infection”, Cell Reports, 2021. DOI:

Provided by University of California- San Diego

Treatment Found to Improve Cognitive Function in Patients With Fragile X Syndrome (Medicine)

Results from phase two study show improved language and daily functioning among participants

An experimental treatment produced improvements in cognitive function and language in patients with fragile X syndrome, according to study results published on April 29 in Nature Medicine. Fragile X syndrome (known as FXS for short) is the most common known genetic cause of autism and the most common cause of inherited intellectual disability.

“These results offer hope for patients with fragile X syndrome and their families,” said Elizabeth Berry-Kravis, MD, PhD, a pediatric neurologist at Rush University Medical Center and principal investigator of the study. “The majority of clinical outcome measures were in favor of the drug. These measures included performance-based assessments, biomarkers, and parent and physician-rated scales, which in combination, suggest a meaningful impact on the global FXS disease process.”

The study was a phase two clinical trial to assess the safety and efficacy of a drug known as BPN14770 in 30 men with between the ages of 18 and 41 years who have fragile X syndrome. BPN1477 inhibits the activity of an enzyme known as phosphodiesterase‐4D (PDE4D), which controls the availability in the brain of cyclic adenosine monophosphate (cAMP), a molecule that is critically involved in memory formation. By inhibiting PDE4D, the drug increases the levels of cAMP in the brain. “It’s exciting that we have a drug that potentially addresses a core biochemical deficit in FXS, a deficiency of cAMP, that has been documented in patients, and which I discovered during my pediatric neurology fellowship 30 years ago,” Berry-Kravis said.

Participants in the study received daily oral doses of BPN14770 twice a day or a placebo for 12 weeks. Parents, caregivers and physician raters were kept unaware of whether the participants received the treatment or the placebo.

The study evaluated the participants using a version of the National Institutes of Health (NIH) Toolbox Cognitive Battery (a cognitive measure) that, in work performed in collaboration with Dr. David Hessl at the UC Davis MIND Institute, was modified to be effective in assessing people with intellectual disabilities. In addition, the study included scales on which parents’ rated improvements from the drug.

“This is the first time that the NIH Toolbox has been able to be used to demonstrate a cognitive change in a trial in people with intellectual disabilities,” Berry-Kravis said. “In just three months, we saw improvement specifically in the verbal subtests of the NIH Toolbox, coupled with parent rating of improvements, particularly in language.”

Cognitive assessments using the NIH Toolbox revealed significant benefit in oral reading recognition, picture vocabulary and the cognition crystallized composite score. Parent/caregiver ratings revealed benefit that was judged to be clinically significant in language and daily functioning.

After 12 weeks of treatment in the study, patients crossed over and took placebo if they had been taking drug, and drug if they had been taking placebo for another 12 weeks. The benefit of BPN14770 was found to persist up to 12 weeks after the crossover from drug to placebo. BPN14770 was very well tolerated, with few adverse events.

In laboratory studies, BPN14770 promoted the maturation of connections between neurons, (which is impaired in patients with fragile X syndrome). BPN14770 is being developed by Tetra Therapeutics ( for the treatment of fragile X syndrome. The drug’s mechanism of action also may have potential to improve cognitive and memory function in Alzheimer’s disease and other dementias, learning/developmental disabilities and schizophrenia. At this time, however, the U.S. Food and Drug Administration only has approved BPN14770 for investigational use, and it will be important to do larger controlled studies in fragile X syndrome to confirm the cognitive benefit of the drug.

Featured image: Elizabeth Berry-Kravis © RUSH

Reference: Berry-Kravis, E.M., Harnett, M.D., Reines, S.A. et al. Inhibition of phosphodiesterase-4D in adults with fragile X syndrome: a randomized, placebo-controlled, phase 2 clinical trial. Nat Med (2021).

Provided by RUSH

How Diet Controls RNA Maturation? (Biology)

Two UNIGE teams have discovered a new mechanism for regulating RNA maturation that depends on diet.

Particularly sensitive to chemical modifications, messenger RNAs (mRNAs) are molecules responsible for transmitting the information encoded in our genome, allowing for the synthesis of proteins, which are necessary for the functioning of our cells. Two teams from the University of Geneva (UNIGE), Switzerland, in collaboration with the Norwegian University of Science and Technology (NTNU), have focused on a specific type of chemical modification – called methylation – of mRNA molecules in the small worm Caenorhabditis elegans. They found that methylation on a particular sequence of an mRNA leads to its degradation and that this control mechanism depends on the worm’s diet. These findings are to be read in the journal Cell.

Several steps take place before a DNA-encoded gene produces the corresponding protein. One of the two strands of DNA is first transcribed into RNA, which then undergoes several processes, including splicing, before being translated into a protein. This process removes unnecessary non-coding sequences (introns) from the gene, leaving only the protein-coding sequences (exons). This mature form of RNA is called messenger RNA (mRNA).

