Leaf-clipping and other leaf-modifying actions among East African chimpanzees as a form of gestural dialects

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University of St. Andrews researchers have discovered that chimpanzees in two nearby groups in Uganda’s Budongo Forest utilize leaf motions in several languages to communicate with one another.

A community of chimpanzees will employ their own preferred way of leaf-modifying motion, and nearby groups can use different ones, resulting in each group having its own gestural language, according to research published on Jan. 5 in Scientific Reports.

Chimpanzee social interactions include a significant portion of gestural communication. Chimpanzees utilize gestures to communicate with one another, ask for food, and settle disputes. Gestures may take many different forms: some require merely the hands, others require touching another individual, and yet others involve manipulating ordinary things like twigs, trees, and leaves that are present in chimpanzees’ natural surroundings.

For instance, leaf gestures might involve altering the leaves by tearing, ripping, or pulling them off the stem with a unique sound.  These leaf-modifying motions, which are observed in practically all of the chimpanzee populations surveyed from East to West Africa, exhibit a striking resemblance to one another. However, for the first time, researchers have demonstrated that each group still uses a distinct dialect or style of leaf-modifying gestures, and that these distinctions cannot be explained simply by variations in their genetic profile or forest habitat.

Gal Badihi, the lead author, said that the various gestures employed by the two communities have similar contexts and appear to represent the same meanings, much like human dialects.

In both human and non-human animal societies, dialects are frequently seen as a fundamentally cultural element. While it has been demonstrated that chimpanzees are excellent at acquiring social skills—such as how to construct the correct tool—from one another, researchers have rarely discovered any evidence that their social environment also affects their communication. This new research reveals that chimpanzees socially learn some parts of their gestural communication, just as other skilled animal communicators like songbirds, whales, and humans.

Dr. Cat Hobaiter, a senior author, said that these behaviors are fairly common, but it can be difficult to detect the details in the dense forest, so they had to try their hand at some chimpanzee “archaeology.” The researchers would follow along and examine the leaf remains after the chimpanzees had performed their gesturing. The researchers could determine who was using either technique by examining the patterns that each type of leaf tearing left behind.

The researchers said that chimpanzees use these leaf-modifying motions for a variety of reasons, but the most common purpose chimpanzees in Budongo use them is as a sort of gestural “pick-up line”—similar to chimpanzee flirting; however, they also need to know how to do it in the local way.

The researchers also added that females who traveled across groups seem to comprehend the dialect of the new community. This demonstrates that throughout their lifespan, even as adults, chimpanzees may adaptably learn to speak and comprehend foreign languages.


Badihi, G., Graham, K.E., Fallon, B. et al. Dialects in leaf-clipping and other leaf-modifying gestures between neighbouring communities of East African chimpanzees. Sci Rep 13, 147 (2023). https://doi.org/10.1038/s41598-022-25814-x


Scientists have found a protein that promotes the metastasis of skin cancer


The most dangerous form of skin cancer, known as melanoma, has been found to be driven by a protein discovered by researchers at Queen Mary University of London, King’s College London, and the Francis Crick Institute. This protein gives the cancer cells the ability to change the shape of their nucleus, which enhances their migration and spread throughout the body.

Skin cancer cells encounter physical barriers during their migration through tissues, and this study published today in Nature Cell Biology models the behavior of aggressive melanoma cells that can alter the shape of their nucleus to avoid these barriers. High quantities of a protein called LAP1 were detected in these aggressive melanoma cells, and the researchers found that this protein was associated with a poor prognosis for melanoma patients.

The skin cancer melanoma can metastasize to other parts of the body. Metastasis, or the spread of cancer, is the primary cause of mortality for those with the disease. Despite a large amount of research, our understanding of what actually triggers metastasis remains limited. The study’s results provide new insight into a process of melanoma progression and may result in the development of new methods of preventing the spread of the disease.

Queen Mary’s Barts Cancer Institute Professor Victoria Sanz-Moreno and King’s College London and Francis Crick Institute’s Dr. Jeremy Carlton co-directed the study.

Researchers in this study tested the ability of aggressive and less aggressive melanoma cells to navigate gaps in an artificial membrane smaller in diameter than the cancer cells’ nuclei. The more aggressive cells originated from a patient’s metastatic site, while the less aggressive cells originated from the patient’s primary melanoma tumor.

Metastasis occurs when cancer cells leave the initial tumor and spread to a new location to begin a new tumor. However, the cramped conditions inside a tumor prevent them from doing so.

