Category Archives: Genetics

The Role of Genetics and Maternal Factors in Retinopathy of Prematurity: A Comparative Study – Medriva

Retinopathy of Prematurity (ROP) is a significant cause of childhood blindness globally and its incidence is on the rise. Understanding the underpinnings of this disease can help us identify potential interventions for ROP. A recent study conducted in Argentina evaluated genetic variants associated with the risk of ROP in premature newborns and compared them with data from other populations. This article will delve into the findings of this study and explore the role of maternal risk factors and genetics in the development of ROP.

The sample for this study included 437 premature infants, of which 75 had ROP and 362 did not. The study aimed to identify maternal risk factors for ROP and analyzed perinatal outcomes. The genetic analysis of these infants involved 14 single nucleotide polymorphisms (SNPs) using a family-based association study approach. The study did not apply the Bonferroni correction test due to its exploratory nature. The researchers also analyzed comorbidities in ROP newborns by creating a network graph to represent associations between events.

Genetic factors play a crucial role in the risk of developing ROP. One of the genes that has been associated with ROP is the methylenetetrahydrofolate reductase (MTHFR) gene. This gene has several isoforms and plays a role in various pathways and interactions. Understanding the variants of this gene can help identify infants at risk of developing ROP.

Along with genetic factors, maternal factors also contribute significantly to the risk of ROP. Identifying these risk factors can help in early intervention and prevention of ROP. The study identified several maternal risk factors including preterm birth, low birth weight, and prenatal complications among others. Understanding these factors can help in developing strategies to reduce the risk of ROP.

Recent research has highlighted the potential of adenosine A2A receptors (A2AR) as a target for early intervention of ROP. A2AR plays a pivotal role in ROP and pharmacological targeting of A2AR signaling may provide an early intervention strategy with distinct therapeutic benefits and mechanisms than the anti-VEGF therapy. Further research is necessary to validate the potential of A2AR in ROP intervention.

This study emphasizes the importance of genetic and maternal factors in the development of ROP. Understanding these factors and their interplay can pave the way for early interventions and better management of ROP. In addition, the potential of A2AR in ROP intervention needs to be further explored. As we continue to expand our knowledge about ROP, we can hope to reduce the incidence of this disease and improve outcomes for premature infants.

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The Role of Genetics and Maternal Factors in Retinopathy of Prematurity: A Comparative Study - Medriva

‘The Idea That Who You Are Is Only Genetics Is the Essence of Evil’ – Books – Haaretz

News Life and Culture Columnists and Opinion Haaretz Hebrew and TheMarker Partnerships

Haaretz.com, the online English edition of Haaretz Newspaper in Israel, gives you breaking news, analyses and opinions about Israel, the Middle East and the Jewish World. Haaretz Daily Newspaper Ltd. All Rights Reserved

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'The Idea That Who You Are Is Only Genetics Is the Essence of Evil' - Books - Haaretz

IPK researchers provide genetic explanations for shade-induced biomass allocation in wheat – EurekAlert

image:

The IPK research team asked how biomass allocation to wheat organs changes under canopy shade and what is the genetic basis for such changes.

Credit: IPK Leibniz Institute

Recent studies have shown a strong correlation between responses to plant density and to low light, indicating that the scarcity of light is often a limiting factor in high-density crop communities. Practices such as tillage, fertilizing the soil, and regulating the water supply can reduce competition for water and nutrients, but they amplify competition for light. These observations suggest that studying the genetic basis of plant responses to changes in the intensity and spectrum of light due to competition from neighbouring plants will advance our understanding of adaptation to the crop environment, says Dr. Guy Golan, first author of the study.

Therefore, the research team applied a new approach that combines principles from plant ecology and quantitative genetics for dissecting light-dependent and size-dependent allocation and identifying genes that regulate allocation to the leaves, stem, spikes, and grains when plants are shaded by neighbours.

One stimulating example comes from the known 'Green Revolution' gene Reduced Height-B1, which has two gene forms. On the one hand, the wild version leads plants to put a lot of their resources into growing tall stems. When these plants sense they are in the shade, they grow even taller to compete for more sunlight. On the other hand, plants with the 'Green Revolution' mutation allocate more resources to the spike, especially in shady conditions, making them more adaptable to low light.

However, allocation to the spike is also size dependent. When the conditions are conducive for growth, the short, semi-dwarf plants allocate significantly more resources to the spike than the tall varieties. Under low resources, when the plants are small, this advantage significantly decreases. This finding helps us understand the results from previous studies which showed that these shorter plants don't always do better than taller ones during droughts when the plants are small, says Dr. Guy Golan.