A “post-it” to block protein synthesis

In addition to these processes, RNA – but also DNA molecules – can undergo a chemical modification: methylation. This consists in adding a methyl group (CH3) which allows to modify the fate of these molecules without altering their sequence. Deposited on the RNA or DNA in very specific places like “post-its”, methyl groups indicate to the cell that a particular fate must be given to these molecules. Methylation of RNA is essential: mice without RNA methylation die at an early embryonic stage.

Two neighboring teams at the UNIGE, one working on RNA regulation and the other specializing in DNA organisation in the worm C. elegans, have studied the role of methylation in controlling gene expression. The laboratories of Ramesh Pillai and Florian Steiner, professors in the Department of Molecular Biology at the UNIGE Faculty of Science, have shown for the first time that methylation at the end of the intron of a particular gene blocks the splicing machinery. The intron cannot be removed and the protein is not produced.

Fine regulation to ensure a fair balance

This gene, whose mRNA is modified by methylation, encodes for the enzyme that produces the methyl donor. “It is therefore a self-regulating mechanism since the gene involved in producing a key factor required for methylation is itself regulated by methylation!”, explains Mateusz Mendel, a researcher in the Department of Molecular Biology at the UNIGE Faculty of Science, and the first author of this study.

Moreover, this modification is dependent on the quantity of nutrients received by the worms. “When nutrients are abundant, the mRNA is methylated, gene splicing is blocked, and the level of methyl donors decreases, which limits the number of possible methylation reactions. On the other hand, when there are few nutrients, there is no methylation of the particular RNA of this gene, so splicing is not blocked and the synthesis of methyl donors increases”, reports Kamila Delaney, a researcher in the Department of Molecular Biology at the UNIGE Faculty of Science. Elements present in the food provide the raw materials required for producing the methyl donor, so methylation-dependent splicing inhibition puts a brake on its production under conditions of a rich diet. “Aberrant methylation reactions – too much or too little – are the cause of many diseases. The cell has set up this very sophisticated regulatory system to ensure a fair balance of methylations in the cell”, summarizes Mateusz Mendel.

Methylation of mRNAs at these specific sequences was discovered in the 1970s by scientists, including Ueli Schibler, a former professor at the UNIGE, before being forgotten. It took 40 years before researchers rediscovered its importance in gene regulation in 2012. With this study, scientists from the Department of Molecular Biology highlight the crucial role of methylation in the control of splicing and in the response to environmental changes.  

Featured image: The nematode C. elegans at two developmental stages: a larva and a developing embryo. © Joanna Wenda

Reference: Mateusz Mendel, Kamila Delaney et al., “Splice site m6A methylation prevents binding of U2AF35 to inhibit RNA splicing”, Cell, 2021. DOI:

Provided by University of Geneve

Study Shows How Meningitis-causing Bacteria May Sense Fever to Avoid Immune Killing (Medicine)

Researchers at Karolinska Institutet in Sweden have discovered a mechanism through which meningitis-causing bacteria can evade our immune system. In laboratory tests, they found that Streptococcus pneumoniae and Haemophilus influenzae respond to increasing temperatures by producing safeguards that keep them from getting killed. This may prime their defenses against our immune system and increase their chances of survival, the researchers say. The findings are published in the journal PLoS Pathogens.

“This discovery helps to increase our understanding of the mechanisms these bacteria use to evade our normal immune defenses,” says co-corresponding author Edmund Loh, researcher in the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet. “It could be an important piece of the puzzle in examining what turns this usually harmless bacterium into a lethal killer.”

Meningitis is an inflammation of the membranes surrounding the brain and the spinal cord. It can be caused by viruses, bacteria, fungi and parasites.

Bacterial meningitis is one of the most severe types and a major cause of death and disability in children worldwide. Several kinds of bacteria can cause the infection, including the respiratory pathogens Streptococcus pneumoniae and Haemophilus influenzae, which can be attributed to some 200,000 meningitis-caused deaths annually.

These two bacteria often reside in the nose and throat of healthy people without making them ill. In some cases they spread into the bloodstream and cause invasive diseases, but the reasons for this remain largely unknown.

In this study, the researchers set out to investigate the connection between temperature changes and survival of these bacteria in a laboratory setting. The experiments were prompted by another recent finding that linked the temperature sensing abilities of the bacterium N. meningitidis to invasive meningococcal disease.

Hannes Eichner, PhD student Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet © Ulf Sirborn

One of the signs of an infection is elevated temperatures and fever, which typically boost our immune system’s ability to fight illness. In this study, however, the researchers found that both S. pneumoniae and H. influenzae activated stronger immune protections when challenged with higher temperatures.

