Dolphins performing acrobatic tricks have, time and again, fascinated and mesmerized people. As early as 1860s, capturers took dolphins and other cetaceans (e.g. whales and porpoises) out of their aquatic habitats and held them in captivity in various parts of Europe and North America. At first, they kept them in a dolphinarium mainly as an amusement for a paying audience. Later on, they discovered that these aquatic marvels could be taught to perform tricks. Since then, people have gravitated to various dolphin shows as one of their “must-dos” off their bucket list.
Dolphins learning tricks
The tricks that dolphins can do seem limitless. Apart from their fantastic leaps and bounds, they can do complex tricks like tail-walking, playing ball, synchronized swimming, and rhythmic gymnastics. How do they learn these tricks? Trainers use positive reinforcement method to teach dolphins the jaw-dropping tricks. Accordingly, they reward them with food whenever they do a trick correctly. Watching them do these tricks, though, seems that they perform not only for the food reward but also for their own enjoyment based on their playful nature.
Wild dolphins’ ballistic jumps
Frequently, wild dolphins leap above the water surface. They do so by swimming fast near the surface, and then execute a ballistic jump. This behavior, called porpoising, seems a demonstration of their playful behavior. Nevertheless, another hypothetical reason surfaced. Accordingly, this porpoising behavior points to the benefit it furnishes. The friction up in the air is less; therefore, porpoising would help save dolphin energy.1
Seeing dolphins doing leaps and bounds in the wild is something that is truly remarkable yet not unusual. However, a pod of playful aquatic creatures in the wild were observed doing a trick rarely seen in the wild. Furthermore, the trick was something that they learned from a formerly captive dolphin.
Wild dolphins’ tail-walking trick
Recently, a study2 reported what they observed in wild dolphins. They saw a pod (particularly, a group consisting of nine dolphins) off the Australian coast that learned from a previously captive dolphin how to “walk” on water using their tail.
Tail walking is one of the fundamental tricks taught to captive dolphins. It involves rising vertically out of the water. Then, the dolphin moves forward or backward on top of the water. This skill is rarely seen in wild dolphins.2
Whale and Dolphin Conservation, together with the universities of St Andrews and Exeter, conducted a thirty-year study where they revealed that dolphins in the wild were able to learn a human-coached tail-walking trick from Billie. Billie is a rescued dolphin from a creek near Adelaide’s Patawalonga River in 1988. The dolphin was in captivity temporarily. During its captivity, it learned how to tail-walk. When it was released into the wild, it taught its companions by continuing to demonstrate the skill. Soon after, its peers copied it. In 2011, nine dolphins began tail walking. However, this spectacular display of “walking” by fins turned out to be just a fad. The number of wild dolphins that tail walk declined over time. As of 2014, only two of them remained to demonstrate the skill. 2
Dolphins, just as all the other living beings, deserve an inhabitable space in order to thrive and keep surviving. The ability of the dolphins to imitate skills could be used in spreading learnt behaviours that could be beneficial to their survival. The lengthy study that tracked the tail-walking behavior of Billie and the local dolphin community for years revealed an important insight. Accordingly, dolphins learning a behavior from each other can persist from one generation to the next. However, there is a tendency that certain learnt behaviors will fade, and, inopportunely, vanish through time.
— written by Maria Victoria Gonzaga
1 Weihs, D. (2002). “Dynamics of Dolphin Porpoising Revisited”. Integrative and Comparative Biology. 42 (5): 1071–1078. doi:10.1093/icb/42.5.1071
2 Whale and Dolphin Conservation. (2018 Aug. 29). WILD DOLPHINS LEARN FROM EACH OTHER TO ‘WALK ON WATER’…BUT IT’S JUST A FAD. Retrieved from https://uk.whales.org/news/2018/08/wild-dolphins-learn-from-each-other-to-walk-on-waterbut-its-just-fad
3 Whale and Dolphin Conservation (WDC). (2014 Nov. 5). Dolphins tailwalking – Port River, Adelaide | Whale and Dolphin Conservation. Retrieved from https://www.youtube.com/watch?v=6tn5TJfR3k4
One of the hallmarks of old age is vascular aging. Researchers found that a biomolecule, β-Hydroxybutyrate (BHB), can serve as a key to turning the time around. Apparently, BHB has anti-aging effects on the vascular system.
β-Hydroxybutyrate – a biomolecule
β-Hydroxybutyrate is a biomolecule with a chemical formula, C4H803. Many regard it as a ketone; however, under a strict definition, it would not technically fit as a ketone. That is because its carbonyl carbon binds to only one instead of two other carbon atoms. Nonetheless, BHB appears to be physiologically related to other ketone bodies (such as acetate and acetoacetate) based on the metabolic aspect. For instance, the tissue level of BHB rises during calorie restrictions, fasting, prolonged intense workout, and when following a ketogenic diet.1 Accordingly, BHB level occurs the highest among the three circulating ketones in the body.
