Researchers in the Van Eck lab perform tomato transformations routinely, as a research method to understand how
individual genes affect tomato growth and development.
Not exact matches
In
individuals affected by SMA, the survival motor neuron - 1 (SMN1)
gene is mutated and lacks the ability to process a key protein that helps neurons function.
«This is exciting because if
genes affected differences between
individuals in these traits, it means they could also change in response to natural selection,» said Dr Bolund.
More and more, researchers are finding that an extra bit of a vitamin, a brief exposure to a toxin, even an added dose of mothering can tweak the epigenome — and thereby alter the software of our
genes — in ways that
affect an
individual's body and brain for life.
In
individuals affected by SMA, the spinal motor neuron - 1 (SMN1)
gene is mutated and lacks the ability to process a key protein that helps muscle neurons function.
The MGH investigators screened the genomes of 40
individuals with arhinia and 55 family members, from a total of 38 families, revealing rare single - nucleotide mutations within the SMCHD1
gene in 84 percent of
affected individuals.
«It doesn't show how the presence or absence of the menopause
affects Darwinian fitness,» how successful an
individual is in passing on his or her
genes to future generations, «which is the all - important evolutionary yardstick.»
We screened a total of 394 Amish research subjects for the KCNH7 mutation; 84 of these
individuals carried at least one copy of the
gene variant, and the lifetime incidence of bipolar spectrum disorders among them was 49 percent (41 people were
affected with the disease).
«Patients»
individual genomes may
affect efficacy, safety of
gene editing: CRISPR - Cas9 and other
gene editing systems may need to be customized to the patient.»
By studying rare «copy number variations,» which are
individual errant insertions or deletions of DNA segments (each of which occur in less than one percent of the population), researchers discovered a new cluster of
genes that are
affected in some autistic
individuals as well as a number of mutations that were present in autistic children but not their parents.
For all 20,000
individual genes, they determined whether those
genes were heritable — controlled by the DNA «dimmer switch» — or largely
affected by environment.
But the new study has underscored the variability in the copy number variants and
genes that can be
affected in autistic
individuals.
Affected individuals do not have a disease: they only carry 1 copy of a hemoglobin
gene variant, and unlike
individuals with 2 copies of the variant, they do not experience symptoms.
«A
gene that
affects how well an
individual does in one environment or the other might
affect how they see each other and how they mate with each other.»
Tomas Marques - Bonet of the Universitat Pompeu Fabra noted that studying
gene flow between ancient humans such as Neanderthals, Denisovans and the ancestors of modern humans has revealed numerous
genes under selection that
affect disease and an
individual's traits.
Using novel technologies developed at HMS, the team looked at how a single sensory experience
affects gene expression in the brain by analyzing more than 114,000
individual cells in the mouse visual cortex before and after exposure to light.
The researchers plan to investigate what percentage of
individuals individuals with intellectual disability and autism may carry CC2D1A mutations and to determine whether other
genes affect neurons in a similar fashion.
«Crohn's disease is a complex disorder with multiple
genes and environmental factors involved, which disproportionally
affects individuals of Ashkenazi Jewish ancestry,» explained lead researcher Inga Peter, Professor of Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai in New York City.
«What we are trying to do is identify the function of
genes and how they
affect the way the
individuals process information and the structure of the brain.
Alexander Wyatt says: «Despite the enormous complexity between patients at the
individual gene level, when we examined the functions of
affected genes, clear commonalities between groups of patients emerged.
This means
affected individuals receive a flawed
gene from each parent in order to have symptoms.
Other medical sequencing projects will use DNA sequencing to: discover new
genes that are involved in common diseases; identify the
genes responsible for dozens of relatively rare, single -
gene (autosomal Mendelian) diseases; sequence all of the
genes on the X chromosome from
affected individuals to identify those involved in sex - linked diseases; and survey the range of variants in
genes known to contribute to certain common diseases.
Such information will help reveal how all traits are
affected by deleting a given
gene in an
individual mouse.
Professor Segal's research has two major directions 1)
Gene regulation — using quantitative and computational models to understand how DNA sequence variation among human
individuals generates phenotypic diversity 2) Microbiome and Nutrition — understanding how the microbial composition of
individuals affect their physiology and health.
