CRISPR gene editing in mice has been used to correct a mutation that can cause rapid ageing, dramatically improving the animals’ health and lifespan.
New gene-editing technology could be used to save species from extinction—or to eliminate them.
In Michelle O’Malley’s lab, a simple approach suggests a big leap forward in addressing the challenge of antibiotic-resistant bacteria.
Scientists have long been aware of the dangerous overuse of antibiotics and the increasing number of antibiotic-resistant microbes that have resulted. While over-prescription of antibiotics for medicinal use has unsettling implications for human health, so too does the increasing presence of antibiotics in the natural environment. The latter may stem from the improper disposal of medicines, but also from the biotechnology field, which has depended on antibiotics as a selection device in the lab.
“In biotech, we have for a long time relied on antibiotic and chemical selections to kill cells that we don’t want to grow,” said UC Santa Barbara chemical engineer Michelle O’Malley. “If we have a genetically engineered cell and want to get only that cell to grow among a population of cells, we give it an antibiotic resistance gene. The introduction of an antibiotic will kill all the cells that are not genetically engineered and allow only the ones we want — the genetically modified organisms [GMOs] — to survive. However, many organisms have evolved the means to get around our antibiotics, and they are a growing problem in both the biotech world and in the natural environment. The issue of antibiotic resistance is a grand challenge of our time, one that is only growing in its importance.”
Biotechnologists at Delft University of Technology have built an artificial chromosome in yeast. The chromosome can exist alongside natural yeast chromosomes, and serves as a platform to safely and easily add new functions to the micro-organism. Researchers can use the artificial chromosome to convert yeast cells into living factories capable of producing useful chemicals and even medicines.
Biotechnologists from all over the world are trying to engineer yeast cells and other micro-organisms such that they can produce useful substances. To do this, they have to make adjustments to the existing genetic material of the cell. For example, they insert a number of genes into the yeast genome using CRISPR-Cas9, or switch off existing genes, thereby gradually transforming yeast cells into ‘cell factories’ that produce useful substances.
The disadvantage of this method is that it is not possible to make all the necessary changes at once, but that several rounds of genetic manipulation are needed. This is time-consuming. Additionally, multiple sessions of DNA-tinkering using CRISPR-Cas9 can lead to mutations that disrupt (essential) functions. The result of this could be, for instance, that the metabolism of the cell is disrupted, causing problems with growth and division.
Alzheimer’s Disease (AD) is probably more diverse than our traditional models suggest.
Postmortem, RNA sequencing has revealed three major molecular subtypes of the disease, each of which presents differently in the brain and which holds a unique genetic risk.
Such knowledge could help us predict who is most vulnerable to each subtype, how their disease might progress and what treatments might suit them best, potentially leading to better outcomes.
Gene therapies are opening up possibilities that were once reserved for science fiction.
At Harvard University, Professor of Genetics David Sinclair says he believes it’s possible to unlock the fountain of youth, and gene therapy is the key.
Continue reading “Gene Therapies and the Promise of the Fountain of Youth” »
Summary: The genetics of neurocognitive skills were associated with higher tolerance of risk, delayed fertility, less healthy-risk behavior, and a greater willingness to forgo immediate gratification.
Source: Columbia University.
Noncognitive skills and cognitive abilities are both important contributors to educational attainment — the number of years of formal schooling that a person completes — and lead to success across the life course, according to a new study from an international team led by researchers at Columbia University Mailman School of Public Health, the University of Texas at Austin, and Vrije Universiteit Amsterdam.
Octopus and squid make strange evolutionary shortcuts in adaptation. Evolution is an intricate process of change.
According to Science Alert, species of squid and octopus may yet have some surprises in store for us. “In a surprising twist, scientists discovered that octopuses, along with some squid and cuttlefish species, routinely edit their RNA (ribonucleic acid) sequences to adapt to their environment,” the article said.
Continue reading “Octopuses, Some Squid Edit RNA Sequences to Adapt to Environment” »
The extent to which nonhuman primate vocalizations are amenable to modification through experience is relevant for understanding the substrate from which human speech evolved. We examined the vocal behaviour of Guinea baboons, Papio papio, ranging in the Niokolo Koba National Park in Senegal. Guinea baboons live in a multi-level society, with units nested within parties nested within gangs. We investigated whether the acoustic structure of grunts of 27 male baboons of two gangs varied with party/gang membership and genetic relatedness. Males in this species are philopatric, resulting in increased male relatedness within gangs and parties. Grunts of males that were members of the same social levels were more similar than those of males in different social levels (N = 351 dyads for comparison within and between gangs, and N = 169 dyads within and between parties), but the effect sizes were small. Yet, acoustic similarity did not correlate with genetic relatedness, suggesting that higher amounts of social interactions rather than genetic relatedness promote the observed vocal convergence. We consider this convergence a result of sensory–motor integration and suggest this to be an implicit form of vocal learning shared with humans, in contrast to the goal-directed and intentional explicit form of vocal learning unique to human speech acquisition.
One of the key preconditions for the development of speech is the ability to adjust vocal output in response to auditory input. Humans are exceptionally proficient at vocal learning. Although effortless speech learning is confined to the early years [1], humans still possess the ability to imitate sounds voluntarily and acquire further languages throughout their lives. Numerous comparative studies have aimed at elucidating the evolutionary origins of vocal learning within the primate lineage, to uncover the extent to which nonhuman primates reveal evidence for vocal plasticity, and whether such plasticity may be conceived as a pre-adaptation for the evolution of speech [2, 3].
Despite considerable research effort, it appears that the ability to learn sounds from auditory experience in most nonhuman primate species is limited. Unlike humans or some songbird species, nonhuman primates are not obligatory vocal learners that require species-specific auditory input to develop their normal vocal repertoires [4, 5]. Early attempts to train a young chimpanzee to produce speech sounds yielded disappointing results and prompted most of the ‘ape language’ projects to turn to another modality, using either symbol systems or sign languages [6]. Studies of the neural basis of vocal production in different monkey species found that the animals lack the neural connections necessary for the volitional control over the fine structure of vocalizations, although they exert greater control over the usage of calls (reviewed in [2]).
Biotin is also known as vitamin H, named for the German words “Haar” and “Haut,” which mean hair and skin. This was due to the fact that even slight deficiencies cause hair thinning, skin rash or brittle fingernails. New research, just published in PNAS, now shows that some forms of severe neurodegeneration, like the frontotemporal dementia seen in Alzheimer’s and Parkinson’s, can directly result from lack of sufficient biotin.
The authors discovered this by looking at fruit flies with dementia. Now, before anyone chuckles, fruit flies actually make a nice model of Alzheimer’s or other diseases when they are given the right genes. Human versions of defective MAPT (tau) genes cause these flies to develop tauopathies that resemble those that occur in our own brains. To delve deeper into the neurotoxicity of tau, they looked at over 7000 fly genes in a forward genetic screen before zeroing in on one significantly modified toxicity of the tauR406W mutant. This gene, Btnd, encodes the biotinidase enzyme that extracts biotin from food sources or recycles it from used enzymes.