The nucleus of a cell is a big, rigid structure that contains the cell’s genetic information but also hinders the cell’s ability to travel through the narrow gaps of the tumor’s surroundings. A more flexible nucleus is required if cancer cells are to squeeze through these openings.

After the migration studies, imaging revealed that the aggressive cells passed through the gaps with higher efficiency than the less aggressive cells because they had formed blebs at the edge of their nucleus. According to genetic tests of the melanoma cells, the LAP1 protein, which is located in the membrane that surrounds the nucleus, was found in greater abundance in the aggressive cells that generated the blebs.

Dr. Jeremy Carlton, whose team is interested in the dynamics of membrane-bound structures within cells revealed that the LAP1 protein loosens the tethering of nuclear envelope to its nucleus, allowing the nuclear envelope to bulge away and develop blebs that make the nucleus more fluid.  So, the cancer cells were able to pass through narrow openings that would have otherwise prevented their spread.

By inhibiting LAP1 protein production, the research team observed that aggressive cells were less able to generate nuclear envelope blebs and less able to squeeze through these gaps when re-challenged to move through pores in laboratory experiments.

The group also saw this LAP1 expression pattern in patient samples of melanoma. The LAP1 levels in melanoma metastatic tissue samples were significantly greater than those in primary tumor tissue samples. Patients with high levels of LAP1 in the cells surrounding the edge of the original tumor had more aggressive cancer and poorer outcomes, suggesting that the protein could be utilized to identify subpopulations of melanoma patients who may be at increased risk of aggressive cancer.

Professor Sanz-Moreno, whose team studies how cancerous tumors utilize environmental cues to multiply and metastasize, said that melanoma is the most aggressive and fatal type of skin cancer. Their laboratory and Dr. Carlton’s have collaborated to uncover new mechanistic insights into LAP1’s role in melanoma progression and to demonstrate that LAP1 is a crucial regulator of melanoma aggressiveness.

Interfering with this molecular mechanism could have a significant effect on cancer metastasis because LAP1 is expressed at high levels in metastatic cells. Since there are no currently available medications that target LAP1, the researchers hope to conduct further research into methods of targeting LAP1 and nuclear envelope blebbing to determine whether or not they can inhibit this progression pathway in melanoma.

The group is interested in learning whether LAP1-driven nuclear envelope blebbing occurs in other cells that contribute to and migrate through a tumor’s environment, such as immune cells, and whether this activity aids or inhibits cancer progression.

According to Dr. Iain Foulkes, Cancer Research UK’s Executive Director of Research and Innovation, studies such as this one are a perfect example of research that deepens the knowledge of what cancer does to the biology of our bodies.

This new knowledge of how the nucleus of a melanoma cell can become more fluid to migrate across the body is valuable for developing the knowledge of how cancer behaves and opens a new path of exploration into strategies to make it harder to spread.


Jung-Garcia, Y., Maiques, O., Monger, J. et al. LAP1 supports nuclear adaptability during constrained melanoma cell migration and invasion. Nat Cell Biol (2023). https://doi.org/10.1038/s41556-022-01042-3


Toxoplasma parasite has the potential to take control of our brain

By Jitinder P. Dubey – http://www.ars.usda.gov/is/graphics/photos/sep08/d1210-1.htm, Public Domain, https://commons.wikimedia.org/w/index.php?curid=25110571

Toxoplasma gondii is a protozoan that causes the illness toxoplasmosis. Numerous species of birds and mammals carry T. gondii, and human infections are frequent. T. gondii infection affects 22.5% of people aged 12 and older, according to the Centers for Disease Control and Prevention (CDC), however immunocompromised individuals usually show no symptoms. Domestic cats serve as the primary infection carriers since they are the only known definitive hosts for the sexual stages of T. gondii. The parasite’s oocysts are excreted by infected cats, and people often get these oocysts through coming into contact with cat waste, in litter boxes, or in garden beds where outside cats urinate.

The life cycle of T. gondii is complex and involves several hosts. When unsporulated oocysts are shed in the cat’s feces, the T. gondii life cycle starts. The environment requires these oocysts to sporulate for 1 to 5 days before they become infectious. Birds and rodents serve as intermediate hosts, becoming infected after consuming soil, water, or plant matter contaminated with the pathogenic oocysts. After being consumed, the oocysts change into tachyzoites that settle in the muscle and neural tissue of the bird or rodent and grow into tissue cysts. Cats who consume birds and rodents with tissue cysts may acquire the infection. Cats and other animals may potentially get the disease by consuming sporulated oocysts that are present in the environment. It’s interesting to note that Toxoplasma infection seems to have the power to alter the host’s behavior. Mice with toxoplasma infection no longer fear cat pheromones. Thus, they become easier prey for cats, promoting the parasite’s transfer to the cat ultimate host.