Our approach provides a basis for exploring the genetic determinants underlying investment strategies in the face of different resource constraints, and will be useful in predicting social behaviours of individuals in a crop community, says Prof. Dr. Thorsten Schnurbusch, head of IPKs research group Plant Architecture.

Agroecological genetics of biomass allocation in wheat uncovers genotype interactions with canopy shade and plant size

8-Feb-2024

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IPK researchers provide genetic explanations for shade-induced biomass allocation in wheat - EurekAlert

River Valley Beef Cattle Conference to explore state of hay availability, cattle genetics and more – Stuttgart Daily Leader

OZARK, Ark. Researchers and extension agents with the University of Arkansas System Division of Agriculture will be bringing the latest in cattle production knowledge to interested attendees at the Feb. 20 River Valley Beef Cattle Conference in Ozark.

With cattle markets soaring throughout 2023 and regional drought conditions affecting the availability and quality of hay and other forages, attendees can expect the conference to address topics key to success in 2024.

I think producers are mostly worried about hay and forage shortages, said Bob Harper, staff chair for the Logan County Cooperative Extension Service. They are also worried about high fertilizer and input costs in the coming year. I think most of them would like to try and up inputs this spring and summer in order to try and get back ahead of their hay situation, but they are concerned that high fertilizer prices may prevent that from happening.

In-person registration for the conference will begin at 8:30 a.m. and the conference will. conclude at 12:15 p.m. with lunch. The cost is $20, payable at the door.

Presenters will include Jesse Taylor, staff chair for the Johnson County Cooperative Extension Service; Kevin Van Pelt, extension agriculture agent for the Conway County Cooperative Extension Service; Maggie Justice, extension beef cattle specialist for the University of Arkansas System Division of Agriculture; Jeremy Powell, professor of animal science for the Division of Agriculture; and Ryan Loy, extension agricultural economist for the Division of Agriculture.

Taylor and Van Pelt will discuss the 2023 hay verification report, which will include the latest findings in verification trials. Justice will discuss understanding expected progeny differences, or EPDs, and genetic tests for cattle breeding. Loy will discuss the input price outlook for 2024.

The conference agenda includes:

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River Valley Beef Cattle Conference to explore state of hay availability, cattle genetics and more - Stuttgart Daily Leader

Harnessing human evolution to advance precision medicine – EurekAlert

image:

People who visit the Andes Mountain Range in South America can feel the physical effects of lower oxygen levels at higher altitudes. However, some people who live there have evolved over hundreds of generations to tolerate these low-oxygen conditions.

Credit: Elysia Cook McDermott

Humans are still evolving, and Tatum Simonson, PhD, founder and co-director of the Center for Physiological Genomics of Low Oxygen at University of California School of Medicine, plans to use evolution to improve healthcare for all.

Her latest research, which was published February 9, 2024 in Science Advances, reveals that a gene variant in some Andean people is associated with reduced red blood cell count at high altitude, enabling them to safely live high in the mountains in low-oxygen conditions. Simonsons UC San Diego lab is applying those findings toward understanding whether there may be a genetic component to why some people with sleep apnea or pulmonary diseases such as chronic obstructive pulmonary disease (COPD) fare better than others.

Explained Simonson, There are people with COPD who breathe a lot and maintain a higher oxygen saturation. Others with the same disease don't breathe as much, and their oxygen saturation is low. Researchers suspect there may be genetic differences underlying this variation, similar to the variation we find in pathways important for oxygen sensing and responses underlying natural selection at high altitude.

Our cells need oxygen to survive. When there isnt enough in the environment, our bodies produce extra red blood cells, which transport oxygen throughout the body. Too many red blood cells, however, create a dangerous condition called excessive erythrocytosis (EE), which makes the blood viscous, which could lead to stroke or heart failure.

Her previous research showed that many mountain-dwelling Tibetans exposed to low-oxygen situations are born with innate mechanisms that protect them from poor outcomes at high altitude, including the overproduction of red blood cells. Part of this is due to changes in the regulation of the EPAS1 gene, which lowers hemoglobin concentrations by regulating the pathway that responds to changing oxygen levels. Advances in genetics have shown that modern Tibetans received this genetic advantage from their ancestors who mixed with archaic humans living in Asia tens of thousands of years agoa unique evolutionary history confined to this population.