β-Hydroxybutyrate – biological sources
The body naturally produces BHB through the process of ketogenesis. Low-carb diet and fasting lead to the rise of BHB level. Firstly, the body breaks down fatty acids to produce acetyl CoA. This precursor goes through a series of reactions leading to acetoacetate synthesis. In turn, the acetoacetate circulates via the bloodstream, and subsequently reaches the liver. The BHB-dehydrogenase enzyme in the liver reduces the acetoacetate to BHB. 1
Another biochemical pathway that leads to the synthesis of this biomolecule uses butyrate. The body metabolizes butyrate and produce D-β-hydroxybutyrate through the aid of the enzyme, hydroxybutyrate-dimer hydrolase.
β-Hydroxybutyrate – biological action
In humans, D-β-hydroxybutyric acid is one of the major endogenous agonist of hydroxycarboxylic acid receptor 2 (HCA2), a receptor protein encoded by the HCAR2 gene. It binds to and activates HCA2. Upon activation, HCA2 can inhibit the breakdown of fats and mediates niacin-induced flushing. Moreover, it induces the dilation of blood vessels.
Based on recent research, BHB might serve as a biomolecule that could help turn time around for the vascular system. Old age faces an increased risk to cancer and cardiovascular diseases since the vasculature ages as well. Dr. Ming-Hui Zou, director at Georgia State University, explains. “When people become older, the vessels that supply different organs are the most sensitive and more subject to aging damage….”2
β-Hydroxybutyrate – vascular study
Zou et al. 2, 3 conducted a study on vascular aging, exploring the link between calorie restrictions and delayed vascular aging. Accordingly, calorie restrictions averted vascular aging.
They found that BHB, the biomolecule naturally produced from the liver, has anti-aging effects, particularly on endothelial cells. The endothelial cells line the interior surface of the vascular system. Based on the results, BHB promoted mitosis of endothelial cells, thus, pre-empting vascular aging.3 Furthermore, they saw that BHB binds to a certain protein, which stimulates a series of reactions that consequently rejuvenate, thus, keep the blood vessels young.2
BHB could eventually become a biomolecular tool that promotes mitosis of endothelial cells. In being able to do so, it could help prevent endothelial cell senescence. Hence, this potential rejuvenating effect on the vascular system may soon become valuable not just in keeping the blood vessels young but also in preventing cardiovascular diseases related to old age.
— written by Maria Victoria Gonzaga
1 Martins, N. (2018 Sept. 26). Beta-hydroxybutyrate or BHB –All You Need to Know. Retrieved from https://hvmn.com/blog/exogenous-ketones/beta-hydroxybutyrate-or-bhb-all-you-need-to-know
2 Georgia State University. (2018 Sept. 10). Researchers Identify Molecule With Anti-Aging Effects On Vascular System. Retrieved from https://www.technologynetworks.com/neuroscience/news/fasting-molecule-delays-vascular-aging-309380
3 Han, Y. M., Bedarida, T., Ding, Y., Somba, B. K., Lu, Q., Wang, Q., Song, P., & Zou, M.H. (2018). β-Hydroxybutyrate Prevents Vascular Senescence through hnRNP A1-Mediated Upregulation of Oct4. Molecular Cell, 71(6):1064-1078.e5. https://doi.org/10.1016/j.molcel.2018.07.036
We often hear that stress can be unsettling as it could make us ill when it becomes chronic and overwhelming. However, is there really a biological ratification behind it? Is it scientifically founded? Apparently, independent studies hinted a biological connection indicating how stress can cause biological damage, and eventually lead to certain ailments. And, the mitochondrial DNA — the genome in the mitochondrion appears to play a role.
Biological features of mitochondria
The mitochondrion (plural: mitochondria) is an organelle that supplies molecular energy for various biological activities. In essence, this rod-shaped structure found within the cell accounts for the generation of ATP, the cell’s major energy source. Thus, the mitochondrion is known to be the “powerhouse of the cell“.
Through the process of cellular respiration, glucose (a monosaccharide) is “churned” to extract energy, primarily, in the form of ATP. Firstly, a series of reactions leads to the conversion of glucose to pyruvate. Then, it uses pyruvate, converting it into acetyl coenzyme A for oxidation via enzyme-driven cyclic reaction called Krebs cycle. Finally, a cascade of reactions (redox reactions) involving the electron transport chain leads to the production of ATPs (via chemiosmosis).
The mitochondria have their own genetic material, called mitochondrial DNA. Because of this, the mitochondrion is regarded as semi-autonomous and self-reproducing organelle. It means it can manufacture its own RNAs and proteins. Generally, we inherit the mitochondrial genome maternally, as opposed to the nuclear genome that we inherit from both parents.
Mitochondrial fate during stress
When confronted with a stressful situation, our body responds intrinsically. We tend to breathe fast. The heartbeat goes wild. Our muscles tense up. And, we sweat profusely. All these responses (so-called “fight-or-flight“) can be an arduous task as they abruptly demand energy. When triggered for so long, eventually, we feel exhausted. Sooner or later, stress sets in and it takes its toll on our health.