Human toxoplasma infections are relatively common; however, the majority of infected individuals show only mild or subclinical symptoms. According to some research, the parasite may be capable of influencing an infected person’s personality and psychomotor performance in a manner similar to how it alters behavior in other mammals. When symptoms do develop, they frequently resemble those of mononucleosis and are typically minor. Asymptomatic toxoplasmosis, nevertheless, can occasionally cause issues. Cysts can linger for years in a number of different human tissues. Immunocompromised individuals may experience the reactivation of these dormant infections following transplantation, cancer treatment, or the onset of an immunological illness like AIDS. Because the immune system is unable to stop T. gondii from growing in bodily tissues in AIDS patients with toxoplasmosis, these cysts can result in encephalitis, retinitis, pneumonitis, cognitive problems, and seizures that can ultimately be deadly.

Tachyzoites, which can spread to the developing fetus through the placenta, increase the risk of toxoplasmosis during pregnancy. The severity of the mother’s illness, the placenta’s damage, the fetus’ gestational age at the time of infection, and the organism’s virulence all affect how much toxoplasmosis harms the developing fetus. Congenital toxoplasmosis can cause central nervous system damage, which can show up as mental retardation, deafness, or blindness. It frequently results in fetal loss or premature delivery. The CDC advises pregnant women to take extra precautions when cooking meat, gardening, and taking care of pet cats. The most common method for diagnosing toxoplasmosis infection during pregnancy is serology, which includes TORCH testing. By employing molecular techniques like PCR to find T. gondii DNA in amniotic fluid, congenital infections can also be diagnosed.

Observing tissue cysts in tissue samples can help doctors diagnose toxoplasmosis in adults. Giemsa- or Wright-stained biopsy samples may show tissue cysts, and infection can also be verified using lumbar puncture, magnetic resonance imaging, and CT scans.

The strongest first-line protection against toxoplasmosis is prevention of infection. After handling raw meat, dirt, or cat litter, you should thoroughly wash your hands. You should also avoid eating any veggies that could have been contaminated with cat excrement. When cooking, the internal temperature of any beef should be 73.9–76.7 °C (165–170 °F).

For Toxoplasma infections, the majority of immunocompetent individuals do not need therapeutic intervention. Pyrimethamine and sulfadiazine can be used to treat immunocompromised individuals, newborns, and pregnant women, with the exception of the first trimester of pregnancy, when these medications have the potential to result in birth abnormalities. Because spiramycin does not cross the placenta, it has been used safely to prevent transmission in pregnant women with primary infection during the first trimester.



Researchers have developed a blood test that may identify the ‘toxic’ protein years before Alzheimer’s symptoms appear

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Most people diagnosed with Alzheimer’s today have already shown typical symptoms including memory loss. Once symptoms have progressed so far, the best treatment choices do nothing more than slow the disease’s progression.

However, studies have revealed that the seeds of Alzheimer’s are planted years, if not decades, before the onset of any cognitive deficits that would allow for a diagnosis. Amyloid beta proteins misfold and cluster into oligomers, which serve as the seeds. Scientists believe that Alzheimer’s disease is caused by the accumulation of “toxic” oligomers of amyloid beta over time.

Laboratory testing has been established to determine amyloid beta oligomer concentrations in human blood, and it was developed by a group of researchers at the University of Washington. Their test, called SOBA, was able to detect oligomers in the blood of patients with Alzheimer’s disease, but not in most participants of a control group who showed no evidence of cognitive deficits at the time the blood samples were taken, as reported in a paper published the week of Dec. 5 in the Proceedings of the National Academy of Sciences.

Conversely, 11 control subjects had oligomers in their blood that were detected by SOBA. Examined again years later, 10 of these people were diagnosed with mild cognitive impairment or brain pathology indicative of Alzheimer’s disease. Thus, for these 10 people, SOBA had discovered the harmful oligomers before the onset of symptoms.

Clinicians and scientists have long sought a reliable diagnostic test for Alzheimer’s disease, ideally an assay that may identify indications of the illness prior to the onset of cognitive impairment rather than merely confirming a diagnosis of Alzheimer’s. That’s critical for both individual well-being and the study of how amyloid beta oligomers become toxic and produce their harmful effects. UW Molecular Engineering & Sciences Institute faculty member and bioengineering professor Valerie Daggett is cited as the paper’s senior author. In this paper, the researchers demonstrate that SOBA has the potential to serve as the foundation for such an examination.