For her latest research, Dr. Simonson, who is also the John B. West Endowed Chair in Respiratory Physiology and associate professor in the Division of Pulmonary, Critical Care, Sleep Medicine & Physiology at UC San Diego School of Medicine, zoomed in on the EPAS1 region of the genome. She and her team focused on a mutation in the gene that is present in some people living in the Andes but is absent in all other human populations. When they scanned whole Andean genomes, they found a pattern surrounding this variant suggesting that the genetic change, which alters only a single amino acid in the protein product, happened by chance, relatively recently (from 9,000 to 13,000 years ago), and spread very quickly through hundreds of generations within the Andean population.

Similar to Tibetans, the EPAS1 gene is associated with lower red blood cell count in Andeans who possess it. However, the researchers were surprised to find that the variant works in a completely different way from the Tibetan version of the gene; rather than regulating its levels, the Andean variant changes the genetic makeup of the protein, altering the DNA in every single cell.

Tibetans have, in general, an average lower hemoglobin concentration, and their physiology deals with low oxygen in a way that doesnt increase their red blood cells to excessively high levels. Now we have the first signs of evidence that Andeans are also going down that path, involving the same gene, but with a protein-coding change. Evolution has worked in these two populations, on the same gene, but in different ways, said Simonson.

This study exemplifies a current approach in research that connects genetic targets of natural selection with complex disease genesunderstanding, for example, how natural genetic variation contributes to adaptive and maladaptive responses to low oxygen, as this study reveals.

In Simonsons lab, that means figuring out what downstream target genes are being turned on in response to low oxygen, among other things. Said Simonson, This paper shows one gene associated with one particular phenotype, but we think there are many different genes and components of oxygen transport involved. Its just one piece of that puzzle, and could provide researchers with information relevant to other populations.

Simonson and her team are working with Latino populations in San Diego and El Centro, California, as well as Tijuana and Ensenada, Mexico, taking them to high altitudes and recording their breathing while awake and asleep. Theyre cross-referencing their findings with publicly available databases to determine whether the findings theyve made in Andeans are also found in local Latinos who may share some genetic variants with the Andeans.

In precision medicine, its important to recognize variation in genetic backgrounds, specifically in historically understudied populations, Simonson said. If we can find some shared genetic factors in populations in an extreme environment, that may help us understand aspects of health and disease in that group and groups more locally. In that way, this study aims to push research forward, and towards comprehensive personalized medicine approaches in clinics here in San Diego.

Co-authors of the study include: Elijah S. Lawrence, Wanjun Gu, James J. Yu, Erica C. Heinrich, Katie A. OBrien, Carlos A. Vasquez, Quinn T. Cowan , Patrick T. Bruck , Kysha Mercader, Mona Alotaibi, Tao Long, James E. Hall, Esteban A. Moya, Marco A. Bauk, Jennifer J. Reeves, Mitchell C. Kong, Rany M. Salem, Keolu P. Fox, Atul Malhotra, Frank L. Powel, Mohit Jain and Alexis C. Komor at UC San Diego, Ryan J. Bohlender, Hao Hu and Chad D. Huff at University of Texas MD Anderson Cancer Center, Cecilia Anza-Ramirez, Gustavo Vizcardo-Galindo , Jose-Luis Macarlupu , Rmulo Figueroa-Mujca, Daniela Bermudez, Noemi Corante and Francisco C. Villafuerte at Universidad Peruana Cayetano Heredia, Eduardo Gaio at Universidad de Braslia, Veikko Salomaa and Aki S. Havulinna at Finnish Institute for Health and Welfare and Andrew J. Murray at Cambridge University and Gianpiero L. Cavalleri at Royal College of Surgeons in Ireland.

This study was funded, in part, by the National Institutes of Health (Grants R01HL145470 [TSS] and T32HL134632 [JEH]), Geographic Society Explorer Award, and John B West Endowment in Respiratory Physiology (TSS), Wellcome Trust Award 107544/Z/15/Z (FCV), Marie Skodowska-Curie grant agreement No 890768 (KAO), National Academies of Sciences, Engineering, and Medicine Ford Foundation Fellowship (CAV), National Science Foundation Grant No DGE-2038238 (PTB), Research Corporation for Science Advancement through Cottrell Scholar Award 27502 (ACK), Science Foundation Ireland 12/IP/1727 (GLC), Finnish Foundation for Cardiovascular Research and Juho Vainio Foundation (VS), and Academy of Finland (ASH).

