Name two ways cells are able to move molecules against their concentration gradient. What is this type of transport called and is it possible to move molecules against their concentration gradient without using ATP?

1. In cystic fibrosis one amino acid is missing in the CFTR protein. Explain why this mutant protein will not end up in the plasma membrane. (You may need to investigate the normal function of this CFTR gene)

2. Why might a mutation in the DNA NOT lead to an abnormally functioning protein?

3. Describe one genetic disorder in which a gene is mutated and leads to abnormal protein folding ( other than Huntington’s). In “your disorder”, name the gene mutated and how it affects the protein.

4. Research Huntington’s disease: Describe the mechanism of the disease and its relationship to protein folding. Cite your references.

1. Through this project, you may have noticed a wide variety of phenological adaptations that different species of trees exhibit. For example, some trees may have developed leaves before flowers, while others may have immediately produced flowers when the spring arrives with their leaves emerging at a later time.

Answer each of the following questions; (2pts.)

• Explain the adaptive significance of developing leaves before flowers.

• Describe the source of sugars when trees produce flowers before the emergence of leaves.

Descriptive epidemiology is used for both scientific and administrative purposes. Describe and provide at least one example of how descriptive epidemiology is used for scientific purposes and describe and provide at least one example of how descriptive epidemiology is used for administrative purposes.

A population consists of 100 individuals of the following genotypes: 60 AA, 20 Aa, 20 aa. Is this population in Hardy-Weinberg equilibrium? Show work for possible partial credit.

1. How to code for repairs, including guidelines for coding of decontamination and debridement and also simple ligation of nerves and exploration of severed structures

A population consists of 100 individuals of the following genotypes: 55 AA, 25 Aa, 20 aa. Is this population in Hardy-Weinberg equilibrium? Show work for possible partial credit.

Microbiology is in the news!All around us!Post a link to an article, blog, report with a short comment/summary of hope this applies to our course.

If you took a commercial hybrid variety (an F1 hybrid) and collected seed (F2) and planted the F2 seeds the next season, how would the F2 progeny compare to the F1 hybrid variety?

Explain the evolutionary characters and similarities that exist among Docodonts, Triconodonts, Symmetrodonts, Multituberculates, Monotremes, Pantotheres, Placentals and Marsupials

I have the data for corn color and texture. These are the follow up questions for the data.

Color of Corn Grains

Number of Purple (Red) Grains: 75

Number of Yellow (White) Grains: 30

Ratio of Purple (Red) Grains: Yellow (White) Grains: 2.5:1

Probable Genotypes of Parents:  

Texture of Corn Grains

Number of Smooth Grains: 85

Number of Wrinkled Grains: 20

Ratio of Smooth Grains: Wrinkled Grains: 4.25:1

Probable Genotypes of Parents:

Grain color is one trait. Grain texture is a second trait. For each, what do you notice about the phenotypic ratios?

R = Purple/Red; r = Yellow/White; S = Smooth; s = Wrinkled

A genetic cross with only one trait is a monohybrid cross.

A genetic cross involving two traits is called a dihybrid cross.

Consider the cross: RRSS x rrss (Parental Generation) F1 is the result of the cross. (Gametes: RS for one parent (e.g. the egg) and rs for another parent (e.g. the sperm). FOR EACH GAMETE, IT IS ONE ALLELE FOR EACH TRAIT. THIS IS WHY YOU SEE TWO LETTERS PER GAMETE.)

What is the expected genotype for the F1 generation?

Will all F1 offspring have the same genotype?

Will all F1 offspring have the same phenotype?

What are the predicted phenotypes for the F2 generation crossing RrSs x RrSs?

In what ratios will they occur?

Purple/Red, Smooth:

Purple/Red, Wrinkled:

Yellow/White, Smooth:

Yellow/White, Wrinkled:

The human pathway for metabolizing alcohol starts with the enzyme alcohol dehydrogenase, which catalyzes the conversion of ethanol (C2H5OH) to acetaldehyde (CH3CHO). This is followed by the aldehyde dehydrogenase 2 (ALDH2, the enzyme of interest in this problem), which catalyzes the conversion of acetaldehyde and HS-CoA to acetyl-CoA (CH3CO–S–CoA). The TCA cycle starts and oxidizes the acetyl-CoA to CO2. Draw two diagrams of this pathway—one for an individual without AFS and another for an individual with AFS. How ALDH2 deficiency combined with ethanol input into the bloodstream could culminate in the accumulation of acetaldehyde in the blood of the patient.