The mitochondria work for an extended time just to meet up the spike of demand for energy. In effect, they become vulnerable to damage from too much work. Inopportunely, the mitochondria have limited repair mechanisms unlike the nucleus.1 And in the end, it results in the disruption of the organelle, thereby, releasing the mitochondrial DNA into the cytoplasm. Eventually, the genetic material reaches the bloodstream where they become genetic cast-offs.
Mitochondrial DNA cast-offs
The ejected mitochondrial DNA, apparently, becomes genetic wastes and stress might have something to do with this outcome. This theory came about based on a series of studies. Firstly, Gong et al. found that chronic mild stress resulted in mitochondrial damage in hippocampus, hypothalamus, and cortex in mouse brains.2
Secondly, another team of researchers (Lindqvist et al.) reported that individuals who had recent suicide attempt had higher plasma level of freely circulating mitochondrial DNA in blood than those of healthy individuals.3
Thirdly, Martin Picard (a psychobiologist at Columbia University), together with his team, observed similar findings in their participants exposed to a stressful situation. Accordingly, their participants – healthy men and women – were asked to defend themselves against a false accusation. Their blood samples were taken before and after the interview. The researchers found that the mitochondrial DNA in the serum of the participants increased twice 30 minutes after the test. 1 Picard explained that the mitochondrial DNA might have acted like a hormone. Furthermore, he theorized that the ejection of these genetic cast-offs might have mimicked the adrenal gland cells releasing cortisol in response to stress. 1
Mitochondrial DNA as an inflammatory factor
Zhang et al. observed that circulating mitochondrial DNA triggered inflammatory responses. Accordingly, the genetic cast-offs can bind to TLR9 (a receptor) on the immune cell. This binding might have incited the immune cell to respond the same way as they do when reacting with antigens. It might have stimulated the cell to release cytokines that call for other immune cells to the site. 1
So far, these conjectures from independent studies disclose the possible direct biological damage due to stress. There could be a biological insinuation that stress could play a part in the manifestation of ill-health conditions. And, the upsurge of circulating mitochondrial DNA cast-offs is one of them. More information and studies on mitochondrial DNA are delineated on a report on mental health published in Scientific American.
— written by Maria Victoria Gonzaga
1 Sheikh, K. (2018 Sept 13). Brain’s Dumped DNA May Lead to Stress, Depression. Scientific American. Retrieved from https://www.scientificamerican.com/article/brain-rsquo-s-dumped-dna-may-lead-to-stress-depression/
2 Gong, Y. Chai, Y., Ding, J. H., Sun, X. L., & Hu, G. (2011).Chronic mild stress damages mitochondrial ultrastructure and function in mouse brain. Neuroscience Letters, 488 (1): 76-80. https://doi.org/10.1016/j.neulet.2010.11.006
3 Lindqvist, D., Fernström, J., Grudet, C., Ljunggren, L., Träskman-Bendz, L., Ohlsson, L., & Westrin, Å. (2016). Increased plasma levels of circulating cell-free mitochondrial DNA in suicide attempters: associations with HPA-axis hyperactivity. Translational Psychiatry, 6 (12), e971–. http://doi.org/10.1038/tp.2016.236
When herbivore, such as an insect, nibbles a plant leaf, the plant sets off an “SOS” or distress signal as one of the various plant defense strategies. This was based on what a team of researchers headed by Masatsugu Toyota observed. Accordingly, the injured leaf makes the distant undamaged leaves aware that it is being eaten.
Masatsugu Toyota worked with Simon Gilroy, Professor of Botany in the University of Wisconsin-Madison.1 Now, Toyota is at Saitama University in Japan and collaborated with a team of researchers from the Japan Science and Technology Agency, Michigan State University and the University of Missouri. Their research findings can be accessed online via the journal Science. 2
Rapid signaling in plant defense mechanism
Previously, Toyota et al. knew that when a plant gets wounded, it releases signaling molecules that fired an electrical charge, and then spread across the plant. However, they did not know what was behind the system.3 Now, the research team deduced that the signal may have been calcium since it carries a charge, and capable of producing such signal. 1
The research team worked on a mutant Arabidopsis. They designed a mutant model plant that would synthesize protein that fluoresces, but only around calcium. In so doing, they can track calcium in real time.
Plant defense involving glutamate
In spite of the fact that the plants lack the nerves and a nervous system of an animal, the plants have a fairly similar systemic signaling system as part of plant defense mechanisms.
In animals, glutamate acts as one of the major and fast excitatory neurotransmitters of the central nervous system. Toyota et al. elucidated that, in plants, glutamate is also present. The injured leaf releases glutamate and this molecule is taken up by glutamate-receptor-like ion channels. Consequently, these ion channels led to a spike in calcium ion concentration. These calcium ions, then, spread out to other plant parts via the phloem vasculature and the plasmodesmata. 2
This video from UW-Madison Campus Connection shows the wave of calcium after supplying glutamate to the tip of a leaf. The plant fluoresces to indicate how the calcium spreads out across the plant.