# # #

Alexis Komor is a member of the SAB of Pairwise Plants, is an equity holder for Pairwise Plants and Beam Therapeutics, and receives royalties from Pairwise Plants, Beam Therapeutics, and Editas Medicine via patents licensed from Harvard University. Mohit Jain and Tao Long are affiliated with Sapient Bioanalytics, LLC.

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Harnessing human evolution to advance precision medicine - EurekAlert

Twins are a mirror to each other and a window into the mysteries of genetics – WAMU 88.5

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Twins are a mirror to each other and a window into the mysteries of genetics - WAMU 88.5

Unveiling the Disparity in Cardiovascular Health: Biological Factors, Dyslipidemia, and Genetics – Medriva

Unveiling the Disparity in Cardiovascular Health

Recent studies have highlighted an alarming health disparity: South Asians are at a significantly higher risk of developing heart disease than their white counterparts. This gap in health outcomes extends beyond geographical borders, affecting South Asians globally. But what contributes to this disparity? A series of recent studies aim to unpack the complex interplay of genetic, biological, and lifestyle factors at play.

Research suggests that unique biological factors may predispose South Asians to heart disease. For instance, South Asians reportedly have a decreased ability to repair blood vessels and lower levels of certain stem cells crucial for regenerating blood vessels. Impaired kidney function, another common issue in this population, further exacerbates the risk. In addition, South Asians have a fourfold higher risk of developing Atherosclerotic Cardiovascular Disease (ASCVD) compared to the general population.

Interestingly, despite having lower levels of low-density lipoprotein cholesterol (LDL C), Indians develop ASCVD about a decade earlier than Western populations. In response to this, the Lipid Association of India (LAI) has updated their cardiovascular risk assessment and lipid management guidelines. These updated recommendations aim to better manage dyslipidemia in Indian patients, with the ultimate goal of curtailing the epidemic of ASCVD among Indians globally.

High total cholesterol, LDL cholesterol, and Non-HDL cholesterol are significant risk factors for coronary artery disease (CAD) in South Asians. Studies reveal alarming trends in increasing population levels of these lipids, particularly in northern and western Indian cities. Emigrant Indians in the UK and USA also reportedly have higher triglycerides compared to Caucasians, underscoring the need for more nationwide surveys and prospective studies to assess the risk of CAD incidence.

Advancements in technology have allowed researchers to delve deeper into the genetic factors influencing heart disease. A study by researchers from Brigham and Womens Hospital, Broad Institute of MIT and Harvard, and Stanford Medicine has revealed links between genetic alterations in cells lining blood vessels and CAD risk. The study identified that a key biological mechanism involved in a rare vascular disease, cerebral cavernous malformations (CCM) signaling pathway, may influence CAD risk by impacting vascular inflammation, thrombosis, and the structural integrity of the endothelium.

While biological and genetic factors are significant, its crucial not to overlook the role of lifestyle and diet in cardiovascular health. Regular physical activity, managing stress, regular check-ups, and making dietary changes can significantly reduce the risk of heart disease among South Asians. Addressing the unique health needs of different ethnic groups will be key to reducing the burden of heart disease globally.

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Unveiling the Disparity in Cardiovascular Health: Biological Factors, Dyslipidemia, and Genetics - Medriva

Parental traits offer new clues to predicting neurodevelopmental disorders in children – News-Medical.Net

Predicting the trajectory of neurodevelopmental and psychiatric disorders like autism or schizophrenia is difficult because they can be influenced by many different genetic and environmental factors. A new study, led by Penn State researchers, demonstrates that evaluating parents for their manifestation of traits of these disorders -; and related diseases like depression and anxiety -; may provide a more accurate method of predicting the prevalence, and potentially severity, of the disorders in affected children than screening for genetic variants alone. This is likely due, at least in part, to genetic variants the parents transmit to the child that would not be routinely picked up in a genetic screen and lead to more severe disease, the researchers explained.

A paper describing the research appeared in the American Journal of Human Genetics. According to the researchers, understanding how both parents contribute to their child's diagnosis could inform genetic counseling and the development of therapeutic intervention plans for children impacted by these disorders.

We looked at the presence of neurodevelopmental and psychiatric traits in children and parents from a large set of families. We saw an increase in the presence of neurodevelopmental disorders in children whose parents both report having the trait, including psychiatric traits like anxiety or depression."

Santhosh Girirajan, interim department head and T. Ming Chu Professor of Biochemistry and Molecular Biology in the Penn State Eberly College of Science and lead author of the paper

The team looked at 97,000 families, many including children with neurodevelopmental disorders such as autism or intellectual disability and evaluated how risk factors -; genetic features and the presence of the traits -; in both parents impact the trajectory of the disease in the children. The datasets included genetic information and questionnaire data from families in a large public biobank, as well as from families from specific studies of neurodevelopmental disorders.