To better understand this complex tissues and its functions — and the diseases that
affect it — a multicenter team led by researchers at the Broad Institute of MIT and Harvard and Massachusetts General Hospital has released a census of the cells that make up the lining of the small intestine, using
gene expression profiles of more than 53,000
individual cells from the mouse gut or gut organoid models.
Full - genome sequencing of
affected individuals and their parents provides a powerful alternative strategy for
gene discovery.
Many medical - genetic syndromes show a clear connection between genetic alteration and typical facial gestalt [49], hence
genes involved in
affected individuals may also contribute to normal variations in facial shape.
An
individual may still be a carrier of (or
affected with) a disease if no variants or only one variant is found in the relevant
gene.
Thus, whole - exome sequencing allowed for direct identification of a disease - causing
gene with just a few samples from
affected individuals.
By analyzing genome sequence data from human populations, including 1269
individuals from sub-Saharan Africa, we identify a diverse array of large copy number variants
affecting the host invasion receptor
genes GYPA and GYPB We find that a nearby association with severe malaria is explained by a complex structural rearrangement involving the loss of GYPB and gain of two GYPB - A hybrid
genes, which encode a serologically distinct blood group antigen known as Dantu.
Results: Our exome variant analysis revealed coding variants in the NLRP7
gene that were present in
affected individuals in two distinct families.
«The new knowledge of the genomic changes in ovarian cancer has revealed that the molecular catalysts of this disease are not limited to small changes
affecting individual genes,» said NCI Director Harold E. Varmus, M.D. «Also important are large structural changes that occur in these cancer genomes.
The focus of the conference was connecting how epigenetics (cellular and physiological phenotypic trait variations that are caused by external or environmental factors that switch
genes on and off and
affect how cells read
genes instead of being caused by changes in the DNA sequence — in other words nutrition and lifestyle choices) impact whether or not an
individual actually develops a specific health issue even though they have a SNP mutation.
Plant Positive (www.plantpositive.com) has some amazing work explaining why we shouldn't use models of these marginalized societies, or of assumed genetic or evolutionary requirements to determine our eating habits (one being that
genes are passed on only by those that live long enough to procreate, and are not
affected by the longevity of that
individual — it just isn't important for «survival of the fittest» in the evolutionary sense).
Most breeders, should they breed for any length of time, may expect to encounter it at some point, as it has been known to
affect individual stud dogs that have been used extensively and which form corner stones of the current Bull Terrier
gene pool.
A clinically normal dog from a litter that had one or no
individuals affected with hip dysplasia (which is a polygenic disorder) is expected to carry a lower amount of liability
genes than a dog with a greater number of
affected littermates.
This area becomes a bit more gray, because while there is a very good argument for not breeding close relatives of
affected and carrier dogs, we also can not afford to eliminate all dogs in the
gene pool who meet this criterion — to do so would risk further constriction of the
gene pool to the point where the remaining «epilepsy - free»
individuals might have higher - than - normal frequency for
genes that contribute to some other genetic disorder.
A dominant mutation is where one defective copy of a
gene is enough to
affect the
individual, whereas a recessive mutation requires that both copies of the
gene carry a mutation for the
individual to be
affected.
For a recessive disease, all offspring of
affected individuals, two thirds of their normal full - siblings, half the offspring of either parent and up to half the full - siblings of both parents carry a deleterious
gene and yet appear normal.
Dogs testing in the abnormal range were generally considered
affected with vWD and at risk for transmitting an abnormal vWF
gene to their offspring, and in some
individuals for expressing an abnormal bleeding tendency.
Since hip dysplasia is a polygenic disorder controlled by several
gene pairs, the disease
affects individual dogs due to different genetic combinations.
As long as the frequency of a
gene for a recessive disorder remains low in the population, the particular
gene may be passed along for many generations before by chance 2 carriers are mated and
affected individuals are born.
It remains unclear why anxiety and mood disorders are less prevalent in East Asian relative to Western cultures, especially given that a majority of
individuals living in East Asia carry the S allele of the serotonin transporter
gene, which is associated in Western populations with negative
affect.
Such interplay between
genes and environment may channel
individual development into different trajectories early in life and
affect the long - term development of mental health and disorder.