In just a couple of minutes, the region receiving the distress signal responds by releasing chemicals. The release of defense-related hormones, for instance, turns the plant unpalatable to the herbivore. In another case, the plant emits volatile chemicals to call for insect allies, such as parasitic wasps. This is an indirect type of a plant defense strategy. The wasps recognize the distress signal that an herbivore feeds on the plant. They, then, go towards the plant to hunt for and lay eggs on the herbivore caterpillar host, thus, killing the latter eventually.4
Plants do not have the capacity to move around at will and in the same way that animals do. And certainly, they cannot run away from herbivores as a prey would to escape a predator. Nevertheless, the plants possess features that strategically protect them against their “predator” despite being firmly rooted in the field. One such plant defense mechanism entails chemicals. In particular, glutamate that acts similarly as neurotransmitter in animals. This demonstrates how a plant can likewise be complex, dynamic, and efficacious with regard to dealing with its “predators”.
— written by Maria Victoria Gonzaga
1 Hamilton, E. (2018 Sept. 13). Blazes of light reveal how plants signal danger long distances. University of Wisconsin-Madison News. Retrieved from https://news.wisc.edu/blazes-of-light-reveal-how-plants-signal-danger-long-distances/
2 Toyota, M., Spencer, D., Sawai-Toyota, D., Jiaqi, W., Zhang, T., Koo, A. J., Howe, G.A., &Gilroy, S. (2018). Glutamate triggers long-distance, calcium-based plant defense signaling. Science, 361 (6407): 1112. DOI: 10.1126/science.aat7744
3 Starr, M. (2018 Sept. 14). An Amazing Reaction Happens When a Plant Gets Hurt, Making Them More Similar to Animals. ScienceAlert.com. Retrieved from https://www.sciencealert.com/plant-damage-response-defence-calcium-ions-glutamate-fluorescent
4 Phillips, K. (2014 Sept. 22). Mown grass smell sends SOS for help in resisting insect attacks, researchers say. Retrieved from https://today.agrilife.org/2014/09/22/mown-grass-smell-sends-sos-for-help-in-resisting-insect-attacks-researchers-say/
Our brain tends to forget things that we wish we would always remember. And yet, it cannot forget certain things we wish never occurred and existed. How does your brain forget? And, can your brain forget on purpose? By nature, the human brain forgets. Inopportunely, the biological mechanism underlying this brain process is poorly understood. Only few studies shed light on this aspect. In May 2012, scientists attempted to explain the molecular biology of active elimination of memories on their report. In September 2018, another team of researchers identified the parts of the brain associated with forgetting. Based on brain frequencies, they analyzed how the human brain voluntarily forgets.
Molecular biology of forgetting
In 2012, an independent research team from the Scripps Research Department of Neuroscience attempted to understand the molecular biology of active forgetting.1 To do so, they used fruit flies (Drosophila) as key model since this species is often used for studying memory. Accordingly, they found that a small subset of dopamine neurons regulated the acquisition as well as the forgetting of memories. In other words, they saw that the neurons that acquired memory on one hand also eliminated the memory on the other hand. Notably, they identified the two dopamine receptors involved, i.e. dDA1 and DAMB.
In this case, dopamine, a neurotransmitter, seemingly performs dual, yet opposing, roles. At first, the dopamine activates the dDA1 receptor of a neuron. In effect, the neuron begins forming memories. However, the same neuron sends out signal via another dopamine receptor, DAMB. As dopamine binds to the DAMB receptor, it activates the receptor. As a result, it triggers events that lead to the forgetting of the recently acquired memory (provided that the memory has not been consolidated yet). A process, called consolidation, protects important memories from being forgotten. In essence, while memory actively forms, a dopamine-based forgetting mechanism works as well. Unless the brain reckoned the memory as important, it erases the forming memory.
Forgetting on purpose
In September 2018, researchers from Ruhr-Universität Bochum and the University Hospital of Gießen and Marburg collaborated with researchers from Bonn, the Netherlands, and the UK.2 In brief, they identified the parts of the brain involved in the process of voluntary forgetting. In particular, these brain areas include the prefrontal cortex and the hippocampus, the brain region associated with memories.
In this recent study, the researchers found that the prefrontal cortex regulates the activity in the hippocampus. One of the leaders of the team, Carina Oehrn, explicated that the prefrontal cortex suppressed hippocampus activity. Further, she noted that the frequency changed. Accordingly, the difference in frequency caused the currently processed information to cease from being encoded. They referred to this frequency as the forgetting frequency.2
Forgetting – crucial to health
As much as recalling is important, forgetting certain things is pivotal to mental and emotional well being. We inherently forget on purpose. Imagine remembering all – both good and bad. Not only we would have to deal with information overload but we would also be long exposed to feelings associated with those memories.