The researchers evaluated parents and their children for symptoms of the various disorders and assessed known genetic mutations that can give rise to such disorders. Their analysis revealed that parents tend to select partners with the same or related disorders, leading to increased prevalence and, potentially, severity of the disorder in their children.

"Most neurodevelopmental disorders are genetically complex, meaning that they aren't caused by a single gene," Girirajan said. "This makes it hard to trace the exact genetic underpinnings of a disorder in an individual and even harder to predict how the disorder will play out in affected children."

The researchers explained that complex genetic diseases can be caused by mutations in many genes, each of which could be inherited from one or both parents, or occur spontaneously in the newly formed genome of the child. The child's disease prognosis results from the combination of mutations that they inherit and how they interact with one another during development. This is called the "multi-hit model" because the disease results from multiple different mutations in many different genes.

"We have been studying one such mutation -; a deletion of a small segment of chromosome 16 -; that has been implicated as a risk factor for several neurodevelopmental disorders," Girirajan said. Symptoms of these disorders can manifest as seizures, schizophrenic features, depression and anxiety, along with characteristics related to addiction. "This mutation is often passed from a parent to a child, but the child regularly has more severe symptoms of the disorder than the parent. We wanted to know if other 'hits' for the disorder could be coming from the other parent. So, we looked at the traits of both parents in a large cohort of families with children with neurodevelopmental disorders."

The research team found that the parent that had passed on the deletion had less severe symptoms than their child or even different but related psychiatric disorders like depression or anxiety. They also found that the other parent often had similar psychiatric traits.

"What we realized, and it's been studied for a long time, is that in people there is a phenomenon called 'assortative mating,'" said Corrine Smolen, a graduate student at Penn State working with Girirajan and the first author of the paper. "Whether it's consciously or unconsciously, people with similar features preferentially find each other as partners. Although there could be other explanations, we see this in our data and that is probably what is leading to what we are seeing in the families that we studied."

The parent that doesn't have the deletion must have these traits because of some other genetic mutations, the researchers explained, and when these mutations are combined with the deletion in the genome of the child, the result is more severe disease. By assessing the traits in both parents, the researchers could more accurately predict the trajectory of the disease in their children than would be possible via genetic screening alone. They also could eventually use this information to try to identify new mutations -; those inherited from the parent without the deletion -; that are involved in causing these traits.

"We found that there is a good correlation between the traits in the parents," Girirajan said. "Someone with schizophrenia is more likely to find a partner with schizophrenia, someone with anxiety and depression is more likely to find a partner with anxiety and depression. This is well-known for other things, like tall people marrying other tall people. Because all of these traits have at least some genetic component that could be similar between the partners, this leads to a situation that is akin, but less pronounced, to consanguineous marriage, when people who are related through ancestry marry."

In this case, Girirajan explained, the assortative mating based on traits -; rather than relatedness -; appears to be driving genetic similarity between the partners which could be leading to more cases and potentially more severe traits in their offspring. As an example, the researchers saw that when neither partner had anxiety, 12.6% of their male children had anxiety. That number jumped to 25.7% when one parent reported having anxiety and to 33.8% when both parents had anxiety. This increase in prevalence is indicative of an increase in severity because more severe traits are more likely to be identified, according to the research team.

In addition to Girirajan and Smolen, the research team includes Matthew Jensen, Lucilla Pizzo, Anastasia Tyryshkina, Deepro Banerjee, Laura Rohan and Emily Huber at Penn State; Lisa Dyer and Jane Juusola at GeneDx, in Maryland; Laila El Khattabi at the Assistance PubliqueHpitaux de Paris in France; Paolo Prontera at the Santa Maria della Misericordia Hospital in Italy; Jean-Hubert Caberg at the Centre Hospitalier Universitaire de Lige in Belgium; Anke Van Dijck and R. Frank Kooy at the University and University Hospital Antwerp in Belgium; Charles Schwartz at the Greenwood Genetic Center in South Carolina; Laurence Faivre, Patrick Callier, and Mathilde Lefebvre at the Universit de Bourgogne Franche Comt in France; Anne-Laure Mosca-Boidron at the Laboratoire de Genetique Chromosomique et Moleculaire in France; Kate Pope, Penny Snell and Paul J. Lockhart at the University of Melbourne in Australia; David J. Amor at the Murdoch Children's Research Institute in Australia; Lucia Castiglia, Ornella Galesi, Emanuela Avola and Maria Grazia Bruccheri at the Oasi Research Institute in Italy; Teresa Mattina, Marco Fichera and Corrado Romano at the University of Catania in Italy; Giuseppa Maria Luana Mandar at ASP Ragusa in Italy; Olivier Pichon, Silvestre Cuinat, Sandra Mercier, Claire Bnteau and Bertrand Isidor at CHU Nantes in France; Cedric Le Caignec at the Universit de Toulouse in France; Radka Stoeva at CHU de Le Mans in France; Sophie Blesson and Dominique Martin-Coignard at Bretonneau University Hospital in France; Ashley Nordsletten at the University of Michigan; and Erik Sistermans at Amsterdam UMC in the Netherlands.

