Auxotroph Yeast and Human DIseases
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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,
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Related Questions
1. These questions will utilize yeast analysis and provide you with mock experimental
data for the phenotypic analysis of yeast growth to infer genotypes. The following
symbols indicate growth or no growth on medium lacking particular components
(examples in 1A are medium lacking methionine "-MET" and medium lacking tryptophan
"-TRP". Growth is indicated by a filled, black circle. No growth on a particular medium is
indicated by an unfilled circle. In cases where we look viability of spores, we would use
absence of a circle to indicate that a spore did not grow at all (for example, it inherited a
lethal mutation).
Growth No growth
1A. You have two haploid strains (Haploid of opposite mating types. Their genotypes
and phenotypes are shown below.
+MET
- TRP - MET +TRP
Haploid 1 MATA: MET2 trp3
Haploid 2 MATalpha: met2 TRP3
You cross each strain to a WT yeast and observe the following:
Haploid 1 x WT= Growth on all three media shown above.
Haploid 2 x WT= Growth on all three media shown…
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Why is “Agrobacterium-mediated genetic transformation” in plants described as natural genetic engineer of plants?
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Before JCVI-syn3.0 was produced, what steps were used to create a synthetic Mycoplasma cell? Put the events below into the correct order.
Drag and drop the events into the proper sequence from left to right.
▸ View Available Hint(s)
First Step
Transformed cells are
detected by the presence
of lacz, which causes
them to cleave Xgal and
produce a blue color.
Yeast is transformed
using Mycoplasma mycoides
fragments.
The synthetic chromosome
is transformed into
Mycoplasma capricolum.
The synthetic
Mycoplasma mycoides
chromosome is purified.
DNA fragments
assemble through
homologous recombination
in yeast.
Reset Help
Last Step
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Flavr savr Tomato Golden rice, Roundup ready soyabean
In order to generate GM foods mentioned above, various gene transfer methods are required
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deliver foreign genes into plants.
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Schizosaccharomyces pombe, also known as "fission yeast," is a powerful model organism in molecular
and cell biology. While performing a genetic screen, you discover an auxotrophic S. pombe strain that
is unable to synthesize one or more vitamins. The following table represents the key experiments you
performed during your genetic screen. Fill in the table with the outcome of each experiment for your
mutant strain (using + for growth and - for no growth).
Medium
Rich media
Minimal media
Minimal media +
all vitamins
Minimal media +
all amino acids
Growth
Wild-type
+
+
+
+
Mutant
+
+
+
>
>
>
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What is the differences in the ability of different strains to grow on different mediums. Propose a hypothesis that helps to explain the presence of red yeast colonies.
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Three haploid fungal mutants that require compound W for growth were isolated.
Each mutant contains a recessive allele in a single gene. Three compounds (A, B and
C) in the biosynthetic pathway to W are known, but their order in the pathway is
unknown. Each compound is tested for its ability to support the growth of each of
the three mutants. Phenotypes of all of the three mutants are shown in the following
table (“+" indicates growth, "-" indicates no growth).
A
C
W
Mutant 1
Mutant 2
Mutant 3
What would be the phenotype of a haploid mutant that contains both mutant alleles
in mutant 2 and 3? Phenotype refers to growth or absence of growth on compounds
A, B, C and WN.
O Like mutant 1
O Like mutant 2
Like mutant 3
O Like wild type
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BICD100 HW6 Prokaryotic Genetics
Question 1. You are interested in three genes in bacteriophage. The recessive mutant alleles cause
plaque phenotypes that were creatively named fuzzy, shaky, and purple. Another lab published the
following map of the three genes:
fuzzy shaky
2.9
17.4
purple
To verify the published map, you cross a purple shaky phage strain with a fuzzy phage strain by co-
infecting E. coli at a high multiplicity of infection (every bacterium infected with both types of phage).
You plate the resulting lysate and analyze the phenotypes of the plaques caused by the progeny phage.
a. State the genotypes of the two parent phage strains:
b. List all eight of the possible phenotypes that could result from this cross. If 400 phage plaques were
examined from this cross, how many plaques of each of the eight phenotypic classes would you expect?
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The figure below shows the life cycle of the fungus Neurospora. The adult stage of the Neurospora is a multicellular haploid.
b) Neurospora has an arginine amino acid synthesis pathway shown below. Suppose I take the strain above that only grows with arginine supplements and cross it to a different mutant Neurospora strain that grows with arginine and citrulline supplements but not with ornithine supplements. Assuming gens A, B, and C are unlinked and there is only one mutation per stain:
What percentage of the progeny will grow on ornithine?
What percentage on citrulline?
What percentage on arginine?