Post-traumatic stress disorder, regarded as a mental disorder, develops when a person has gone through a traumatic event. People with this condition face higher risks of inflicting self-harm, or worse, committing suicide.3 Hyperthymesia, a condition wherein an individual can extraordinarily recall much of one’s life in vivid and perfect detail, can be off-putting and distressing to the affected individual. Based on one such case, the patient recounted how the ability to remember constant, uncontrollable chain of memories could be exhausting and a burden.4
The metaphorical inability to forget hinders a person to move on and focus on the tasks at hand. Traumatic events seem to be ingrained deeply in mind and soul. For instance, loss of a loved one, warfare, and sexual assaults prove to be difficult to ignore. Thus, we need more insights on the neuro- and molecular biology of forgetting. More studies could help shape up future therapeutic intervention. It may not necessarily lead to the absolute incapacity to recall. But, hopefully, it can help set aside spiteful memories. In that way, affected individuals could be freed from the traps of the past, and help them live life with a sanguine hope for a future.
— written by Maria Victoria Gonzaga
1 Sauter, E. (2012, May 14). “Team Identifies Neurotransmitters that Lead to Forgetting”. The Scripps Research Institute. Retrieved from https://www.scripps.edu/newsandviews/e_20120514/davis.html
2 Ruhr-University Bochum. (2018, September 7). This is how the brain forgets on purpose: Two brain regions apparently play a pivotal role in forgetting. ScienceDaily. Retrieved from www.sciencedaily.com/releases/2018/09/180907110501.htm
3 Bisson, JI; Cosgrove, S; Lewis, C; Robert, NP (2015, November 26). “Post-traumatic stress disorder”. BMJ (Clinical research ed.). 351: h6161. doi:10.1136/bmj.h6161. PMC 4663500
4 Parker ES, Cahill L, McGaugh JL (2006, February). “A case of unusual autobiographical remembering”. Neurocase. 12 (1): 35–49. doi:10.1080/13554790500473680.
Dubbed as “rosehip neuron“, a new brain neuron recently discovered is unique based on its morphology and the set of genes it activates. Neuroscientists recently uncovered this new type of neuron from postmortem human brain samples. They presumed that this rosehip neuron occurs in the brain of humans but not in rodents.
Rosehip neurons found in human brains
What makes human brain special? What sets it apart from other animal brains? Humans have this sort of consciousness and intelligence that make them different from other species. Apart from the complexity and the size of the human brain, its cellular components seem to be different from that of the other animals. Neuroscientists found rosehip neurons in human brain. These cells have not yet been observed in the brains of mice and other well-studied laboratory animals. Researchers reported this recent discovery in Nature Neuroscience.1 Nevertheless, they were fast to warn not to make haste assumptions. The rosehip neurons may not be unique to humans. More studies are on the way to confirm it.
What their findings implicate is the suitability of rodent brains as experimental models. Rodent brains lack such neurons. Thus, they may not be fit as laboratory models, especially when one tries to understand human neurologic diseases and how the brain works.
Current info on human rosehip neurons
Since rosehip neurons are a recent discovery, there is currently little information about them. What the neuroscientists know is they appear bushy. In fact, their bushy appearance accounts for their name “rosehip“. Rosehip originally refers to the accessory fruit of the rose plant. The rosehip neuron looks like the accessory fruit of the rose after petals are shed.
Researchers discovered the rosehip neurons from the top layer of the cortex of the brain from the postmortem brains of two men in their 50s. The rosehip neuron belongs to a group of inhibitory neurons. This means that it works by inhibiting other neuronal activity in the brain.
Researchers from the Allen Institute collaborated with the J. Craig Venter Institute. They found that the rosehip neurons seemed to have a different genetic signature. The rosehip neurons turned on a unique set of genes. They also formed synapses with pyramidal neurons. Pyramidal neurons are a different type of brain cells named after their shape.
Future research on rosehip neurons
Researchers have yet to fully recognize the purpose and importance of rosehip neurons in the human brain. In doing so, they may gain a significant insight regarding their role in neurologic function and diseases. They also aim to check the presence of rosehip neurons in other human brain parts as well as in the brains of other animals. Details on their recent work on rosehip neurons is published in Nature Neuroscience.2
— written by Maria Victoria Gonzaga based on the news release and materials from the Allen Institute website
1 Allen Institute. (27 Aug. 2018). Scientists identify a new kind of human brain cell. Retrieved from http://www.alleninstitute.org/what-we-do/brain-science/news-press/articles/scientists-identify-new-kind-human-brain-cell
2 Boldog, E. et al. (2018). Transcriptomic and morphophysiological evidence for a specialized human cortical GABAergic cell type. Nature Neuroscience. DOI: 10.1038/s41593-018-0205-2
One of the crucial needs that arise during or after a devastating natural disaster is the availability of the “universal” blood type O. The increased demand for blood surges following the aftermath of a catastrophy. Storms, hurricanes, and earthquake calamities are major causes for an abrupt call for blood donations. Researchers from the University of British Columbia headed by Stephen Withers knew so well the gravity of this need that they are adamant in finding a way to somehow curb the limitations hampering the availability of a universal, friendlier blood type. Withers and his team recently identified a potential enzyme candidate that appears to be efficient and at the same time cost-effective in converting blood types into type O.