The acronym SOBA stands for soluble oligomer binding assay and is used to take advantage of a specific property of the hazardous oligomers. Misfolded amyloid beta proteins generate an alpha sheet shape when they start to cluster together in oligomers. Previous study by Daggett’s group demonstrated that alpha sheets had a tendency to bond to other alpha sheets. Alpha sheet are so seldom observed in nature. SOBA relies on a synthetic alpha sheet developed by her team to bind oligomers in cerebrospinal fluid or blood. The oligomers bound to the test surface are then confirmed to be amyloid beta proteins using industry-standard techniques.

The scientists put SOBA to the test on blood samples from 310 study participants who had donated blood and medical data for Alzheimer’s disease study. At the time of the blood draws, the patients were not showing any symptoms of dementia, Alzheimer’s disease, or moderate cognitive impairment.

Researchers using SOBA found oligomers in the blood of people with Alzheimer’s disease ranging from mild cognitive impairment to severe cases. Autopsy confirmed the diagnosis of Alzheimer’s disease in 53 of the study’s participants, and toxic oligomers were found in the blood samples of 52 of them, obtained years before their deaths.

Records demonstrate that participants in the control group who later acquired moderate cognitive impairment were similarly found to have oligomers by SOBA. Toxic oligomers were absent in the blood samples of the unaffected members of the control group.

Currently, Daggett’s group is collaborating with researchers at UW spinout company AltPep to transform SOBA into an oligomer diagnostic test. They also demonstrated the ease with which SOBA may be modified to identify hazardous oligomers of a different protein type linked to Parkinson’s disease and Lewy body dementia.

It has been shown that many human illnesses are linked to the buildup of harmful oligomers into alpha sheet formations, as Daggett put it. These include not just Alzheimer’s and Parkinson’s but also type 2 diabetes and others. Since SOBA is able to detect this distinct alpha sheet structure, the researchers are optimistic that this approach may prove useful in the diagnosis and investigation of a wide variety of disorders caused by “protein misfolding.”

Daggett thinks there’s a lot of room for growth in the test.

The researchers believe that SOBA might help in identifying persons at risk or incubating the illness, as well as act as a readout of therapy efficacy to aid in development of early therapies for Alzheimer’s disease.


Shea, D., Colasurdo, E., Smith, A., Paschall, C., Jayadev, S., Keene, C. D., Galasko, D., Ko, A., Li, G., Peskind, E., & Daggett, V. (2022). SOBA: Development and testing of a soluble oligomer binding assay for detection of amyloidogenic toxic oligomers. Proceedings of the National Academy of Sciences of the United States of America119 (50), e2213157119. https://doi.org/10.1073/pnas.2213157119

University of Washington. (2022, December 5). New blood test can detect ‘toxic’ protein years before Alzheimer’s symptoms emerge, study shows. ScienceDaily. Retrieved January 7, 2023 from www.sciencedaily.com/releases/2022/12/221205153722.htm

The ability of elephants to remain in their seasonal habitat despite environmental change

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Dr. Rhea Burton-Roberts, a biologist and lecturer at Bangor University, found that elephants had extremely stable seasonal migratory patterns over years. In Kruger National Park, Rhea found that elephant family groups prefer to stay in regions that they know well, but a scarcity of food during very dry seasons might lead them to move their foraging to less known habitats. Her research was published in Scientific Reports.

Rhea’s Ph.D. research on animal movement ecology used 8 years of elephant geographic data collected from 13 elephant family groups in the Kruger National Park, South Africa, as part of a collaborative project involving researchers from the University of KwaZulu-Natal (UKZN), the Indian Institute of Sciences, the Ashoka Trust, and South African National Parks.

Rhea said that the data they got from the GPS collars on the elephants tracked their location every 30 minutes, providing a fascinating look into their migratory behavior throughout various seasons as food supply and environmental circumstances varied.

Elephants, according to Rhea’s research, have a strong preference for certain habitats and regions within the National Park’s total size of 20,000 sq. kms. Elephants have a seasonal diet, with a preference for grass during the wetter months and for woody vegetation during the drier months. The amount of precipitation, especially during the dry season, drove the most change in their seasonal migratory behavior.

The researchers said that if rainfall was more than normal heading into the dry season, the elephants chose to remain faithful to their home area, preserve their energy, and make the most of the prolonged quality and amount of vegetation.

