The expression levels for two genes measured at four times are: Compute the correlation coefficient for this pair of genes. Make a plot of the gene1 levelsagainstthe gene 2levels.Isthe informationinthe plot consistent with the implication of the correlation coefficient? Comment on potential hazards of using the correlation coefficient based on your findings.

The expression levels for two genes measured at four times are: Compute the correlation coefficient for this pair of genes. Make a plot of the gene1 levelsagainstthe gene 2levels.Isthe informationinthe plot consistent with the implication of the correlation coefficient? Comment on potential hazards of using the correlation coefficient based on your findings.

Concepts of Biology

1st Edition

ISBN:9781938168116

Author:Samantha Fowler, Rebecca Roush, James Wise

Publisher:Samantha Fowler, Rebecca Roush, James Wise

Chapter10: Biotechnology

Section: Chapter Questions

Problem 13CTQ: Identify a possible advantage and a possible disadvantage of a genetic test that would identify...

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. The human IGF2 gene is autosomal and maternallyimprinted. Copies of the gene received from themother are not expressed, but copies received fromthe father are expressed. You have found two allelesof this gene that encode two different forms of theIGF2 protein distinguishable by gel electrophoresis.One allele encodes a 60K (Kilodalton) blood protein;the other allele encodes a 50K blood protein. In ananalysis of blood proteins from a couple named Billand Joan, you find only the 60K protein in Joan’sblood and only the 50K protein in Bill’s blood. Youthen look at their children: Jill is producing only the50K protein, while Bill Jr. is producing only the 60Kprotein.a. With these data alone, what can you say about theIGF2 genotype of Bill Sr. and Joan?b. Bill Jr. and a woman named Sara have two children, Pat and Tim. Pat produces only the 60K protein and Tim produces only the 50K protein. Withthe accumulated data, what can you now say aboutthe genotypes of Joan and Bill Sr.?
stion 6 of 18 Suppose that a geneticist discovers a new mutation in Drosophila melanogaster that causes the flies to shake and quiver. She calls this mutation quiver, qu, and determines that it is due to an autosomal recessive gene. She wants to determine whether the gene encoding quiver is linked to the recessive gene for vestigial wings, vg. She crosses a fly homozygous for quiver and vestigial traits with a fly homozygous for the wild-type traits, and then uses the resulting F, females in a testcross. She obtains the flies from this testcross. Phenotype Number of flies vg* qu+ 230 vg qu 224 vg qut vg* qu 97 99 Test the hypothesis that the genes quiver and vestigial assort independently by calculating the chi-squared, X², for this hypothesis. Provide the X2 to one decimal place. X2 = Does the X value support the hypothesis that the quiver and vestigial genes assort independently? Why or why not? the partial table of critical values for X2 calculations to test this hypothesis.
This is about Prediction of Genetic Gain. Kindly provide me the answer with solution.
I know the answer is e but can you thoroughly explain the answer choices? like what does constitutive, inducible, expressed mean? and how do these conditions come about?
Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand thecause of the aberrant phenotypes and develop newtherapeutic measures. However, such mice are not always as useful to investigators as it might seem at firstglance. Suppose that you have a mouse knockoutmodel for a human disease caused by homozygosityfor a null allele of a gene. Discuss how the followingsituations might complicate investigations of the human disease based on this mouse model.a. Mice have a shorter life span than humans.b. Mice homozygous for certain knockout mutationsdie in utero.c. Mouse genomes may have additional copies of thegene whose mutation causes the disease in humans.d. Mice from different inbred lines homozygous forthe same gene knockout vary in the penetrance andexpressivity of the phenotype.e. Manipulations to create the knockout mouse, suchas the presence of a drug resistance gene that allowsthe selection of cells containing the knockout (seeFig. 18.9),…
Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand thecause of the aberrant phenotypes and develop newtherapeutic measures. However, such mice are not always as useful to investigators as it might seem at firstglance. Suppose that you have a mouse knockoutmodel for a human disease caused by homozygosityfor a null allele of a gene. Discuss how the followingsituations might complicate investigations of the human disease based on this mouse model.a. Mice have a shorter life span than humans.b. Mice homozygous for certain knockout mutationsdie in utero.c. Mouse genomes may have additional copies of thegene whose mutation causes the disease in humans.
A complex biochemical pathway is shown below, along with the alleles that either promote or inhibit each step of the pathway leading to a phenotype. Gene A has alleles A and a, B has alleles B and b, and so forth. Genes B and C are duplicate dominant epistatic lethal as heterozygotes (i.e. Bb Cc are lethal). Genes D and E are duplicate dominant epistatic (i.e. dd eg = desired phenotype). If I were to cross AA Bb cc Dd Ee with aa BB Cc Dd e, (i) (ii) What proportion of all offspring don't show the phenotype? What proportion of offspring survive? Gene A Gene B B Gene D a Gene C Gene E
What is dosage compensation? Give its importance. explain please
1. DO NOT ROUND OFF YOUR ANSWERS PREMATURELY. Use the unrounded and complete values when computing for the genetic gain; 2. Upon encoding, all final answers should be rounded-off to TWO decimal places. Examples: 3.5798 = 3.58, 0.0079 = 0.01, 0.00000008 = 0.00; 2. Report your answers as NUMERIC VALUES only. Please exclude the units; 3. Write ONLY one answer for each question. Avoid using "or", "/", "&" and "and". Provide only what is asked to you; 4. AVOID using unnecessary PUNCTUATIONS (. , ? 1; ; etc.), SYMBOLS ( []{ } etc.) and SPACES (before or after your answer). Please follow these instructions carefully. Prediction of Genetic Gain. If the milk yield of a herd of cow is 6,479 kg while those kept for breeding is 6,890 kg, and the h2 estimate of milk yield is 0.85. And the generation interval of dairy cattle is 4 years. What will be the expected genetic gain in the milk yield (kg/year) of the next generation?
e. You also study the expression of 2 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? o If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above).
Identify a possible advantage and a possible disadvantage of a genetic test that would identify genes in individuals that increase their probability of having Alzheimer’s disease later in life.
Explain at the biochemical or enzymatic level, the phenotypic consequencesof alleles incase of following cross. Rr (pink flower) x Rr (pink flower) (progeny are 1 RR (red flower) :2 Rr (pink flower): 1rr(white flower) how alleles contribute to a phenotype through metabolism.