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In this activity you will analyze the results of experiments that investigate nutritional requirement of
several mutant strains of yeast. The mutations in these strains cause a nutritional requirement for an
amino acid, such that the strains will not grow in media that lack one specific amino acid. Any mutant
that has a nutritional requirement is called an auxotroph, and is incapable of growing in a "minimal
medium" containing only a carbon source (e.g., glucose), a simple nitrogen source (e.g., ammonium
sulfate), and various salts and minerals. Such strains can be supported on a medium supplemented
with only the missing nutrient or on a "rich" medium that contains amino acids, vitamins, nitrogenous
bases, etc. (often in the form of an extract from yeast). The wild-type individual that can synthesize
the metabolic component is a prototroph, and is capable of growth on minimal medium.
The mutant strains in this activity are unable to synthesize tryptophan, lysine, or histidine; one…
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Wild type yeast can normally grow on solid or liquid minimal medium; you isolate three mutant strains which are no longer capable of growing on minimal medium alone, however, they can grow on medium supplemented with adenine.
All three yeast strains are homozygous for the underlying alleles.
When you cross mutant strain 1 and mutant strain 2, the offspring cannot grow on minimal medium alone and require adenine supplementation;
when you cross mutant strain 1 and mutant strain 3, the offspring can grow on minimal medium alone and do not require adenine.
After crossing the F1 generation of the cross between mutant strains 1 and 3, you count and determine the phenotypes of 1,000 colonies (here a colony is equivalent to an individual): 563 colonies that can grow on minimal medium alone; 437 colonies that require adenine…
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Wild type yeast can normally grow on solid or liquid minimal medium; you isolate three mutant strains which are no longer capable of growing on minimal medium alone, however, they can grow on medium supplemented with adenine.
All three yeast strains are homozygous for the underlying alleles.
When you cross mutant strain 1 and mutant strain 2, the offspring cannot grow on minimal medium alone and require adenine supplementation;
when you cross mutant strain 1 and mutant strain 3, the offspring can grow on minimal medium alone and do not require adenine.
A. What conclusions can you make about the alleles of mutant strains 1, 2, and 3 and their relationships with each other?
B. What phenomenon is occurring in the cross between mutant strains 1 and 3?
After crossing the F1 generation of the cross between mutant strains 1…
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Wild type yeast can normally grow on solid or liquid minimal medium; you isolate three mutant strains which are no longer capable of growing on minimal medium alone, however, they can grow on medium supplemented with adenine.
All three yeast strains are homozygous for the underlying alleles.
When you cross mutant strain 1 and mutant strain 2, the offspring cannot grow on minimal medium alone and require adenine supplementation;
when you cross mutant strain 1 and mutant strain 3, the offspring can grow on minimal medium alone and do not require adenine.
A. What conclusions can you make about the alleles of mutant strains 1, 2, and 3 and their relationships with each other?
B. What phenomenon is occurring in the cross between mutant strains 1 and 3?
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After preparing cultures and completing a six-hour growth and viability trial, you
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concentration experimental culture. Your medium and high concentration
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based on
“Targeted polyelectrolyte complex micelles treat vascular complications in vivo”, PNAS 2021, Vol. 118 No. 50 e2114842118;107:110210; https://doi.org/10.1073/pnas.2114842118
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21:14
+4G
KB/S LTED 41 96
09.00 Vo
Microsoft Word - Assignment 02.docx
Assignment 02
1. Groups of alleles associated with the lactose operon are as follows (in order of
dominance for each allelic series): repressor, IS (superrepressor), I *(inducible), and
I "(constitutive); operator, OC (constitutive, cis dominant) and 0+ (inducible, cis-
dominant); structural, Z and Y.
(a) Which of the following genotypes will produce B-galactosidase and B-galactoside
permease if lactose is present: (1) 1*0* Z* Y*, (2) 1 *OCZ+ Y+, (3) OCZ+ Y+, (4) IS O+ Z+
Y+, and (5) 10+ Z+Y+?
(b) Which of the above genotypes will produce ß-galactosidase and ß-galactoside
permease if lactose is absent? Why?
2. By what mechanism does the presence of tryptophan in the medium in which E. coli
cells are growing result in premature termination or attenuation of transcription of
the trp operon?
3. Suppose that you used site-specific mutagenesis to modify the trpL sequence such
that the two UGG Trp codons at positions…
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#22) You have identified five genes in S. cerevisiae that are induced when the yeast are grown in a high-salt (NaCl) medium. To study the potential roles of these genes in acclimation to the growth in high-salt conditions, you wish to examine the phenotypes of loss-and-gain-of-function alleles of each. How will you do this?
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Cap, EA1, and Sap are all genes/proteins of interest in this study. For each gene, what gene product is encoded and where is the gene (the literal DNA sequence) located physically in the cell?
I need help fimiding this in the artticle and answer as short as possible
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106848/
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52.
