Kensey H. Barrett
BIO3344-Principles of Genetics SU01
Week 1 Discussion
Professor Dr. Hoban
September 23, 2021
As a 35-year-old female, with family history of cystic fibrosis, hypertension, and heart disease who is not interested in having more children, I would want to check for these types of health risk. Doing a Nutrigenetics testing would be interesting to see how that plays a role in daily activities and food intake (Lewis, 2020, p. 421). Knowing what a possibility is genetically of having such as osteoporosis, hypertension, type 2 diabetes, or heart disease could help motivate for prevention (Lewis, 2020, p. 420). Listing cystic fibrosis, my curiosity is because I know my mother and father are both carriers. I have two children and one have asthma like symptoms constantly. I chose to not be tested while pregnant and now I wonder if it is possible for him. However, it would have to be my husband and I both having the gene for CF. While it could be a coincidence, I often wonder about getting genetic testing for that reason.
The biochemical composition of the DNA is that DNA is deoxyribonucleic acid that can be located in chromosomes. It is the house of inherited information that is made up of nucleotides and it makes genes (Lewis, 2020, p. 168). DNA is a double helix that has a phosphate group, deoxyribose, and a base. It has four bases which are Adenine (A), Thymine (T), Guanine (G), and Cytosine (C) (Lewis, 2020, p. 168). The structure of DNA began in 1909 when Russian-American biochemist Pheobus Levene found the 5-carbon sugar ribose as part of some nucleic acids (Lewis, 2020, p. 168). Then in 1929, he discovered a similar sugar deoxyribose in other nuclei acids. In the early 1950s, two lines of experimental evidence converged to connecting the dots that finally revealed the full DNA structure (Lewis, 2020, p. 168). The replication of DNA happens when it is copied so that the information can be maintained and passed to future cell generations. DNA replication happens during S phase of the cell cycle (Lewis, 2020, p. 174). It first unwinds and then separates. The hydrogen bonding that holds the base pairs together break and two identical nucleotide chains are built from one (Lewis, 2020, p. 174). This is the new complementary pairs. The role of specific RNA is in the process of protein transcription and translation starts with cells using two process to manufacture proteins using genetic instructions. Transcription first synthesizes RNA molecule that is complementary to one strand of the DNA double helix for a gene (Lewis, 2020, p. 174). The RNA copy is taken from the nucleus and into the cytoplasm. The process of translation takes the information in the RNA to manufacture a protein by aligning and joining the amino acids. Then, the protein folds into a three-dimensional form for its function (Lewis, 2020, p. 174).
All of the genes that mutations increase susceptibility to, or cause cancer, affect three basic cellular pathways which is cell fate, cell survival, and genome maintenance (Lewis, 2020, p. 374). Cell fate is the differentiation or specialization. Cell survival is the oxygen availability and preventing apoptosis. Genome maintenance refers to the abilities to survive in the presence of reactive oxygen species and toxins, to repair DNA, to maintain chromosome structure, and to correctly splice mRNA molecules (Lewis, 2020, p. 374).
A cancer cell has a different look than a normal cell. Cancer cells can be rounder than the cells they descend from because they do not conform to surrounding normal cells as strongly as other cells do (Lewis, 2020, p. 377). Their plasma membrane is more fluid, different substances cross it. A cancer cell’s may have different antigens that are on other cells or different numbers of the antigens that are also on normal cells (Lewis, 2020, p. 377). Mitosis is similar to a runaway train that is racing along without signals or controls, this is the red flag. Cancer starts when a cell divides more frequently than noncancerous cells that is comes from (Lewis, 2020, p. 375). The timing, rate, and number of mitoses a cell undergoes will depend on protein growth factors, the transcription factors from within, and signaling molecules from outside the cell. Cancer cells arise more quickly because mitoses are frequent (Lewis, 2020, p. 375). However, the immune system steps in to destroy cancer cells after recognizing tumor-specific antigens on their surfaces. The checkpoints that control the cell cycle can reveal how the cancer started (Lewis, 2020, p. 375). A mutation in a gene that normally halts the cell cycle can lift the constraint, leading to inappropriate mitosis. The failure to halt long enough to repair DNA can allow a mutation in an oncogene or tumor suppressor gene to persist. This loss of control can contribute to cancer by affecting the cell cycle (Lewis, 2020, p. 375).
Lewis, R. (2020). Human Genetics (13th Edition). McGraw-Hill Higher Education (US). https://digitalbookshelf.southuniversity.edu/books/9781260539189