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Genetics Exam 3

Terms in this set (232)

Mark the scenarios that are likely due to epigenetic modifications

-A male smoker has less DNA methylation at certain parts of the AHRR gene. After quitting smoking, methylation patterns in DNA are reversed.
-Mother with a mutation in the BRCA1 gene wants her son and daughter tested. The mother inherited the mutation from her father. The son develops prostate cancer, despite inheriting the mutation from his mother. The daughter did not inherit the mutation and does not develop cancer.
- Female rats exposed to dioxin, a toxin, during pregnancy have offspring with a high rate of kidney disease. Females from the first generation who were not directly exposed to the toxin during pregnancy also have offspring with disease. This pattern continues for three generations. There is no evidence that dioxin generates mutations in the DNA.
- Wild radish plants damaged by caterpillars are known to turn bitter and grow spines. The caterpillars release a toxin in the plants that was discovered to methylate MET164 and DDM1 genes. Offspring of damaged plants will have similar levels of defenses as damaged plants.
-Himalayan rabbits carry the C gene, which is required for the development of fur pigmentation and its expression is regulated by temperature. Specifically, C gene is methylated (inactive) above 35°C, and it is maximally active from 15°C to 25°C. Rabbits carrying the dark allele in gene C are born with black feet (because temperature is lower in extremities during development) and white in the rest of the body (because temperature is higher in these regions). The pigmentation pattern is maintained throughout the rabbits life regardless of temperature.
Assignment: Which of the following characteristics would be considered a quantitative traits?
Select all that apply.

Two Indian Paintbrush flowers raised in the same environment were crossed. One parent was yellow and the other was reddish orange. Of the cross, the F2 generation showed a diverse distribution of colors from yellow to reddish orange. This differs from the flower color of Mendel's peas where the F2 individuals were either purple or white, the two parental phenotypes.

It has been found that there is a gene involved in the mechanism of tasting bitter taste such as PTC, this is TAS2R3 found in chromosome 7. The ability to sense bitter taste is dominant over not being able to perceive said taste.

Two identical twins were born, but separated at birth, growing up in completely different environments. IQ tests were performed on the twins when they turned eight years old. The IQ test of one twin was much higher than the other, even though identical twins have the same DNA.

Research has shown that the concentration and metabolism of serum lipids, which includes cholesterol, LDL, HDL and triglycerides, in the blood of pigs have been linked to numerous loci in the genome.

The flower Gaillaridia pilchella has been known to show variation in flower diameter. This trait is controlled by a number of genes.

About 80 percent of an individual's height is believed to be determined by the DNA variants that they inherit. Height is controlled largely by a combination of genetic variants that each have modest effects on height, plus a smaller contribution from environmental factors like nutrition. More than 700 gene variants have been discovered and many more are expected to be identified.

One of the first species described by Carl Linnaeus was Plumeria rubra, a type of plant found throughout Mexico, Central America, and the top of South America. Now, it's cultivated and sold around the world. The color of Plumeria rubra flowers has been found to be controlled by one gene at a loci and the location of the plant does not impact phenotypic ratios.

Primary Hypertension (High Blood Pressure) has been studied to be influenced by genes at different loci. 45% of Adults in the U.S. have hypertension.

Presence or absence of leprosy. Susceptibility to leprosy is determined by multiple genes and numerous environmental factors.
Researchers are actively trying to define the causes of high susceptibility for a critical case or long-term case of Covid 19. On the genetic side, a GWAS is a good start approach.
Here is the abstract of a recently published paper about a GWAS performed regarding COVID 19
Host-mediated lung inflammation is present1 (Links to an external site.), and drives mortality2 (Links to an external site.), in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3 (Links to an external site.). Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10−8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10−8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10−12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10−8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defense mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice.
You can find the article here:
Genetic mechanisms of critical illness in COVID-19 (Links to an external site.)

What can be concluded from this abstract?

Alleles that code for low levels of IFNAR2 or high levels of TYK2 directly cause critical cases of Covid 19
Alleles that code for low levels of expression of IFNAR2 or high expression of TYK2 are associated with critical Cases of Covid19
IFNAR 2 and TYK2 are the only 2 genes involved in critical cases of Covid 19
We can definitely now treat Covid 19 by creating iRNA against IFNAR2 and TYK2