Auxotroph Yeast and Human DIseases

.docx

School

New Mexico State University *

*We aren’t endorsed by this school

Course

2110L

Subject

Biology

Date

May 2, 2024

Type

docx

Pages

4

Uploaded by gradoabigail1001 on coursehero.com

Abigail Grado BIOL- 2110L April 23, 2024 Yeast and Human Diseases Phototrophic yeast is the common strain, which can obtain all the needed nutrients from single vitamin and sugar, while auxotrophic yeast occurs due to a mutation of genes in phototrophic yeast that have created alleles of genes which code defective enzymes (Marion, et. al., 2018). This auxotrophic yeast may be described by unique genotypes and not being able to synthesize AMP. The mutation prevents auxotrophic yeast to complete these pathways, forcing these to require other supplemental nutrients. Alkaptonuria is an inherited disorder, in which patient urine turns black, and has the same pathway as phenylketonuria (PKU). Individuals that suffer from PKU have the inability to metabolize phenylamine and other related compounds (Marion, et. al., 2018). PKU has such an unusual phenotype which the patients were mentally retarded, had a distinct odor which resulted from phenylpyruvic acid, and had lighter-colored hair/skin than relatives. Both of these human diseases are abnormalities in specific enzymes. One of the most notable similarities between auxotrophic, PKU, and alkaptonuria is that certain proteins may not be metabolized/synthesized. All lack an enzyme that initiates the breakdown caused by a mutation. The auxotrophic yeast is not capable of synthesizing AMP, this molecule consists of adenine, ribose, and a phosphate group. Auxotrophic yeast may result in red pigmentation due to excess reactants accumulated as these have not been transformed into products. Meanwhile, PKU and alkaptonuria are both incapable of metabolizing/absorbing phenylalanine (Marion, et. al., 2018). As patients that suffer from PKU are unable to metabolize compounds such as phenylalanine, due to the absence of the enzyme that catalyzes this protein in
the liver. Additionally, the mutations of PKU and alkaptonuria result in the formation of enzymes which are no longer functional, and the auxotrophic yeast may have enzymes present, but these are uncapable of developing pathways which permit synthesis. Moreover, some pigment alterations can be caused by auxotrophic yeast and PKU. As noted, auxotrophic yeast strains may result in red pigmentation due to excess accumulation of certain reactants, while PKU may result in lighter pigmentation (Marion, et. al., 2018). Thus, auxotrophic yeast and the human diseases share similarities regarding inability to synthesize certain proteins, absences of enzymes, and in some cases pigment alteration. Despite auxotrophic yeast and these human diseases sharing some similarities, there are other differences that can be identified. Even if PKU and auxotrophic yeast strains may alter pigmentation, these are caused by completely different reasons. As previously mentioned, auxotrophic yeast results in red pigmentation due to excess reactants accumulated as they have not transformed into products, while PKU causes lighter pigmentation as pigment melanin made from tyrosine is not synthesized but obtained in diets (Marion, et. al., 2018). Alkaptonuria and PKU result from gene mutations, but patients with these diseases do not need supplementary nutrients as the auxotroph yeast do. Moreover, auxotroph yeast are in the haploid stage of their life compared to the human diseases. The auxotroph yeast is capable of growing/ dividing during this stage unlike human diseases. Lastly, it can be noted that yeast can be considered an organism, which can mate, grow and divide, in comparison the human disease discussed are only mutations in a patient’s genes rather than organisms living inside of them. There are many ethical, social, and legal implications that must be considered for genetic testing. Regardless of the indisputable effect genetic testing has on medicine and public health, there are some boundaries that need to be set (National Library of Medicine, 1994). For instance,
Your preview ends here
Eager to read complete document? Join bartleby learn and gain access to the full version
  • Access to all documents
  • Unlimited textbook solutions
  • 24/7 expert homework help