Grants from the U.S. National Institutes of Health, the South Carolina Department of Disabilities and Special Needs, and the Italian Ministry of Health-Ricerca Corrente supported the research.

Source:

Journal reference:

Smolen, C., et al. (2023). Assortative mating and parental genetic relatedness contribute to the pathogenicity of variably expressive variants.The American Journal of Human Genetics. doi.org/10.1016/j.ajhg.2023.10.015.

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Parental traits offer new clues to predicting neurodevelopmental disorders in children - News-Medical.Net

Cheetahs Are Extremely Inbred: 50 Interesting Genetics Facts You May Have Missed At School – Bored Panda

There is a gene called TP53 - its referred to as the guardian of the genome - it is a tumor suppressor gene and prevents cancer of all types. Humans have two copies and if one is broken/mutated it causes an inherited condition called Li Fraumeni. People with this have a very very high risks for cancer, and the condition can be passed down in families. Elephants have 20 copies of TP53 and therefore rarely get cancer. The Li Fraumeni foundation uses the elephant as its mascot and hopefully we can someday figure out how to replace faulty TP53 genes for these families.

OrangeMonarchQueen , Chokniti Khongchum (not the actual photo) Report

Perhaps my favourite biology fact is about pharmacogenetics, how your genetics determines the efficacy of drugs on your system due to prevalence of receptors of different types that the drugs target to produce an effect:

"90% of drugs only work on 30-50% of the population."

I find it so truly wild. But most people I've talked to about it seem to agree that some drug or other doesn't work for them. This really highlights how much of a process finding the right drug for a person is. I had a lecture on this in uni in about 2016 and it said the future of pharmacology is individual genetic screens for drug effectiveness meaning people don't have to keep trying different drugs until they find the one that works, you would be tested then your doctor would have that info. I just hope it overcomes the pushback from Big Pharma in my lifetime cause it would be a true game-changer.

jimbo-g , Christine Sandu Report

While it might sound like a cross between dystopian fiction and body horror, some researchers believe that there is a lot of potential to store data and information in our DNA. After all, in one sense, thats exactly what DNAs actual function is. That being said, most of us probably dont want to walk around with our own DNA turned into a sort of USB flash stick when we can literally buy this device in most stores.

Comically, as sci-fi as this idea sounds, it might already be out of date. Research into this topic has found that encoding data into our DNA is not only more costly but less reliable and slower to read than the various means of data storage we already have. So if you really want to get cyberpunk, perhaps get a QR code tattooed or investigate the wonderful world of chipping your palms.

That if you unraveled all of the DNA in your body, and stretched it out in a straight line, you'd be dead.

volume_two Report

Since navel oranges have no seeds, they are all clones of the original mutated fruit discovered by a Brazilian monk a century ago. The billions and billions of navel oranges that have been grown, sold and consumed since are all genetically identical.

JK_NC , Shang Ning Report

Cheetahs are extremely inbred. They had a massive bottleneck about 10,000 years ago and had too little diversity to fully recover.

confusedbox03 , Pixabay Report

For simplicity, let's say your mother is 50% Chinese & 50% Spanish. That does **not** mean you are 25% of each.

On paper it would seem so but you can have any combination of those two equaling to 50%. It's not a clean cut in half. It's a *random* 50% given and 50% not. Although, yes there are dominate genes that can give all the kids a certain nose shape or eye color. Still, you and your siblings might get these DNA combos from mom:

- you: 30% C & 20% S

- brother: 12% C & 38% S

- sister: 5% C & 45% S

So if you ever wondered why your sister looks more Spanish than you its because genetics wise she just is more Spanish.

a_person1852 Report

If you set aside ethics and set out to do it, it would only take 33 generations to create a human being who was the descendant of everyone currently alive and able to have children.