They did so through mechanisms involving four specific so-called RNA thermosensors (RNATs), which are temperature-sensitive non-coding RNA molecules. These RNATs helped boost the production of bigger protective capsules and immune modulatory Factor H binding proteins, both of which help shield these bacteria from immune system attacks.

“Our results indicate that these temperature sensing RNATs create an additional layer of protection that helps the bacteria colonize their normal habitat in the nose and throat,” says the paper’s first author Hannes Eichner, PhD student at the same department. “Interestingly, we saw that these RNATs do not possess any sequence similarity, but all retain the same thermosensing ability, which indicates that these RNATs have evolved independently to sense the same temperature cue in the nasopharynx to avoid immune killing.”

More research is needed to understand exactly what triggers these pathogens to breach from the mucous membrane into the bloodstream and further into the brain. Future studies encompassing in vivo infection model are warranted to characterize the role of these RNATs during colonization and invasion, the researchers say.

The work was supported by grants from the Knut and Alice Wallenberg Foundation, the Swedish Foundation for Strategic Research, the Swedish Research Council, the Stockholm County Council and Karolinska Institutet.

Featured image: Edmund Loh, researcher Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet © Francesco Righetti

Publication: “RNA thermosensors facilitate Streptococcus pneumoniae and Haemophilus influenzae immune evasion,” Hannes Eichner, Jens Karlsson, Laura Spelmink, Anuj Pathak, Lok-To Sham, Birgitta Henriques-Normark, Edmund Loh, PLoS Pathogens, online April 29, 2021, doi: 10.1371/journal.ppat.1009513

Provided by Karolinska Institute

Machine Learning Algorithm Helps Unravel the Physics Underlying Quantum Systems (Quantum)

Protocol to reverse engineer Hamiltonian models advances automation of quantum devices

Scientists from the University of Bristol’s Quantum Engineering Technology Labs (QETLabs) have developed an algorithm that provides valuable insights into the physics underlying quantum systems – paving the way for significant advances in quantum computation and sensing, and potentially turning a new page in scientific investigation.

In physics, systems of particles and their evolution are described by mathematical models, requiring the successful interplay of theoretical arguments and experimental verification. Even more complex is the description of systems of particles interacting with each other at the quantum mechanical level, which is often done using a Hamiltonian model. The process of formulating Hamiltonian models from observations is made even harder by the nature of quantum states, which collapse when attempts are made to inspect them.

In the paper, Learning models of quantum systems from experiments, published in Nature Physics, quantum mechanics from Bristol’s QET Labs describe an algorithm which overcomes these challenges by acting as an autonomous agent, using machine learning to reverse engineer Hamiltonian models.

The team developed a new protocol to formulate and validate approximate models for quantum systems of interest. Their algorithm works autonomously, designing and performing experiments on the targeted quantum system, with the resultant data being fed back into the algorithm. It proposes candidate Hamiltonian models to describe the target system, and distinguishes between them using statistical metrics, namely Bayes factors.

Excitingly, the team were able to successfully demonstrate the algorithm’s ability on a real-life quantum experiment involving defect centres in a diamond, a well-studied platform for quantum information processing and quantum sensing.

The algorithm could be used to aid automated characterisation of new devices, such as quantum sensors. This development therefore represents a significant breakthrough in the development of quantum technologies.

“Combining the power of today’s supercomputers with machine learning, we were able to automatically discover structure in quantum systems. As new quantum computers/simulators become available, the algorithm becomes more exciting: first it can help to verify the performance of the device itself, then exploit those devices to understand ever-larger systems,” said Brian Flynn from the University of Bristol’s QETLabs and Quantum Engineering Centre for Doctoral Training.

“This level of automation makes it possible to entertain myriads of hypothetical models before selecting an optimal one, a task that would be otherwise daunting for systems whose complexity is ever increasing,” said Andreas Gentile, formerly of Bristol’s QETLabs, now at Qu & Co.

“Understanding the underlying physics and the models describing quantum systems, help us to advance our knowledge of technologies suitable for quantum computation and quantum sensing,” said Sebastian Knauer, also formerly of Bristol’s QETLabs and now based at the University of Vienna’s Faculty of Physics.

Anthony Laing, co-Director of QETLabs and Associate Professor in Bristol’s School of Physics, and an author on the paper, praised the team: “In the past we have relied on the genius and hard work of scientists to uncover new physics. Here the team have potentially turned a new page in scientific investigation by bestowing machines with the capability to learn from experiments and discover new physics. The consequences could be far reaching indeed.”

The next step for the research is to extend the algorithm to explore larger systems, and different classes of quantum models which represent different physical regimes or underlying structures.

Featured image: The nitrogen vacancy centre set-up, that was used for the first experimental demonstration of QMLA. © Gentile et al.

Paper: Gentile, A.A., Flynn, B., Knauer, S. et al. Learning models of quantum systems from experiments. Nat. Phys. (2021). Link when paper is live:

Provided by University of Bristol