Once the rain stopped during the transition from the wet to dry season, elephants began exploring new areas of their home range in search of food. It appears that Kruger’s elephant population is adapting its seasonal movement pattern to environmental circumstances so that it can satisfy its high energy and nutritional needs. An adult female requires a diet of around 150 kg per day.

Professor Rob Slotow (UKZN), a key collaborator and data source, said that as a result of global warming, rainfall patterns and temperatures in Africa’s savannas are becoming more unstable. Understanding how elephants cope with these changes is important for saving the species, especially as droughts become more often and food becomes scarce.

Changing migration patterns, however, may pose problems in locations where habitat is already fragmented, and human interference is high.

Elephants are an intriguing study subject because, despite their massive size and broad feeding preferences, they consistently use the same essential habitats, as noted by coauthor Graeme Shannon.


Rhea Burton-Roberts et. al. (2022). Seasonal range fidelity of a megaherbivore in response to environmental change, Scientific ReportsDOI: 10.1038/s41598-022-25334-8


The transformation of a tentacle into a foot

By Flatters & Co. (photograph) – Original source: Marvels of the universe. A popular work on the marvels of the heavens, the earth, plant life, animal life, the mighty deep, with an introd. by Lord Avebury and with contributions by leading specialists, etc., published in 2 vols in London 1911-1912. Page 264 [1]., Public Domain, https://commons.wikimedia.org/w/index.php?curid=8263409

Differentiated cells are the building blocks of all multicellular organisms, including humans, animals, and plants. Thus, the cells that make up the skin are not the same as the cells that line the digestive tract, nor do they serve the same purpose. However, how these cells are able to maintain their unique characteristics remains uncertain.

One of the important regulators, the transcription factor Zic4, was identified by a team from the University of Geneva (UNIGE) and the Friedrich Miescher Institute for Biomedical Research (FMI) in Basel while studying the freshwater polyp known as Hydra. Researchers discovered that when Zic4 expression was suppressed, tentacle cells in a Hydra transformed into foot cells, giving the animal functioning feet on its head. The findings are published in Science Advances.

Stem cells, found in all multicellular organisms, divide and give rise to specialized cells as an organism grows and develops. To become specialized, cells undergo a process known as differentiation. Because of this, the cells that make up the skin’s surface will differ in morphology and physiology from the cells that make up the digestive tract or the nervous system. Seldom, certain differentiated cells can undergo a change in shape and function, and hence their identity, later in their lifetime. Transdifferentiation is the term for this phenomenon.

While the processes responsible for differentiation are widely understood, how a specialized cell is able to keep its identity and not undergo dedifferentiation or transdifferentiation are still a mystery. Species with the ability to repair or replace damaged parts of their bodies, or even complete regeneration, are excellent case studies. Some cells in such creatures undergo a temporary identity crisis or transformation before regenerating and taking on a new function. The freshwater hydra, a little invertebrate around 1.5 cm in length, fits this description well since it can regenerate any severed component throughout its lifetime.

This animal model has been used by scientists at the University of Geneva (UNIGE) and the Friedrich Miescher Institute for Biomedical Research (FMI) in Basel to identify the transcription factor Zic4, a protein found in the nuclei of hydra cells that regulates the expression of a series of target genes.

First author, senior research, and teaching assistant in the Department of Genetics and Evolution at the Faculty of Science and the Institute of Genetics and Genomics (iGE3) at UNIGE, Matthias Christian Vogg, explains that the work shows more specifically that Zic4 plays a vital role in the production and maintenance of the cells that make up the tentacles.

Scientists showed that epithelial cells on the tentacles’ outer layer may be converted into foot epithelial cells by lowering Zic4 expression by 50%. The hydra’s foot, also known as its basal disk, is its lowest body part. Its cells are highly specialized, producing mucus that helps it adhere to its surroundings. A few days after Zic4 was suppressed, the tentacle cells began to transdifferentiate, resulting in the development of feet instead of tentacles, the study’s supervisor, Brigitte Galliot, an emeritus professor in the Department of Genetics and Evolution in the Faculty of Science and at the iGE3 of the UNIGE, explains.

The research team also learned that transdifferentiated cells enter the cell cycle again before dividing. Because of this, they are no longer in their original identities. Charisios Tsiairis, a junior group leader at the FMI and co-last author of the paper, notes that these cells restart the process of DNA synthesis, and hence of chromosomal duplication, which is at work during cell proliferation but falls short of mitotic division.