Also, pedigree collapse: no living person has as many unique ancestors as they mathematically should. Every person has, biologically, 2 parents, 4 grandparents, 8 great-grandparents, etc, doubling every generation. 30 generations back without any degree of inbreeding would require over a billion unique 28x great grandparents, more than the entire world population for 1100 AD. Every single human's family tree is full of people marrying and having children with cousins of some genetically-unimportant degree over the last thousand years.

Triton1017 , Tyler Nix (not the actual photo) Report

not everyone may know is that your genes play a role in determining whether you are more likely to be a morning person or a night owl

Either-Growth9518 Report

1. Most genetics studies were, and are still, done on white western populations. Some things that we "know" about genetics turn out to not work so well in non-white or non-western populations. Loose example: diagnostic tests to check for certain diseases sometimes misdiagnose Americans with African ancestry, because sometimes we don't actually know exactly how certain diseases will look in non-European ancestry patients, we just assume it will be the same.

2. Africa, as a whole, is the most genetically diverse continent for human genetics. Humans outside of Africa went through a population bottleneck, resulting in an overall lack of diversity moving forward. The human blender of genetics in Europe just didn't have many starting ingredients. There are things called linkage disequilibrium maps, which basically map out sections of the genome that are usually found inherited together. In Europe, these maps are quite "chunky", with large identifiable sections that are sort of reliably found intact. But in Africa, the blender was always running and never had a bottleneck, so those maps are basically a much finer puree, with a lot more mixing. This presents certain challenges, as many studies rely on those maps to make predictions, and it's harder to do that when the map for Africa as a whole is basically way more complex.

3. Everyone's cancer is its own unique genetic disease. There is no one true single disease called "lung cancer", just as there is no one single true human genome. Everyone is genetically unique (yes even identical twins), and every cancer is unique.

4. Chromothripsis is a thing where a chromosome pretty much shatters and gets stuck back together all out of order. And... this is sometimes okay. There are cases of people who have chromosomes that have undergone chromothripsis, and they have mild to moderate symptoms, but they're not dead, which is miraculous.

5. Remember in biology class when you learn about mitosis? And there's that step called metaphase where all the chromosomes line up in a line before being separated into two new cells? That spot in the middle of the "X"-shaped chromosomes where the spindles attach to line them up is called the centromere. And it's sort of mysterious black hole of genetics. There aren't usually any genes there, just a chaotic cluster-f**k of repetitive sequence that gets chopped forwards, backwards, repeated 7 times, swapped around and repeated again, etc etc in an area that's hundreds of thousands of nucleotides long. But what's even crazier is that we don't really know *why* they are how or where they are, because *you don't need the wacky wasteland of repeats for them to work*. Almost all centromeres in all animals look like this, but there are exceptions. A very notable exception is that very very rarely in humans, a "mar-del" chromosome can form where a chromosome accidentally loops on itself and pinches (think of that heart thing people do with their thumb and forefinger), resulting in a circular chromosome that still has its centromere, and a "butterfly" chromosome that does not. Without a centromere, a chromosome can't be duplicated into daughter cells successfully, and cells can't live without the genes on that butterfly chromosome so this should be lethal if it happens early on in development. But surprise, a centromere can and has spontaneously formed on the butterfly chromosome, making them tiny, viable chromosomes that work pretty much fine! But like I said this is super rare, with only a few recorded cases ever. Centromeres in general are very cool and very mysterious.

6. Everything about modern next-generation genetic sequencing is super interesting, yet not well known to the general public. I won't brain dump about it, but if you want to know more, ask and I will!

Mooshan Report

Birthing identical twins is not an inherited trait. Its random. Fraternal twinning is inherited, but only from mother to daughter. My MIL took credit for me having identical twins because she had fraternal twin siblings. When I explained that genetics proved her wrong she was not having it!!

JellyfishEastern8184 , Becerra Govea Photo (not the actual photo) Report

When youre pregnant, bits of DNA from your baby invade your body and settle all over permanently - including in your brain. Researches found this by looking for male DNA in the brains of deceased 70 year olds. Interestingly, mouse studies have also shown that fetal cells within the mother have restorative properties and will rush to places like the heart, kidneys, lungs, liver if its injured and can even become cells that begin beating. One of the theories I have seen but I dont know if anyone knows for certain if this is true is that these cells enter our bodies so a host is less likely to reject the parasite baby.