Blood group systems overview
The blood is the circulating fluid in our body that performs multifarious functions. Its major functions are for transporting nutrients, delivering oxygen, moves metabolic byproducts for excretion, providing immune defense, and homeostasis. It is comprised mainly of plasma (55%) and cellular elements (45%) (e.g. red blood cells and white blood cells). The red blood cells (RBCs) are the major cellular component of the blood and are essential for their role in delivering oxygen throughout the body. The white blood cells (WBCs), in turn, are involved in the detection of non-self particles (antigens) and the subsequent immune action against them.
Blood type (or blood group) is a classification system used to identify which type the blood belongs to. The blood type is determined based on the presence (or absence) and types of antigens present on the cell surface of the RBCs. Various blood classification systems are used to classify types; however, the ABO and the Rh systems are the most important ones. The ABO system is used to classify blood into types A, B, AB, and O. The Rh system, in turn, is used to denote blood as either positive (+) or negative (-) based on the presence and absence of the Rh factor, respectively.
Why type O blood?
Type O blood is considered as the universal blood because it has neither A nor B antigens on the surface of the RBCs. Type AB blood, in contrast, has both A and B antigens. If A antigens are present on the cell surface of the RBCs, the blood is typified as type A whereas type B has B antigens. Determining blood type is important because blood administered into the body that does not match with the innate blood type can trigger an immune response. Transfusion involving a blood type different from one’s own can instigate the WBCs of the body to attack the transfused blood cells, and this could lead to serious effects. Thus, an individual with type A (Rh-), for instance, can receive transfusions of type A (Rh-) and type O (Rh-). Based on this precept, type O (especially Rh-) can be administered to any blood type.
Metagenomics for creating a universal type of blood
Blood banks constantly need type O. Withers and his team focused their research works in searching for enzymes that can convert types A and B to type O by applying metagenomics. Accordingly, they found enzymes from the human gut that apparently can turn type A and B into O as much as thirty times more efficiently than previously identified enzymes.1 Withers said, “We have been particularly interested in enzymes that allow us to remove the A or B antigens from red blood cells. If you can remove those antigens, which are just simple sugars, then you can convert A or B to O blood.”
In reaching their goal, they focused on mucins, which are glycoproteins secreted by the mucous membranes in the gut wall. These mucins in the gut wall display a number of sugars, including antigen A and antigen B. They found that the gut microbiome can cleave these sugars from the gut wall and use them as food source. Using metagenomics, they identify genes from these gut microbial species that code for proteins that cleave target antigens on the cell surfaces of RBCs. Thus, type A blood, for instance, can be converted into type O blood through the enzymes that remove antigen A from the RBCs. The goal is to identify the most economical, most efficient, and safest enzyme that can be used to turn donated blood into a particular type as needed.
Disastrous events take so much of human properties and lives. Apart from the apparent destruction of homes and livestock as an aftermath of natural calamities, blood donations become crucial to save lives of the people needing blood transfusions. Suddenly, life takes a stance on the edge between survival and death. Blood transfusions have to be extensive, safe, and economical. Although research on how to turn blood types into a more universal type has still a long way to go before it can be approved for medical use, this is a significant development.
— written by Maria Victoria Gonzaga
1 American Chemical Society. (2018, August 21). Gut bacteria provide key to making universal blood (video). American Chemical Society.. Retrieved from https://www.acs.org/content/acs/en/pressroom/newsreleases/2018/august/gut-bacteria-provide-key-to-making-universal-blood-video.html?_ga=2.17288057.1746138702.1535160738-1328130083.153516073
Scientists are excited over a gene-silencing drug that recently won an approval from the US Food and Drug Administration (FDA). This approval is historic because it is the first of its kind. The drug works by silencing genes that otherwise lead to the production of damaged proteins associated with certain diseases. The drug is called patisiran and it recently got its approval for use to treat the hereditary transthyretin amyloidosis, a fatal rare hereditary condition associated with damaged nerves.
Gene basis of hereditary transthyretin amyloidosis
The hereditary transthyretin amyloidosis is a rare and fatal hereditary condition that manifests as an autosomal dominant neurodegenerative disease. Because it is dominant, this means that the offspring inheriting the defective autosomal gene will acquire the condition. A defective transthyretin (TTR) gene located on human chromosome 18q12.11 is the genetic cause. The most common type of mutation is the replacement of valine by methionine at position 30.