Zic4 gene suppression was achieved by “electroporating” chemicals that silence the gene into the animal’s epidermis. Then, the researchers double labeled the cells to find a marker for tentacle cells as well as a marker for foot cells, demonstrating that these cells are transdifferentiating through a stage in which they are both tentacle and foot cells. The transdifferentiating process may be recognized by this transitional state, Chrystelle Perruchoud, a research assistant at the iGE3 of the UNIGE and in the Department of Genetics and Evolution in the Faculty of Science, says.

These findings offer new insights into the phenomenon of transdifferentiation. It’s possible that these discoveries will lead to the development of novel medicines for regenerating certain cell types in individuals that have been damaged. Many issues are still unclear at this time. In other species, does Zic4 serve the same purpose? Suppose it is possible to further suppress its expression, would it pave the way for the creation of new cell types? Furthermore, it is likely that there are additional key regulators of transdifferentiation that have not yet been identified according to the researchers.


Matthias Christian Vogg et al. (2022). The transcription factor Zic4 promotes tentacle formation and prevents epithelial transdifferentiation in Hydra, Science Advances. DOI: 10.1126/sciadv.abo0694


The process by which humans began to lose their body hair

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Humans don’t have it, but other mammals like orangutans, mice, and horses do. For a long time, it has been mysterious to scientists why humans have such a small amount of body hair compared to other mammals. However, the story of how humans and other mammals lost their locks is just beginning to be revealed thanks to a groundbreaking analysis of genetic codes from 62 animals.

University of Utah Health and University of Pittsburgh researchers write in the journal eLife that humans seem to have the genes for a full coat of body hair, but such evolution has blocked them. These findings identify a group of genes and regulatory areas of the genome that are required for hair growth.

Important questions concerning the mechanisms that produce this basic human feature are addressed by the findings. According to the researchers, this could pave the path for novel treatments in balding, chemotherapy-induced hair loss, and other hair loss problems.

This research further demonstrates that this similar method has been used by nature at least nine times before in mammalian species from vastly diverse evolutionary lineages. When they lost their hair and fur, the ancestors of modern rhinos, naked mole rats, dolphins, and other hairless mammals all followed a similar evolutionary route.

Human geneticist at U of U Health Nathan Clark, Ph.D., who conducted much of the research at the University of Pittsburgh with Amanda Kowalczyk, Ph.D., and Maria Chikina, Ph.D., says that they have adopted the unique approach of harnessing biological diversity to learn about human DNA. With this information, they can zero in on certain parts of human genome that play a role in health.

Hairiness takes many forms across the animal kingdom, from the harsh hair of a monkey to the silky fur of a cat. It’s the same with being bald. Although humans have that distinctive crown on the heads, body hair is so fine that we considered “hairless.” Some of these other mammals include the hairless elephant, the hairless pig, and the mustachioed walrus.

A receding hairline can be advantageous in some situations. Elephants benefit from reduced body heat retention in hot areas while walruses benefit from less drag in the water when they don’t have thick coats of hair. Kowalczyk’s research of this and other hairless mammals discovered that they share mutations in many of the same genes, despite the different reasons. Among these are genes for keratin and other components of the hair shaft that are necessary for hair growth.

The research also demonstrated the significance of regulatory areas of the genome. Although they don’t directly code for hair-producing structures, these areas do have an impact on hair production. The timing and location of gene activation, as well as the quantity produced, are controlled by these factors.

In addition, the analysis located genes for which the function in hair growth was unknown. When considered in combination with other evidence, such as skin-based indicators of activity, these results suggest a new collection of genes that may play a role in hair development.

In regard to genetics, the researchers don’t know much about a good number of genes. They hypothesize it play a part in hair development and maintenance.

Clark, Kowalczyk, and Chikina sought to uncover the mystery of mammalian hair loss by looking for genes in hairless animals that had developed at quicker rates than their equivalents in hairy animals.

Clark believes that as animals experience evolutionary pressure to reduce hairiness, the role of the genes responsible for hair loss decreases in significance. This is because they increase the rate of natural selection-permitted genetic alterations. Hair thinning could be caused by alterations in one’s genes.

The researchers used computer approaches that allowed for the simultaneous comparison of hundreds of genomic areas to conduct the search. They examined 19,149 genes and 343,598 regulatory regions that were conserved among various mammalian species. They did this by actively discounting genomic areas that contribute to the evolution of other species-specific features, such as the ability to thrive in aquatic environments.

Clark explains that the success of the strategy was shown by the fact that known hair genes were found through the unbiased screen. In addition, it shows that the less well-defined genes found in the screen may be just as crucial for hair development (or lack thereof).