Sweaty-Peanut1 Report

I'm a geneticist with a mediocre master's degree in biology and currently pursuing a PhD in Bioinformatics. Here are some insights:

1. The accuracy of consumer and clinical genetic tests is often questionable due to the rapid pace of scientific advancements outpacing their application in the industry. The notable exceptions are information about Neanderthal ancestry (which is significant enough to have earned a Nobel Prize in Medicine) and a few critical mutations like the sickle cell variant and others related to blood.

2. Genetically, most humans are nearly identical, with differences being incredibly minute. This means that, barring age and sex, achieving success in various fields whether it's social, intelligence, or physical appearance is possible without genetic modifications. Everyone likely has a unique genetic trait that gives them a significant advantage, however. This is currently identifiable only in a lab setting. Understanding your unique trait, which often involves the expression of certain molecules, might require professional scientific interpretation.

3. Many severe genetic diseases, such as insulin-dependent diabetes, are only about 50% determined by genetics. Factors like early developmental conditions, including a mother's diet during early pregnancy and infections, play a paramount role.

4. Despite common belief, Neanderthals were not a separate species but rather a part of the human family. For perspective, Europeans and the Khoisan people of South Africa have been genetically divergent for about 300,000 years, not much less than the 500,000-year divergence between humans and Neanderthals.

5. Factors beyond genetics, such as living in a highly controlled environment (like a prison), having access to specific nutrition, owning a car and a separate house, and engaging in mental activities like language learning, math, statistics, and team video games, can significantly impact personal development. Genetics helps us understand and appreciate the influence of these non-genetic factors. The field of genetics is incredibly dynamic and continually evolving, offering many more fascinating insights.

nevermindever42 Report

Genetic chimera is arguably the most interesting condition. It is possible (and documented) for a woman to give natural birth but the baby not match her DNA test.

Essentially, 2 fertilized eggs merge at a very early stage and developing into a single organism. Different parts of the body comprised of obe or the other genome.

It's most commonly discovered in domestic animals that have unexplainable color combinations, often (but not always) divided symmetrically.

Eagle_1776 , Dominika Roseclay (not the actual photo) Report

Trauma can be inherited (look up transgenerational trauma).

So if you feel more sensitive than most people it might be because your grandma experienced something horrible.

On average it takes three generations to heal a trauma if I remember correctly. But only if properly treated and the parents do not retraumatize their kids with their unconscious trauma-responses. This way unhealthy behaviors would become the norm and eventually become genetically preferred automatic behavior for future generations.

Even-Ad-6783 Report

One in 40 Ashkenazi Jewish women has a BRCA gene mutation. Mutations in BRCA genes raise a person's risk for getting breast cancer at a young age, and also for getting ovarian and other cancers. That is why Ashkenazi Jewish women are at higher risk for breast cancer at a young age.

Walter_Piston Report

Twins can be half identical. Like same egg split but two different sperms so they share about 75% genetic similarities compared to 100% in identical twins and 50% in fraternal twins/siblings. They can even be boy and girl twins.

SunRemiRoman , Pixabay (not the actual photo) Report

There are more combinations than just XX and XY.

And some of the variations have no outward signs, so you could have one of them and have no idea without genetic testing.

NotMyNameActually Report

Pretty much everybody is clueless about 99.9% of genetics.

hapidaron Report

Humans are closer genetically to bonobos than chimpanzees.

I wish I was a bonobo.

MyMudEye Report

Get tested for hereditary high cholesterol (familial hypercholesterolemia). It's a comparatively common genetic disorder.

It shows next to no symptoms but can clog your arteries and kill you, no matter how healthy your diet and lifestyle. It rarely skips a generation.

The treatment is usually a medication called statins.

LarryLongBalls_ Report

The green eyed gene is a recessive gene when compared to brown eyed gene; it is dominant when compared to blue eye gene.

illuminatedcake Report

UV gives you cancer because literally makes your DNA stick so tightly the only way to fix it is remove the entire section then "guess" what was there. More this happens, more chance cell becomes cancerous.

Bacteria don't have this polymerase repair so it's why UV kills them or mutates them.

Plant one - Hexaploid wheatpossesses 42 chromosomes derived from its three ancestral genomes. The 21 pairs of chromosomes can be further divided into seven groups of six chromosomes (one chromosome pair being derived from each of the three ancestral genomes)... This is mainly because of how much humans have bred it it's literally inbred.

arabidopsis , Jesse Schoff (not the actual photo) Report

Read more:
Cheetahs Are Extremely Inbred: 50 Interesting Genetics Facts You May Have Missed At School - Bored Panda