A normal, functional TTR gene codes for transthyretin (TTR) protein that is involved in the transportation of thyroxine (thyroid hormone) and retinol (vitamin A). TTR protein is produced mainly in the liver, and is then secreted into the bloodstream. TTR proteins from a defective TTR gene tend to misfold and stick together, forming amyloids. This building-up of amyloids in tissues is called amyloidosis. In hereditary transthyretin amyloidosis, pathogenic amyloids form especially in the peripheral nervous system, which may eventually lead to a progressive sensory and motor polyneuropathy.
Gene silencing by RNA interference
Normally, the cell performs what is now known as RNA interference (RNAi). It is also known as quelling, co-suppression, and post-transcriptional gene silencing. In this process, the RNA molecules inhibit the translation of a gene. They do so when they neutralize targeted mRNA molecules. RNAi is different from CRISPR, which is a gene-editing tool that makes use of a guide RNA. CRISPR is used to switch off a gene and has a potential therapeutic use to treat cancers. It also had FDA approval in 2016 for use in a clinical trial study. However, recent studies on CRISPR raised issues about its safety since it was found to cause unexpected mutations that involve large deletions and complex genomic rearrangement at target sites.2 To learn more about CRISPR, read: CRISPR caused gene damage? … Unlike CRISPR, the RNAi is presumed not to bring permanent changes to DNA.3
Patisiran as gene-silencing drug
Patisiran is RNA-based drug that recently received the first FDA approval for use as a gene-silencing tool. People with hereditary transthyretin-mediated amyloidosis can now be treated with it. The drug interferes with the production of transthyretin. It doses so by preventing the mRNA involved in the translation of the gene that codes for the problematic protein. This is good news to people with such fatal rare condition. FDA has now approved a drug that can be administered to them. The downside, though, is the chillingly high cost. The cost of the therapy is estimated to be about $450,000 in a year.4
New therapeutic technologies that delve into the molecular and gene mechanisms hold so much promise especially in conditions that until now lack an efficacious treatment. RNAi is a precise gene-silencing tool and scientists are excited in its historic FDA approval. This means that it is a glorious start for contemporary therapies involving targeted gene silencing and alterations. The cost of the therapy may be encumbering but it is still a step forward, certainly a scientific feat to reckon.
— written by Maria Victoria Gonzaga
1 TRANSTHYRETIN; TTR. (n.d.). OMIM.org. Retrieved from https://omim.org/entry/176300
2 Gonzaga, M. V. (17 July 2018). CRISPR caused gene damage? Rise and pitfall of the gene-editor. Biology-Online.org. Retrieved from https://www.biology-online.org/crispr-caused-gene-damage-rise-pitfall-gene-editor/
3 Nield, D. (14 Aug. 2018). A First of Its Kind Gene-Silencing Drug Just Got Historic Approval From The FDA. ScienceAlert. Retrieved from https://www.sciencealert.com/first-drug-silencing-genes-approved-by-fda-for-disease-treatment
4 Lipschultz, B. & Cortez, M. (10 Aug. 2018). Rare-Disease Treatment From Alnylam to Cost $450,000 a Year. Bloomberg. Retrieved from https://www.bloomberg.com/news/articles/2018-08-10/alnylam-wins-first-u-s-drug-approval-in-rare-genetic-disease
How do cells know when to separate during mitosis? A molecule called BubR1 was found to regulate the timing of the division of a parent cell into two progeny cells. Researchers who identified the role of BubR1 were optimistic that their discovery could lead to a potential cancer treatment by inducing cancer cells to undergo premature mitosis.
Phases of mitosis
When a cell enters the Synthesis phase (S phase) of the cell cycle, it is likely that it will subsequently go through the sequential phases of mitosis in which a single cell ultimately gives rise to two cells, each with its own copy of chromosomes. Firstly, the cell enters prophase, which is the phase of mitosis largely characterized by the condensation of chromatin (becoming distinct chromosomes), the beginning of spindle fiber formation, and the disintegration of the nucleolus, nuclear membrane, and organelles. This is then followed by a phase, called metaphase, wherein the chromosomes align along the metaphase plate and the microtubules attach to the kinetochores. Then, the chromosomes are pulled apart toward the opposite poles of the cell during anaphase. In the last phase of mitosis called telophase, the chromosomes have completely moved to the opposite poles of the cell resulting in two sets of nuclei. The cytoplasm divides ultimately giving rise to two new cells.
Delaying strategy of BubR1 during mitosis
Researchers from Institute of Cancer Research reported in their paper published in Molecular Cell the role of BubR1 in mitosis. Accordingly, the spindle assembly checkpoint (SAC) prevents the separation of sister chromatids until all chromosomes are properly attached to the spindle. It also catalyzes the formation of the Mitotic Checkpoint Complex (MCC).1 The BubR1 is part of this molecular complex that regulates the Anaphase Promoting Complex/Cyclosome (APC/C). In particular, the BubR1 is part of the molecular machinery that delays the onset of anaphase during mitosis. The delay is crucial as it ensures the chromosomes to be properly positioned before they will be segregated.2
The researchers further reported that the N-terminal half of BubR1 contains two ABBA motifs. When they mutated these BubR1motifs, the cells become unable to normally delay mitosis. Moreover, the two resulting cells following mitosis had unevenly divided chromosomes. They explained that without the normal ABBA sequences of BubR1, the MCC failed to bind to the APC/C. Consequently, mitosis progressed despite the chromosomes not yet being properly positioned.