Papaya plants are very susceptible to the papaya ringspot virus (PRSV), which stunts the growth of the fruit and negatively impacts the taste. By 1995, PRSV wiped out the Hawaiian papaya crop completely and made it impossible to produce papaya commercially. In 1998, Cornell University developed a genetically modified papaya called Rainbow that was resistant to PRSV and introduced it to Hawaii. Currently, 80% of the papaya cultivated in Hawaii is genetically modified to be resistant to PRSV.Which of the following rows identifies the effect of PRSV on the original papaya population and the reason why the population recovered?
Select one:
a.
Effect on the Original Population
Reason for Recovery
Population bottleneck
Some papaya had the PRSV-resistance gene.
b.
Effect on the Original Population
Reason for Recovery
Increased gene flow
The PRSV-resistance gene had to be artificially introduced to the papaya genome
c.
Effect on the Original Population
Reason…
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a- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866609/pdf/pnas.201800195.pdfb- (Article is no longer available)
Here are the articles provided within the question - They are not needed but are available if additional information is warranted - The figures being mentioned are already provided. This is Biochemoistry, please answer each part to the best of your ability. There are a max of 3 parts due to guidelines and please answer each part with clear and efficient work with answers. Thank you
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Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able…
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Robert Bost and Richard Cribbs studied a strain of E. coli (araB14) that possessed a nonsense mutation in the structural gene that encodes Lribulokinase, an enzyme that allows the bacteria to metabolize the sugar arabinose (R. Bost and R. Cribbs. 1969. Genetics 62:1–8). From the araB14 strain, they isolated some bacteria that possessed mutations that caused them to revert back to the wild type. Genetic analysis of these revertants showed that they possessed two different suppressor mutations. One suppressor mutation (R1) was linked to the original mutation in L-ribulokinase and probably occurred at the same locus. By itself, this mutation allowed the production of L-ribulokinase, but the enzyme produced was not as effective in metabolizing arabinose as the enzyme encoded by the wild-type allele. The second suppressor mutation (SuB) was not linked to the original mutation. In conjunction with the R1 mutation, SuB allowed the production of L-ribulokinase, but SuB by itself was not able…
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Cystic fibrosis (CF) is a genetic disorder affecting a number of organs, including
the lung airways, pancreas, and sweat glands.
Mutations in both copies of the CFTR gene causes cystic fibrosis.
Imagine that you have sweat gland samples from several Cystic Fibrosis patients
(A-C) with unknown mutations in CFTR.
You also have normal (+) sweat gland sample to use as a positive control.
А В С
А В С
Choose which mutation would explain the
RNA and protein results in A, B, & C:
1. Promoter/Regulatory mutation
2. Silent mutation
3. Missense mutation
4. Deletion mutation
5. Splice site mutation
6. Nonsense mutation
RNA gel
Protein gel
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In the early 1990s, Carolyn Napoli and her colleagues were working on petunias, attempting to genetically engineer a variety with dark purple petals by introducing numerous copies of a gene that encodes purple pigment in the flower petals (C. Napoli, C. Lemieux, and R. Jorgensen. 1990. Plant Cell 2:279–289). Their thinking was that extra copies of the gene would cause more purple pigment to be produced and would result in a petunia with an even darker hue of purple. However, much to their surprise, many of the plants carrying extra copies of the purple gene were completely white or had only patches of color. Molecular analysis revealed that the amount of mRNA produced by the purple gene was reduced 50-fold in the engineered plants compared with wild-type plants. Somehow, the introduction of extra copies of the purple gene silenced both the introduced copies and the plant’s own purple genes. Provide a possible explanation for how the introduction of numerous copies of the purple gene…
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Experiment:
Page 6 de can exist stably in either a haploid or a diploid state. A haploid S. cerevisiae
mes. When certain haploids come into contact, they fuse their cell walls and
membranes, followed by the fusion of their nuclear membranes. The single nucleus now has 32
chromosomes, 16 from each parent strain, and is thus a diploid.
Haploid yeast strains divide mitotically to give rise to haploid progeny, and diploid strains divide
mitotically to give rise to diploid progeny. Certain haploids can fuse to form diploids. Haploid S.
cerevisiae exists in two "mating types," called a and a Mating occurs only between a and a cells; no
mating occurs between cells of identical mating type.
We have a collection of eight a haploid mutant strains and eight & haploid mutant strains of yeast
unable to synthesize tryptophan (trp). These will be combined (mated) in all possible combinations
to yield diploid strains. If the diploids can grow on minimal medium, complementation occurred
between the…
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What is “translocation”? Why it is essential for plants.
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Human Biology- MILESTONE 6 X
P genetics-and-biotechnology-glo
O
https://app.sophia.org/spcc/human-biology-2-mile
->
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UNIT 6 – MILESTONE 6
Which of the following is a gene abnormality in which two
nonhomologous parts rearrange and fuse together?
O Translocation
O Deletion
None of these,
O Duplication
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