To define genomic areas implicated in cancer prevention, lifespan extension, and the knowledge of other health issues, Clark and colleagues are currently employing the same approach.

Clark explains that this strategy is useful because it allows researchers to identify the universal genetic pathways that underlie a wide variety of traits.


Kowalczyk, A., Chikina, M., & Clark, N. (2022). Complementary evolution of coding and noncoding sequence underlies mammalian hairlessness. eLife11, e76911. https://doi.org/10.7554/eLife.76911


As a result of coral bleaching, reef fish needs to relearn the rules of interaction

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New research shows that mass coral bleaching events are making it tougher for some reef fish species to distinguish between rivals.

After widespread loss of coral due to bleaching, scientists studying reefs in five parts of the Indo-Pacific discovered that butterflyfish individuals’ capacity to detect competing species and respond appropriately was compromised. As a result of this change, the butterflyfishes are less likely to make good choices and more likely to get into fights that aren’t necessary.

Researchers think these changes may affect species’ chances of survival as the effects of climate change continue to worsen.

Proceedings of the Royal Society B released the study’s findings in an article titled “Rapid resource depletion on coral reefs disrupts competitor recognition processes among butterfly species.”

According to the study’s senior author, Dr. Sally Keith of Lancaster University’s Department of Marine Biology, by detecting a competitor, individual fish can make judgments about whether to advance, or retreat from a conflict thereby saving energy and avoiding harm.

These ground rules of engagement developed on a certain field, but that field is shifting. Butterflyfish rely on corals for food, yet repeated disturbances like bleaching occurrences change both the quantity and variety of corals. When it comes to making adjustments to their behavior, it’s unclear if these fishes have the capacity to keep up with their rule book.

More than 3,700 observations of 38 different species of butterflyfish were made on reefs before and after coral bleaching events and compared their behaviors.

Less signaling occurred between fish of different species after the bleaching event, and more than 90% of fish interactions escalated into chases (up from 72% before the event). After bleaching, fish chased off potential rivals for longer distances, using more energy than they would have otherwise.

Researchers believe environmental disruptions are impacting fish recognition and responses because bleaching events, which kill many corals, are causing fish species to alter and diversify their diets and territories. Therefore, these widespread alterations to the environment are upsetting the delicate balance that has allowed many different kinds of fish to coexist.

The researchers can start to anticipate how ecological communities can evolve in the future by examining at how behavior responds to real-world changes in the environment and seeing that those changes are the same regardless of location.  These seemingly minor mistake in deciding how to use energy could prove fatal.


Rapid resource depletion on coral reefs disrupts competitor recognition processes among butterflyfish species, Proceedings of the Royal Society B: Biological Sciences (2023). DOI: 10.1098/rspb.2022.2158


What is decompression sickness?

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When the internal pressure of the body drops too low, a condition known as decompression sickness (DCS) can set in. DCS occurs when gases that were previously dissolved in the blood or other body tissues become undissolved. Divers who come up to the surface of the water too quickly are susceptible to this illness, as are pilots flying at high altitudes in planes without pressurized cabins. The term “the bends” is commonly used by divers to describe the joint pain that is a sign of decompression sickness.

Decompression sickness is always caused by a drop in barometric pressure. Because pressure is generated by the weight of the column of air above the body pressing down on the body, barometric pressure is significantly lower at high altitude compared to the surface of the Earth. Extremely high pressures exerted on divers at depth are also caused by the weight of a water column bearing down on the body. The fast drop in pressure that divers experience when they rise up from the high pressure of deep water to the now low pressure of sea level is what causes decompression sickness (DCS), which occurs at normal barometric pressure (at sea level). A dive in a deep alpine lake, where the atmospheric pressure at the lake’s surface is lower than that at sea level, is more likely to result in decompression sickness (DCS) than a dive in water at sea level.

When DCS occurs, the blood’s dissolved gases, primarily nitrogen, rapidly escape their dissolved state, causing bubbles to develop in the blood and other tissues. This happens because a lower gas pressure above the liquid reduces the amount of gas that may remain dissolved in the liquid. The proper distribution of gases in the blood is maintained by the pressure exerted by the atmosphere. Less gas is left dissolved when the pressure is lowered. When you open a can of soda, you observe this phenomenon firsthand. When the bottle’s seal is broken, the gas pressure exerted over the liquid is reduced. Because of this, bubbles form as the gas (carbon dioxide) escapes from solution in the liquid.