Premature mitosis for cancer cells
The researchers made note of the importance of the ABBA sequence of BubR1. It served as a “safety catch” – preventing the machinery from progressing prematurely. Accordingly, cancer cells rely on this safety catch much more than normal cells as they usually have extra chromosomes to be put into place, and thereby need more time for mitosis.2 This could therefore be used to design cancer treatment, such as a drug that could switch off the “safety catch” of BubR1, and forcing cancer cells to divide prematurely with an unevenly divided chromosomes following mitosis.
— written by Maria Victoria Gonzaga
1 Fiore, B.D., Wurzenberger, C., Davey, N.E., & Pines, J. (2018).Molecular Cell. https://doi.org/10.1016/j.molcel.2016.11.006
2 Institute of Cancer Research. (2016, December 8). Scientists reveal ‘safety catch’ within all dividing cells: Major discovery could lead to new cancer treatments. ScienceDaily. Retrieved August 7, 2018 from www.sciencedaily.com/releases/2016/12/161208143306.htm
Scientists from Cardiff University’s School of Biosciences reported that a father’s gene may have an impact on the quality of care that is furnished by the mother to her newborn offspring. One of the most crucial roles of a mother is being able to provide and attend to the needs of her offspring, especially during the time of conception up to the time of nursing the offspring. Good quality maternal care is essential to ensure a healthy development of the newborn and the recent study on mice suggests that a father’s gene may have an effect on the mother’s nurturing behavior towards her offspring before and after they are born.
Imprinting of genes
In humans, the zygote is a diploid cell that results from the union of two haploid sex cells. This means that the zygote will possess two copies of the genome, i.e. one coming from the mother and the other one from the father. The autosomal genes of the zygote would therefore occur in pairs or as two copies. Their expressions occur simultaneously except for a few genes whose expressions will depend on the parent-of-origin. Depending on the parent source, one of the gene copies will be imprinted, which means it will be ”silent”. For example, a father’s gene that is imprinted will be “silent” and will not be expressed but the other copy of the gene (from the mother) will be expressed, or “vice versa“. This phenomenon is called genomic imprinting. An imprinted gene is one in which the DNA is methylated. A methylated gene means that its expression is suppressed.1
Phlda2 gene – overview
Pleckstrin homology-like domain family A member 2 (Phlda2) gene is an example of a gene whose expression accords to the phenomenon of genomic imprinting. The gene is located in the cluster of imprinted genes on chromosome 11p15.5.2 It encodes for the Phlda2 protein. It was also found that only one copy of the Phlda2 gene is “switched on” and that the other copy of the gene that is “silent” comes from the father.3 In rodents, one of its physiological roles is identified to be associated with the regulation of the activity of the placental cells called spongiotrophoblasts, which are cells responsible for the production of placental hormones. It was reported that the Phlda2 gene controls their size, and therefore their hormone production activity. 3
Phlda2 gene – impact on mother’s behavior
Scientists from Cardiff University’s School of Biosciences found that female mice carrying pup embryos with two active Phlda2 genes, and thus with relatively higher Phlda2 levels and probably reduced placental hormone activity, exhibited decreased nursing and grooming of pups but with an increased focus in nest building. On the contrary, mothers carrying pup embryos with lower Phlda2 levels were more focused at nurturing their pups than on nest building. They also identified corresponding changes in the brain regions essential for maternal care behavior (particularly, hippocampus and hypothalamus) of the mothers during pregnancy. Their findings implicate that the Phlda2 gene activity may have an effect on the maternal care behavior of mice.3
Based on the recent findings, scientists speculate that Phlda2 gene activity may also have an impact in human pregnancies. Many regard motherhood as an epitome of a woman’s existence. Apparently, there are instances when the quality of maternal care provided to the child is inadequate due to various factors. If these findings are relevant to humans, then, this is a potential aspect to probe in order to understand the biology of maternal care behavior – one that involves Phlda2 gene.
— written by Maria Victoria Gonzaga
1 Genomic imprinting. (n.d.). Biology-Online Dictionary. Retrieved from https://www.biology-online.org/dictionary/Genomic_imprinting
2 PHLDA2 pleckstrin homology like domain family A member 2 [Homo sapiens (human)]. (8 July 2018). National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved from https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=7262
3 Creeth, H.D.J., McNamara, G.I., Tunster, S.J., Boque-Sastre, R., Allen, B., Sumption, L., et al. (2018). Maternal care boosted by paternal imprinting in mammals. PLoS Biol, DOI: 10.1371/journal.pbio.2006599