Genes inherited from Denisovans, extinct human relatives, may help Papua New Guineans in the lowlands fight off infection, while mutations to red blood cells may help highlanders live at altitude.
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The brain is one of the most complex entities in biology. For thousands of years, humans have wondered how the human brain works, but only in the past few years has technology evolved so that scientists can actually answer some of the many questions we have. What are the causes of brain disorders? How do our brains develop? How does the brain heal after a head injury? While we still have a long way to go before we can understand the many facets of the human brain, one technology – CRISPR – has allowed us to start answering these questions on a genetic level.
What is CRISPR?
What if someone handed you a tool and said that you could better the lives of people before their birth by changing their genes? Would you do it?
CRISPR-Cas9 is one such tool. It’s an efficient and effective gene-editing technology that works by tagging a section of DNA with an RNA segment, and then using a protein called Cas9 to cut the DNA at the specified point. Then, the cell’s own DNA machinery works to add or delete DNA.
This technology opens up the pathway to a variety of gene-editing applications, from eliminating HIV in living organisms to creating a potential cure for Huntington’s disease. There is especially high potential for single-gene disorders to be eradicated. For example, promising results from the successful removal of a gene known to cause fatal heart disease from the embryo will not only save lives but also prevent the passing down of the gene.
Down syndrome (DS) is one of the most prevalent genetic disorders in humans. The use of new approaches in genetic engineering and nanotechnology methods in combination with natural cellular phenomenon can modify the disease in affected people. We consider two CRISPR/Cas9 systems to cut a specific region from short arm of the chromosome 21 (Chr21) and replace it with a novel designed DNA construct, containing the essential genes in chromatin remodeling for inactivating of an extra Chr21. This requires mimicking of the natural cellular pattern for inactivation of the extra X chromosome in females. By means of controlled dosage of an appropriate Nano-carrier (a surface engineered Poly D, L-lactide-co-glycolide (PLGA) for integrating the relevant construct in Trisomy21 brain cell culture media and then in DS mouse model, we would be able to evaluate the modification and the reduction of the active extra Chr21 and in turn reduce substantial adverse effects of the disease, like intellectual disabilities. The hypothesis and study seek new insights in Down syndrome modification.
Keywords: Down syndrome, CRISPR/Cas9, Designed DNA construct, Poly D L-lactide-co-glycolide (PLGA), Nano-carrier, Chromosome 21 inactivation.
Summary: Preschool children actively influence their own development to align with their genetic dispositions. By examining how toddlers interact with their environment, including activities like reading and puzzles, researchers found that children’s preferences impact how they engage in cognitive stimulation at home.
This active involvement helps shape their brain development alongside environmental factors. The findings emphasize the dynamic interplay between genetics and environment in early childhood, challenging the traditional views of passive developmental processes.
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Putting more meat on the theory that dinosaurs’ closest living relatives are modern-day birds, molecular analysis of a shred of 68-million-year-old Tyrannosaurus rex protein — along with that of 21 modern species — confirms that dinosaurs share common ancestry with chickens, ostriches, and to a lesser extent, alligators.
The work, published this week in the journal Science, represents the first use of molecular data to place a non-avian dinosaur in a phylogenetic tree that traces the evolution of species. The scientists also report that similar analysis of 160,000-to 600,000-year-old collagen protein sequences derived from mastodon bone establishes a close phylogenetic relationship between that extinct species and modern elephants.
Continue reading “Molecular analysis confirms T. Rex’s evolutionary link to birds” »
Two eggs fertilized by two sperm coincided in a uterus and, instead of giving rise to two sisters, they fused to form a single person: Karen Keegan. When she was 52 years old, this woman from Boston suffered very serious kidney failure, but luckily she had three children willing to donate a kidney to her. The doctors did genetic tests to see which offspring was most compatible and they got a major surprise: the test said that two of them were not her children. The reality was even more astonishing: Karen Keegan had two different DNA sequences, two genomes, depending on the cell you looked at. Biologist Alfonso Martínez Arias maintains that this chimeric woman is conclusive proof that DNA does not define a person’s identity.
The most inspiring science book of all time is The Selfish Gene, according to a survey carried out by the Royal Society of the United Kingdom. In this famous work from 1976, British biologist Richard Dawkins defended that the DNA molecule uses the human being as a mere envelope in order to be transmitted to the next generation and become immortal. “We are survival machines, robot vehicles blindly programmed to preserve the selfish molecules known as genes,” Dawkins stated. Almost half a century later, Martínez Arias refutes this perspective of the selfish gene and proposes a much more romantic alternative: the altruistic cell. “An organism is the work of cells. Genes merely provide materials for their work,” he says in The Master Builder, a fascinating and provocative book from the London publisher Basic Books that will also be published in Spanish this year.
Martínez Arias, 68, argues that the DNA sequence of an individual is not an instruction manual or a construction plan for their body, but a box of tools and materials for the true architect of life: the cell. The Madrid-born biologist argues that there is nothing in the DNA molecule that explains why the heart is located on the left, why there are five fingers on the hand or why twin brothers have different fingerprints. Cells are what “control time and space,” he proclaims. They are the ones who know where right and left are, and where exactly a person’s foot or an elephant’s trunk should end.
A study from the Hackett group at EMBL Rome led to the development of a powerful epigenetic editing technology, which unlocks the ability to precisely program chromatin modifications.
Understanding how genes are regulated at the molecular level is a central challenge in modern biology. This complex mechanism is mainly driven by the interaction between proteins called transcription factors, DNA regulatory regions, and epigenetic modifications – chemical alterations that change chromatin structure. The set of epigenetic modifications of a cell’s genome is referred to as the epigenome.
Advancements in Epigenome Editing.
A breakthrough study by the Institut Curie reveals that embryonic cell compaction in humans is caused by cell contraction, offering new insights to enhance assisted reproductive technology success rates.
In human development, the compaction of embryonic cells is a vital process in the early stages of an embryo’s formation. Four days post-fertilization, the cells tighten together, helping to form the embryo’s initial structure. If compaction is flawed, it can hinder the development of the essential structure needed for the embryo to attach to the uterus. During assisted reproductive technology (ART), this stage is meticulously observed before the embryo is implanted.
An interdisciplinary research team led by scientists at the Genetics and Developmental Biology Unit at the Institut Curie (CNRS/Inserm/Institut Curie) studying the mechanisms at play in this still little-known phenomenon has made a surprising discovery: human embryo compaction is driven by the contraction of embryonic cells. Compaction problems are therefore due to faulty contractility in these cells, and not a lack of adhesion between them, as was previously assumed. This mechanism had already been identified in flies, zebrafish, and mice, but is a first in humans.