Joint discomfort is the most common symptom of DCS, followed by headache and visual abnormalities (10-15 percent of cases). Extreme DCS can be fatal if left untreated. Pure oxygen is used as an emergency treatment. Afterwards, the patient is taken to a hyperbaric chamber. A hyperbaric chamber is an enclosed space that is pressured to a level higher than that of the atmosphere. Repressurizing the body with this treatment is effective for DCS because it allows for a more progressive pressure reduction. Increased blood oxygen levels result from the hyperbaric chamber’s method of administering oxygen at high pressure. The result is that some of the nitrogen in the blood gets swapped out for oxygen, which is more manageable in its gaseous form.



Learning the rules of tissue-specific immunity could pave the way to a more promising future

Image by Masum Ali from Pixabay

New discoveries in immunology have been driven by the recent push to increase vaccine efficacy, revealing several innovative approaches with unrealized medicinal possibilities. Tissue-resident memory T cells (TRM cells) are the subject of a rapidly expanding field of study because of the long-term immunity they give against infections that target certain organs and tissues.

Researchers from the University of California San Diego School of Medicine released a new study on TRM cell biology in the gut on December 28, 2022 in Immunity. Their findings have the potential to lead to a new generation of precision treatments against infection, cancer, and autoimmune disease.

Memory T cells are left behind by the immune system after an infection. These cells keep a molecular memory of the pathogen and are activated to its reappearance. Some memory T cells are intended to travel throughout the body via the bloodstream, protecting the entire organism from infection, while others are located in different organs and are programmed to combat only the pathogens that threaten that particular organ. TRM cells have the potential to offer lifelong protection at the target tissue, but their overactivation can contribute to autoimmune disorders.

According to senior author and UC San Diego School of Medicine professor John T. Chang, MD, TRM cells are the initial defenders, right at the front lines of infection.  Most of the vaccinations aim to establish systemic immunity, but higher protection may be achieved by targeting the tissue-specific cells that come into contact with the pathogen directly.

Improving TRM cell function in the intestines may be the most effective way to treat pathogenic gut microbes, whereas improving TRM cell function in the nose and lungs may be the most effective way to combat a respiratory virus. Thus, the aim is to create therapies that can either increase TRM cell development and maintenance or, in the case of autoimmune illness, eliminate immune cells by altering the same pathways.

However, there is still much that has to be learned about what aids TRM cell formation and survival, and it’s possible that the criteria are very different for different types of tissues.

The researchers conducted a series of studies on mice to describe TRM cells from four distinct regions of the gastrointestinal tract: the small intestine, the colon, the ileum, and the jejunum.

In addition to substantial transcriptional, epigenetic, and functional heterogeneity, the analysis demonstrate that TRM cells in each tissue type expressed cytokines and granzymes in unique patterns. That is to say, identical immune cells from various regions of the gut appeared to have significantly different molecular compositions, functions, and reliance on chemical stimuli.

Further supporting this notion is the observation that Eomesodermin (Eomes), a transcriptional factor known to influence TRM cell growth, is required at varying levels by each cell group. Previous findings from the skin, liver, and kidney suggested that Eomes inhibited TRM cells, but the current trials showed the opposite to be true in the small intestine. There, Eomes had an unexpected function in TRM cell viability. But, the colon was an exception, demonstrating that context matters even inside the digestive tract.

Defining the principles for TRM cell development and maintenance in other tissues and revealing what drives their specialization will continue to be a focus of future research. The authors propose, for instance, that TRM cells have unique requirements because of the differences in the microbiome of the small intestine and the colon; hence, microbiome manipulation may be an additional strategy for regulating gut immune cells.

The researchers want to be thinking about vaccinations and other therapies that are tailored to the individual demands of each organ. The best immune responses against disease can be provided by understanding the requirements of each tissue type for the development and maintenance of TRM cells.


Lin, Y. H., Duong, H. G., Limary, A. E., Kim, E. S., Hsu, P., Patel, S. A., Wong, W. H., Indralingam, C. S., Liu, Y. C., Yao, P., Chiang, N. R., Vandenburgh, S. A., Anderson, T. R., Olvera, J. G., Ferry, A., Takehara, K. K., Jin, W., Tsai, M. S., Yeo, G. W., Goldrath, A. W., … Chang, J. T. (2022). Small intestine and colon tissue-resident memory CD8+ T cells exhibit molecular heterogeneity and differential dependence on Eomes. Immunity, S1074-7613(22)00643-4. Advance online publication. https://doi.org/10.1016/j.immuni.2022.12.007